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S Dohi

Publications and source records attributed to S Dohi.

At least 37 records · Page 2Linked to original sources
PubMed2001

The differential effects of stereoisomers of ropivacaine and bupivacaine on cerebral pial arterioles in dogs.

UNLABELLED: We investigated whether the stereoisomers of ropivacaine and bupivacaine exert differential effects on the cerebral microcirculation. Pentobarbital-anesthetized dogs (n = 16) were prepared for measurement of cerebral pial vessel diameters by using a closed cranial window preparation. We administered three different concentrations (10(-7), 10(-5), and 10(-3) M) of each of three drug solutions [R(+), racemic, and S(-) forms of ropivacaine (n = 8) or bupivacaine (n = 8)] under the window in a randomized manner and measured cerebral pial arteriolar diameters. Various physiologic data were obtained before and after topical application of each test solution. All three forms of ropivacaine constricted cerebral pial arterioles, each in a concentration-dependent manner. The rank order for degree of vasoconstriction was S(-) ropivacaine > racemic ropivacaine > R(+) ropivacaine. In contrast, R(+) and racemic bupivacaine dilated, but S(-) bupivacaine constricted, cerebral pial arterioles, each in a concentration-dependent manner. We could find no difference in vascular reactivity to these drugs between large (> or = microm) and small (<100 microm) arterioles. Topical application of these drugs induced no changes in mean blood pressure or heart rate. The observed differences in the microvascular alterations induced by the stereoisomers of ropivacaine and bupivacaine suggest that the vasoactive effects of these drugs on cerebral arterioles could, at least in part, depend on their chirality. IMPLICATIONS: The differential effects of the stereoisomers of ropivacaine and bupivacaine on cerebral pial vessels could, at least in part, depend on their chirality.

Amides↗
PubMed2001

Effect of beta-hydroxybutyrate, a cerebral function improving agent, on cerebral hypoxia, anoxia and ischemia in mice and rats.

Although improving energy metabolism in ischemic brain has been accepted for the treatment of cerebrovascular diseases, administration of glucose, as an energy substrate, would aggravate ischemic brain damage via activating anaerobic glycolysis, which leads to lactate accumulation. Beta-hydroxybutyrate (BHB) is one of the ketone bodies that can be utilized as an energy source during starvation. The purpose of our study was to define the protective effects of BHB on brain damage induced by hypoxia, anoxia and ischemia. The isotonic solution of BHB administered 30 min before the induction of ischemia at doses over 50 mg x kg(-1) x h(-1) showed remarkable protective effects against hypoxia and anoxia. BHB administered immediately after a bilateral carotid artery ligation at a dose of 30 mg x kg(-1) x h(-1) significantly suppressed the elevation of cerebral water and sodium contents as well as maintaining high ATP and low lactate levels. In contrast, glycerin, a hypertonic agent, substantially reduced the water content but did not show any significant effect on other parameters. We demonstrated that BHB, unlike glycerin, when used as an energy substrate in ischemic brain, has protective effects on cerebral hypoxia, anoxia and ischemia-induced metabolic change.

3-Hydroxybutyric Acid↗
PubMed2001

Coronary artery bypass grafting with cardiopulmonary bypass is safe and contributes to favorable long-term results.

The aim of this study was to determine the indication for minimally invasive direct coronary artery surgery based on the operative and long-term results of conventional coronary artery bypass grafting with cardiopulmonary bypass. Operative results: The subjects included 505 patients who underwent isolated elective coronary artery bypass grafting with cardiopulmonary bypass from January 1995 through August 1999. The mean age at the time of surgery was 61.9 and the mean number of grafts per patient was 2.6. Long-term results: From January 1984 to December 1995, a total of 907 patients received coronary artery bypass grafting with cardiopulmonary bypass using the internal thoracic artery to the left anterior descending artery with or without saphenous vein grafts to other coronary arteries. The rates of complete and incomplete revascularization were 69.3% (n = 629) and 30.7% (n = 278), respectively. Mean follow-up was 5.95+/-3.0 years. The operative results revealed low output syndrome occurred in 14 patients (2.8%), perioperative myocardial infarction with the appearance of new Q-waves in 5 (1.0%), renal failure requiring transient dialysis in 16 (3.2%), stroke with persistent sequelae in 5 (1.0%), and mediastinitis in 5 (1.0%). Two patients (0.4%) died in the hospital. The long-term results for the 907 patients revealed the 10-year actuarial survival, 10-year cardiac death free, and 10-year cardiac event free rates were 85.7%, 94.1%, and 77.3%, respectively. The 10-year survival rates was 88.4% among patients receiving complete revascularization and 79.3% among those receiving incomplete revascularization (p = 0.0334). The 10-year cardiac death free rate among patients undergoing complete revascularization was 96.3% and 88.7% among those receiving incomplete revascularization (p = 0.0016). The 10-year cardiac event free rates were 82.3% and 67.9%) among patients undergoing complete and incomplete revascularization, respectively (p = 0.0118). In view of the favorable operative and long-term results of conventional coronary artery bypass grafting, especially complete revascularization, we conclude that minimally invasive direct coronary artery grafting is an appropriate treatment for multi-vessel disease in carefully selected patients at a high risk for stroke and major comorbidities due to old age.

Adult↗
PubMed2001

[Finding appropriate endotracheal tube position by Trachlight in children].

Finding appropriate endotracheal tube position in children is important, because the trachea length of a child is shorter than that of an adult, and the position of the endotracheal tube is easy to be altered by head position, rotary movements, and flexion as well as extension. We confirmed the correct depth of the endotracheal tube by transillumination method using the Trachlight device in children. Twenty children were intubated orally with a rigid laryngoscope according to the distance of the formula height/10 + 5 cm at the lips. We measured the distance from the tip of the tube to the sternal notch where the bright light of the Trachlight disappeared. The tip of the endotracheal tube (4.5, 5.0 or 5.5 mm tube size) was placed approximately 1.5 cm beyond the sternal notch. The distance between the carina and the tube tip measured by chest radiography was more than 1 cm. Trachlight device was simple and reliable to ensure the appropriate endotracheal tube position in children. We consider that the appropriate depth of the endotracheal tube using any of 4.5, 5.0 or 5.5 mm tube size is 1.5 cm beyond the point the bright light of the Trachlight disappears.

Anesthesia, General↗
PubMed2001

[Perioperative mortality and morbidity for the year of 1999 in 466 Japanese Certified Anesthesia-training Hospitals: with special reference to ASA-physical status--report of Committee on Operating Room Safety of Japan Society of Anesthesiologists].

Perioperative mortality and morbidity in Japan for the year 1999 were studied retrospectively. Committee on Operating Room Safety of the Japan Society of Anesthesiologists (JSA) sent confidential questionnaires to 774 Certified Training Hospitals of JSA and received answers from 60.2% of the hospitals. We analyzed their answers with special reference to ASA physical status (ASA-PS). The total number of anesthetics analyzed was 655, 644. Mortality and morbidity due to all kinds of causes including anesthetic management, intraoperative events, co-existing diseases, and operation were as follows. The incidence of cardiac arrest (per 10,000 anesthetics) was 0.68, 3.76, 14.37, 67.03, 0.36, 4.68, 27.96, 206.30 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The incidences of critical events including cardiac arrest, severe hypotension, and severe hypoxemia were 8.93, 26.99, 71.30, 188.52, 8.68, 31.27, 136.16, and 790.92 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The mortality rates (death during anesthesia and within 7th postoperative day) after cardiac arrest were 0.16, 0.94, 5.71, 33.51, 0.00, 1.46, 16.41 and 167.76 per 10,000 anesthetics in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The overall mortality rates were 0.24, 1.66, 12.16, 67.03, 0.00, 3.51, 34.65 and 417.14 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. Overall mortality and morbidity were higher in emergency anesthetics than in elective anesthetics. ASA-PS correlated well with overall mortality and with morbidity, regardless of etiology. The incidences of cardiac arrest totally attributable to anesthesia were 0.24, 0.45, 1.47, 8.38, 0.36, 1.75, 2.43 and 11.34 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The incidences of all critical events totally attributable to anesthesia were 4.92, 8.81, 14.74, 20.95, 4.34, 11.40, 15.80 and 22.67 in patients with ASA-PS of I, II, III, IV, I E, II E, III E, and IV E, respectively. The mortality rates after cardiac arrest totally attributable to anesthesia were 0.00, 0.00, 0.61 and 4.53 in patients with ASA-PS of I-IV, I E-II E, III E, and IV E, respectively. The overall mortality rates totally attributable to anesthesia were 0.00, 0.04, 0.18, 0.00, 0.00, 0.61 and 4.53 in patients classified to ASA-PS of I, II, III, IV, I E-II E, III E, and IV E, respectively. Only one death, due to overdose of anesthetics, was reported among patients with good physical status (ASA-PS of I, II, II E and II E). Anesthetic management was mainly responsible for critical events in patients with good physical status, while co-existing diseases were in those with poor physical status. The major co-existing diseases or conditions leading to critical events were heart diseases in elective anesthetics, and hemorrhagic shock in emergency anesthetics. We reconfirmed that ASA-PS is beneficial to predict perioperative mortality and morbidity. It also seems likely that we should make much more efforts to reduce anesthetic morbidity in patients with good physical status, and to improve preanesthetic assessment and preparation of cardiovascular conditions in those with poor physical status.

Anesthesiology↗
PubMed2001

[Perioperative mortality and morbidity in 1999 with a special reference to age in 466 certified training hospitals of Japanese Society of Anesthesiologists--report of Committee on Operating Room Safety of Japanese Society of Anesthesiologists].

Perioperative mortality and morbidity in Japan from Jan. 1 to Dec. 31, were studied retrospectively. Committee on Operating Room Safety of Japanese Society of Anesthesiologists (JSA) sent confidential questionnaires to 774 Certified Training Hospitals of JSA and received answers from 60.2% of the hospitals. We analyzed their answers with a special reference to the age group. The total number of anesthetics available for this analysis was 732,788. All cases were divided in to 7 groups; group A(< 1 months), group B(< 12 months), group C(< 5 years), group D(< 18 years), group E (< 65 years), group F(< 85 years), and group G(> 85 years). The incidences of all critical events including cardiac arrest, severe hypotension, and severe hypoxemia were 168.14, 47.86, 24.63, 14.65, 28.43, 50.4, and 43.68 per 10,000 in patients with group A, B, C, D, E, F, and G, respectively. The overall mortality rate (death during anesthesia and within 7th postoperative day) were 74.10, 6.63, 3.30, 3.07, 4.82, 13.74, and 11.84 per 10,000 anesthetics in patients with group A, B, C, D, E, F, and G, respectively. The incidences of cardiac arrest were 54.15, 8.84, 5.08, 2.56, 4.84, 11.02, and 6.66 per 10,000 in patients with group A, B, C, D, E, F, and G, respectively. The mortality rates after cardiac arrest were 42.75, 2.95, 2.54, 1.70, 2.00, 6.56, and 5.18 in patients with group A, B, C, D, E, F, and G, respectively. The incidences of all critical events, the incidence of cardiac arrest, and the overall mortality rate were much higher in group A than other groups and lower in group D. Mortality and morbidity due to all kinds of causes including anesthetic management, intraoperative events, co-existing diseases, and operation were as follows. The incidence of all critical events attributable to co-existing disease were the highest in these four groups, and 94.04, 15.46, 7.87, 6.13, 7.26, 17.38, and 16.29 per 10,000 in patients with group A, B, C, D, E, F, and G, respectively. The incidences of all critical events attributable to anesthetic management were 31.35, 16.94, 4.60, 6.09, 10.77, and 14.07 per 10,000 in patients with group A, B, C, D, E, F, and G, respectively. The incidence of cardiac arrest in group A was much more attributable to co-existing disease and operation than other causes. The incidences of cardiac arrest attributable to anesthetic management were 0.00, 1.47, 0.25, 0.34, 0.83, 0.92, and 0.22 per 10,000 in patients with group A, B, C, D, E, F, and G, respectively. The mortality rates in these groups were 0.00, 0.00, 0.00, 0.17, 0.07, 0.05, and 1.48, and no death was found in cases under 5 years of age. The two cases of death in G group were due to too high anesthesia levels in spinal anesthesia. Other causes including overdose of anesthetics, toxic effect of local anesthetic, improper management of airway, and incompatible blood transfusion were preventable with the anesthesiologists' effort in protocol development and skilled assistance.

Adolescent↗
PubMed2001

[Non-opioid analgesics in cancer pain].

Non-opioid analgesics such as NSAIDs play a central role for patients with cancer pain as well as for those with acute pain. Pain management using non-opioid analgesics need to avoid potential side effects, and the analgesic action of NSAIDs, cyclooxygenase inhibitors, would synergistically potentiate opioids' effects via the activation of the periaquaductal grey of the midbrain. The analgesic action of opioids would also be potentiated by the activation of alpha 2-adrenoceptors of the spinal cord. Thus the use of non-opioid analgesics for cancer patients taking opioid needs meticulous care. Undertreatment of pain is a persistent clinical problem for patients with cancer. Although changing medical practice is difficult and improving pain management with the rational use of combination of drugs may especially difficult, supplementation of non-opioid analgesics for opioid treatment would provide a better quality of life of cancer patients.

Adrenergic alpha-Agonists↗
PubMed2001

[Annual report of perioperative mortality and morbidity for the year 1999 with a special reference to anesthetic methods at Certificated Training Hospitals of Japanese Society of Anesthesiologists].

The Committee on Operating Room Safety of Japanese Society of Anesthesiologists (JSA) sends annually confidential questionnaires of perioperative mortality and morbidity to Certificated Training Hospitals of JSA. This report is on perioperative mortality and morbidity in 1999 with a special reference to anesthetic methods. Four hundred and sixty-seven hospitals reported the number of cases referred to anesthetic methods and total numbers of cases were 727,723. The incidences of cardiac arrest per 10,000 cases due to all etiology are estimated to be 6.77 cases in average, 5.33 cases in inhalation anesthesia, 34.26 cases in total intravenous anesthesia (TIVA), 5.26 cases in inhalation anesthesia plus epidural or spinal or conduction block, 5.29 cases in TIVA plus epidural or spinal or conduction block, 0.73 cases in spinal with continuous epidural block (CSEA), 2.85 cases in epidural anesthesia, 1.63 cases in spinal anesthesia, 2.53 cases in conduction block and 46.51 cases in other methods. However, the incidences of cardiac arrest per 10,000 cases totally attributable to anesthesia are estimated to be 0.78 case in average, 0.51 case in inhalation anesthesia, 1.35 cases in TIVA, 0.97 case in inhalation anesthesia plus epidural or spinal or conduction block, 1.51 cases in TIVA plus epidural or spinal or conduction block, 0.73 case in CSEA, 1.71 cases in epidural anesthesia, 0.54 case in spinal anesthesia, 2.52 cases in conduction block and 1.08 cases in other methods. The incidences of severe hypotension per 10,000 cases due to all etiology are estimated to be 16.64 cases in average, 13.61 cases in inhalation anesthesia, 100.36 cases in TIVA, 13.32 cases in inhalation anesthesia plus epidural or spinal or conduction block, 9.07 cases in TIVA plus epidural or spinal or conduction block, 3.65 cases in CSEA, 6.26 cases in epidural anesthesia, 7.31 cases in spinal anesthesia, 2.52 cases in conduction block and 28.12 cases in other methods. On the other hand, the incidences of cardiac arrest per 10,000 cases totally attributable to anesthesia are estimated to be 2.40 cases in average, 1.65 cases in inhalation anesthesia, 0.81 cases in TIVA, 3.92 cases in inhalation anesthesia plus epidural or spinal or conduction block, 2.77 cases in TIVA plus epidural or spinal or conduction block, 2.56 cases in CSEA, 3.42 cases in epidural anesthesia, 2.71 cases in spinal anesthesia, zero case in conduction block and zero case in other methods. The incidences of severe hypoxia per 10,000 cases due to all etiology are estimated to be 5.32 cases in average, 6.7 cases in inhalation anesthesia, 9.17 cases in TIVA, 5.16 cases in inhalation anesthesia plus epidural or spinal or conduction block, 4.53 cases in TIVA plus epidural or spinal or conduction block, 2.56 cases in CSEA, zero case in epidural anesthesia, 1.08 cases in spinal anesthesia, zero case in conduction block and 1.08 cases in other methods. On the other hand, the incidences of severe hypoxia per 10,000 cases totally attributable to anesthesia are estimated to be 2.39 cases in average, 3.22 cases in inhalation anesthesia, 2.43 cases in TIVA, 2.26 cases in inhalation anesthesia plus epidural or spinal or conduction block, 2.77 cases in TIVA plus epidural or spinal or conduction block, zero case in CSEA, zero case in epidural anesthesia, 0.54 cases in spinal anesthesia, zero case in conduction block and 1.08 cases in other methods. The mortality rates of cardiac arrest per 10,000 cases due to all etiology are estimated to be 3.56 cases in average, 2.82 cases in inhalation anesthesia, 24.55 cases in TIVA, 1.4 cases in inhalation anesthesia plus epidural or spinal or conduction block, 1.51 cases in TIVA plus epidural or spinal or conduction block, zero cases in CSEA, 0.57 cases in epidural anesthesia, 0.27 cases in spinal anesthesia, zero case in conduction block and 42.18 cases in other methods. On the other hand, the mortality rates of cardiac arrest per 10,000 cases totally attributable to anesthesia are estimated to be 0.08 case in average, 0.09 case in inhalation anesthesia, 0.27 case in TIVA, 0.05 case in inhalation anesthesia plus epidural or spinal or conduction block, zero case in TIVA plus epidural or spinal or conduction block, zero case in CSEA, 0.57 case in epidural anesthesia, zero case in spinal anesthesia, conduction block and other methods. The outcomes of cardiac arrest totally attributable to anesthesia are 70.2% of full recovery without any sequelae, 10.5% of death within 7 days, 1.8% of vegetative state and 17.5% of unknown results while the outcome of critical events including severe hypotension and severe hypoxia totally attributable to anesthesia is 94.9% of full recovery without any sequelae, 0.4% of death within 7 days, 0.2% of vegetative state and 4.5% of unknown results. These results indicate that there are no differences in mortality and morbidity totally attributable to anesthesia among anesthetic methods in 1999 at Certificated Training Hospitals of Japan Society of Anesthesiologists.

Anesthesia↗
PubMed2001

[Perioperative mortality and morbidity for the year 1999 in 466 Japanese certified anesthesia-training hospitals: with special reference to operative regions--report of Committee on Operating Room Safety of Japanese Society of Anesthesiologists].

Perioperative mortality and morbidity in Japan for the year 1999 were analyzed retrospectively with special reference to operative regions. The total number of analyzed cases was 701,940. The percentages for each operative region were as follows, craniotomy 4.5%, thoracotomy 3.3%, heart and great-vessels 3.9%, thoracotomy with laparotomy 0.8%, laparotomy except caeserian-section 31.7%, ceserian-section 3.2%, head-neck and otolarynx 14.5%, chest-abdomen-perineum 11.1%, spine 3.5%, extremity including peripheral-vessel 16.5%, and others 6.9%. The incidence of serious events, including cardiac arrest and severe hypotension and hypoxemia suggesting impending cardiac arrest was 34.58 per 10,000 cases in all operative regions. The events were observed more frequently in heart and great-vessels 247.26, thoracotomy with laparotomy 128.91 and thoracotomy 61.55, and less frequently in chest-abdomen-perineum 13.52 and extremity including peripheral-vessel 16.99. Regarding the prognosis of events, the cases with no sequela were 69.9% in all operative regions. While there were fewer cases with no sequela in craniotomy 50.4%, thoracotomy with laparotomy 54.3% and heart and great-vessels 58.6%, there were more cases in head-neck and oto-larynx 95.2% and chest-abdomen-perineum 90.5%. The incidence of serious events totally attributable to anesthetic management was 7.79 per 10,000 cases in all operative regions. The events were observed more frequently in thoracotomy 12.82, heart and great-vessels 12.29 and spine 11.06, and less frequently in extremity including peripheral-vessel 5.17 and chest-abdomen-perineum 6.05. Regarding the prognosis of events, the cases with no sequela were 93.1% in all operative regions. There were fewer cases with no sequela in thoracotomy with laparotomy 80.0% and craniotomy 81.8%. The main cause of events in thoracotomy and spine was the inadequate airway management, and in heart and great-vessels was the overdose or miss-selection of drugs. Although the incidence of serious events totally attributable to anesthetic management was one fourth of all events, most of them resulted from human factors. Thus, the more efforts are necessary to improve the outcomes. While the total deaths from 701,940 cases, including death on the operation day or within 7 days after it, were 528 cases (7.52 per 10,000 cases), the deaths totally attributable to anesthesia were 7 cases (0.10 per 10,000 cases).

Anesthesia↗
PubMed2001

[Annual study of perioperative mortality and morbidity for the year of 1999 in Japan: the outlines--report of the Japan Society of Anesthesiologists Committee on Operating Room Safety].

Anesthetic mortality and morbidity in Japan Society of Anesthesiologists (JSA) Certified Training Hospitals (CTH) for the year 1999 were reported as continuation of annual studies started in 1993. The JSA Committee on Operating Room Safety (CORS) sent confidential questionnaires to 774 CTH and received valid responses from 60.3% of hospitals. A total number of 793,840 anesthetics were documented. The respondents were asked to report all cases of cardiac arrests and other critical incidents (serious hypotension, serious hypoxemia and others), and their outcomes (death in operating room, death within 7 days, transfer to vegetative state and rescue without sequelae) as well as one principal cause for each incident from list of 52 items. They were also requested to submit the tabulation of patients by ASA physical status, age distribution, surgery sites and anesthetic methods. Analysis was made by total incidents under anesthesia/surgery, and also by incidents totally attributable to anesthetic management (AM), due to preoperative complications (PC), due to intraoperative pathological events (IP) and due to surgery (SG), with special reference to each of four tabulation groups and the whole group of patients. This paper focused analysis on all patients, as analyses with special reference to ASA physical status, age distribution, surgery sites and anesthetic methods were previously reported. Total incidence of cardiac arrest under anesthesia/surgery was 6.53 per 10,000 anesthetics. PC, IP and SG represented principal causes in 42.9%, 22.0% and 21.4% causes of total cardiac arrest cases, respectively. AM was noted as the principal cause in 12.0% of cases, with an incidence rate of 0.78 per 10,000. In 52 more detailed classification of principal causes, the most frequent cause of cardiac arrest was preoperative hemorrhagic shock, 20.3% of all cardiac arrests. The second cause was massive hemorrhage and/or hypovolemia due to surgical procedures (13.1%), and the third was intraoperative myocardial infarction/coronary ischemia/coronary spasm (9.5%). Prognoses of cardiac arrest cases declined due to PC: 71.1% of cardiac arrests died in the operating room or within 7 days after surgery and only 19.8% survived without sequelae. The best prognoses were found in cardiac arrest cases due to AM: 69.4% survived without sequelae and 12.9% died. The mortality rate post-cardiac arrest was 3.44 per 10,000 anesthetics, of those 0.10 due to AM, 0.57 due to IP, 1.99 due to PC and 0.76 due to SG. The mortality rate after critical incidents other than cardiac arrest such as severe hypotension and severe hypoxemia was 3.75, of those 0.03 due to AM, 0.28 due to IP, 2.31 due to PC and 1.13 due to SG. The final mortality rate attributable to anesthesia/surgery including deaths post-cardiac arrest and after other critical incidents was 7.19 per 10,000 anesthetics and very close to 7.18 [6.22, 8.13], that of mean [95% C.I.] in 1994-1998. The final mortality rate totally attributable to anesthesia was 0.13 per 10,000 anesthetics, which was significantly improved from 0.21 [0.15, 0.27], that of mean [95% C.I.] in 1994-1998. IP, PC and SG showed the final mortality rate of 0.84, 4.30 and 1.89, respectively. Five major causes of all critical incidents were massive hemorrhage due to surgical procedures (20.8%), preoperative hemorrhagic shock (10.7%), surgical technique (8.0%), inappropriate airway management (5.2%) and intraoperative myocardial infarction and coronary ischemia (4.5%). Drug overdose or selection error (3.9%) and overdose of main anesthetic (2.9%) as a result of human error occupied the 7th and 10th places. As far as anesthetic management to reduce mortality and morbidity related to anesthesia is concerned, we should increase vigilance to avoid human errors in addition to improving preanesthetic preparations and assessment of cardiovascular status as well as intraoperative management of cardiovascular events.

Anesthesia↗
PubMed2000

Enhancement by sphingosine 1-phosphate in vasopressin-induced phosphoinositide hydrolysis in aortic smooth-muscle cells: involvement of p38 MAP kinase.

We previously reported that sphingosine 1-phosphate (S-1-P), a sphingomyelin metabolite, activates p44/p42 mitogen-activated protein (MAP) kinase and p38 MAP kinase in aortic smooth-muscle A10 cells. In the present study, we investigated the effect of sphingomyelin metabolites on phospholipase C-catalyzing phosphoinositide hydrolysis induced by arginine vasopressin (AVP) in A10 cells. C(2)-ceramide and sphingosine had little effect on inositol phosphate (IP) formation stimulated by AVP. S-1-P, which alone slightly stimulated the IPs formation, dose-dependently amplified the AVP-induced formation of IPs. Tumor necrosis factor-alpha enhanced the AVP-induced formation of IPs. However, S-1-P did not enhance the formation of IPs by NaF, a heterotrimeric GTP-binding protein activator. Pertussis toxin inhibited the effect of S-1-P. PD98059, an inhibitor of the upstream kinase that activates p44/p42 MAP kinase, had little effect on the enhancement by S-1-P. SB203580, an inhibitor of p38 MAP kinase, suppressed the effect of S-1-P on the formation of IPs by AVP. SB203580 inhibited the AVP-induced phosphorylation of p38 MAP kinase. Pertussis toxin suppressed the phosphorylation of p38 MAP kinase by S-1-P. These results indicate that S-1-P amplifies AVP-induced phosphoinositide hydrolysis by phospholipase C through p38 MAP kinase in vascular smooth-muscle cells.

Aorta↗
PubMed2000

Patient anxiety scores after low-dose ketamine or fentanyl for epidural catheter placement.

PURPOSE: To compare the effect of low-dose ketamine with that of low-dose fentanyl on patient anxiety during the identification of the epidural space and catheterization. METHODS: Sixty patients were randomly assigned to one of three groups: saline group (n=20), saline 2 ml; ketamine group (n=20), 5 mg ketamine; or fentanyl group (n=20), 50 microg fentanyl. Each drug was administered intravenously (iv) five to ten minutes before the epidural procedures began. After epidural catheter placement had been accomplished, anxiety and pain were rated using a visual analog scale. RESULTS: The anxiety scores given for ketamine(20.2 +/- 18.5, mean +/- SD) and fentanyl (24.6 +/- 20.3) were similar, and both were lower than that for saline (44.1 +/- 32.7) (P=0.0034 and 0.0153 vs saline group, respectively). Pain scores were similar for all three groups. A decrease in hemoglobin oxygen saturation during the procedure was only observed in the fentanyl group, and two patients in fentanyl group had SpO2 <90%. CONCLUSION: Ketamine, 5 mg iv, is as effective as 50 microg fentanyl, iv, in alleviating patient anxiety and in providing adequate sedation during the procedures necessary for epidural catheter placement, without inducing severe complications.

Adult↗
PubMed2000

Antinociception by epidural and systemic alpha(2)-adrenoceptor agonists and their binding affinity in rat spinal cord and brain.

UNLABELLED: This study was designed primarily to relate the antinociceptive and hemodynamic effects of clinically available alpha(2)-adrenoceptor agonists to their binding affinity for alpha(2)-adrenoceptors in the spinal cord and brain. In rats with chronic indwelling epidural catheters, the percentage maximal possible effect on tail-flick latency was measured after epidural or IM dexmedetomidine (DXM), clonidine (CL), or tizanidine (TZ) administration. To examine their binding affinities, isolated spinal cord and brain membranes with an alpha(2) agonist were incubated with (3)H-UK14304, a selective alpha(2) agonist, and the radioactivity in the reaction mixtures was measured by liquid scintillation spectrometry. Epidural DXM (0.5-10 microg), CL (10-500 microg), and TZ (5-500 microg) all produced dose-dependent antinociceptive effects; the rank order of potencies was DXM > CL > TZ, the same as for their systemic administration. The antinociceptive effects were blocked by epidural yohimbine. The receptor binding affinities expressed as the concentration that inhibits 50% for spinal cord and brain, respectively, were 0.25 and 1.3 nM (DXM), 10.8 and 12.5 nM (CL), and 48.2 and 96.8 nM (TZ). The changes in arterial blood pressure and heart rate evoked by antinociceptive doses did not correlate with the rank order of antinociceptive potencies. The relative antinociceptive potencies of epidural alpha(2) agonists may depend on their binding affinities to alpha(2)-adrenoceptors in the spinal cord, but their cardiovascular effects may result from actions both inside and outside the central nervous system. IMPLICATIONS: Spinal antinociception caused by the epidural administration of alpha(2) agonists is well correlated with their binding affinity to spinal alpha(2)-adrenoceptors.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

Localized airway anesthesia with lidocaine partially suppresses cardiovascular responses To lung inflation.

UNLABELLED: Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H(2)O. Both lungs inflated at 20 cm H(2)O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H(2)O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes. IMPLICATIONS: Localized airway anesthesia with lidocaine is unlikely to suppress the cardiovascular responses to lung inflation. This suggests that a limited number of neurogenic mechanisms are involved in the cardiovascular responses to lung inflation in anesthetized humans.

Adult↗
PubMed2000

Antinociceptive action of epidural K+(ATP) channel openers via interaction with morphine and an alpha(2)- adrenergic agonist in rats.

Potassium (K(+)) channels may play some role in the analgesic actions of mu-opioid agonists and alpha(2)-adrenergic agonists (alpha(2) agonists). We examined whether the adenosine triphosphate-sensitive K(+)(K(+)(ATP)) channel openers, levcromakalim and nicorandil, (given epidurally), might have antinociceptive effects in a tail flick test in adult male Sprague-Dawley rats implanted with a lumbar epidural catheter. The interactions with morphine and an alpha(2) agonist were also examined. The epidural administration of levcromakalim (10 microg, 100 microg) or nicorandil (10 microg, 100 microg) alone did not produce antinociception, but 100 microg levcromakalim or nicorandil did potentiate the antinociceptive effect induced by epidural morphine. Epidural glibenclamide (10 microg), a K(+)(ATP) channel blocker, or naloxone (10 microg) antagonized this potentiation. Systemic administration of levcromakalim or nicorandil (at the same dose as that given into the epidural space) did not potentiate the epidural morphine-induced analgesia. A combination of epidural dexmedetomidine (1 microg) and morphine (1 microg) (each at a subantinociceptive dose) had a significant antinociceptive effect, and epidural glibenclamide (10 microg) partly antagonized this antinociception. These data suggest that levcromakalim and nicorandil potentiate the analgesic action of both morphine and dexmedetomidine, probably via an activation of K(+)(ATP) channels at the spinal cord level.

Adenosine Triphosphate↗
PubMed2000

The effects of pentobarbital, isoflurane, and propofol on immediate-early gene expression in the vital organs of the rat.

General anesthetics are known to transiently increase the expression of messenger ribonucleic acids (mRNAs) of immediate-early genes in the brain. We investigated whether the expression of two immediate-early genes in vital organs were modulated by various anesthetics. Inhaled isoflurane (n = 20), intraperitoneal pentobarbital (n = 20), and IV propofol (n = 20) were administered to male Sprague-Dawley rats, and five from each group were decapitated at 5, 30, 60, or 120 min after the induction of anesthesia. Control, nonanesthetized rats (n = 5) were handled gently and then decapitated. Reverse transcriptase-polymerase chain reactions were performed on total RNA from samples of the brain, heart, liver, and kidney to detect the expressions of c-fos and c-jun mRNAs. As internal control, cyclophilin mRNA was amplified simultaneously. The products were separated by electrophoresis, and the optical density of the bands was quantified. The expression of c-fos mRNA was transiently increased in the brain, and more strikingly and for longer times, in the kidney with all three anesthetics; the expression of c-fos mRNA was decreased in the heart with isoflurane and pentobarbital and increased in the liver with isoflurane and propofol. The expression of c-jun mRNA was increased in the heart, liver, and kidney with isoflurane, increased in the heart and kidney with pentobarbital, increased in the heart, liver, and kidney with propofol, and decreased in the brain with pentobarbital. Our results suggest that the appropriate anesthetics to be used to anesthetize animals differ in accord with the target organs in which the expressions of immediate-early genes in response to stimuli were studied.

Adjuvants, Anesthesia↗
PubMed2000

Characteristics of ropivacaine block of Na+ channels in rat dorsal root ganglion neurons.

UNLABELLED: When used for epidural anesthesia, ropivacaine can produce a satisfactory sensory block with a minor motor block. We investigated its effect on tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant (TTX-R) Na(+) currents in rat dorsal root ganglion (DRG) neurons to elucidate the mechanisms underlying the above effects. Whole-cell patch-clamp recordings were made from enzymatically dissociated neurons from rat DRG. A TTX-S Na(+) current was recorded preferentially from large DRG neurons and a TTX-R Na(+) current preferentially from small ones. Ropivacaine shifted the activation curve for the TTX-R Na(+) channel in the depolarizing direction and the inactivation curve for both types of Na(+) channel in the hyperpolarizing direction. Ropivacaine blocked TTX-S and TTX-R Na(+) currents, but its half-maximum inhibitory concentration (IC(50)) was significantly lower for the latter current (116 +/- 35 vs 54 +/- 14 microM; P: < 0.01); similar IC(50) values were obtained with the (R)-isomer of ropivacaine. Ropivacaine produced a use-dependent block of both types of Na(+) channels. Ropivacaine preferentially blocks TTX-R Na(+) channels over TTX-S Na(+) channels. We conclude that because TTX-R Na(+) channels exist mainly in small DRG neurons (which are responsible for nociceptive sensation), such selective action of ropivacaine could underlie the differential block observed during epidural anesthesia with this drug. IMPLICATIONS: Whole-cell patch-clamp recordings of tetrodotoxin-sensitive and tetrodotoxin-resistant Na(+) currents in rat dorsal root ganglion neurons showed ropivacaine preferentially blocked tetrodotoxin-resistant Na(+) channels over tetrodotoxin-sensitive Na(+) channels. This could provide a desirable differential sensory blockade during epidural anesthesia using ropivacaine.

Amides↗