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S Dohi

Publications and source records attributed to S Dohi.

At least 73 records · Page 4Linked to original sources
PubMed1998

Prediction of patients with higher order multifetal pregnancy at risk for postpartum pulmonary edema.

OBJECTIVE: This retrospective study aims to verify the factors for the development of maternal pulmonary edema in higher order multifetal pregnancy. STUDY DESIGN: We analyzed medical profiles of a total of 13 triplet, quadruplet and quintuplet pregnancies for the years 1992 through 1997. Some treatments were applied in attempts to promote these multifetal pregnancies. All underwent cesarean section, two of which developed pulmonary edema within a few hours of delivery. There had been no evidence for the development of pulmonary edema antepartum. RESULTS: In the patients affected by pulmonary edema, postoperative values of PaO2/FIO2<250 mmHg showed close association to a value perioperative fluid loading index (FLI)>0; the index consists of an intraoperative fluid balance and preoperative infusion volume within 24 h prior to surgery. Two patients with postoperative pulmonary edema had a perioperative FLI>0, whereas the others had values 0 may have a much higher risk for postoperative pulmonary edema, suggesting the predictive role of the perioperative FLI value.

Adult↗
PubMed1998

Marked increases of aminotransferase levels after cresol ingestion.

A 26-year-old woman developed marked increases in levels of aminotransferases about 24 hours after ingestion of 70 mL of 50% cresol. Responding to supportive measures, the patient recovered without any significant complications. Cresol and/or its metabolite may have caused transient hepato-cellular injury in this patient. In cresol poisoning, hepato-cellular injury can manifest even after a 24-hour asymptomatic period.

Adult↗
PubMed1998

The vascular effects of topical and intravenous alpha2-adrenoceptor agonist clonidine on canine pial microcirculation.

UNLABELLED: To assess the direct cerebrovascular effects of clonidine, we investigated the pharmacological responses of pial vessels to its topical and i.v. administration using a cranial window. Forty-six dogs anesthetized with pentobarbital had the cranial window implanted. We administered six different concentrations of clonidine (10(-8), 10(-7), 10(-6), 10(-5), 10(-4), 10(-3) mol/L) dissolved in artificial cerebrospinal fluid under the window and measured the pial arterial and venous diameters. After pretreating pial vessels with either yohimbine, an alpha2-adrenoceptor antagonist, or glibenclamide, an adenosine triphosphate-sensitive K+-channel blocker, their action was examined after applying clonidine. We also evaluated the effects of i.v. clonidine (5 microg/kg) on pial vascular tone. Topical clonidine produced significant constriction of the pial large and small arteries and veins in a concentration-dependent manner (P < 0.05). Yohimbine abolished the clonidine-induced pial arterial (large P < 0.005; small P < 0.0005) and venous constriction (large and small P < 0.0001). Glibenclamide potentiated the clonidine-induced pial arterial constriction (P < 0.05). I.v. clonidine did not cause significant changes in pial arteries, but it caused significant constriction of small veins. These were associated with a significant decrease in heart rate and an increase in serum potassium level and glucose concentration. In the present study, we demonstrate that the topical application of clonidine constricts both pial arterial and venous vessels in a concentration-dependent manner and suggest that mechanisms of such action are caused by the activation of alpha2-adrenoceptors and adenosine triphosphate-sensitive K+-channels, whereas i.v. clonidine constricts only pial small veins. IMPLICATIONS: In this study, we describe the direct and i.v. effects of clonidine on pial vessels using a cranial window in anesthetized dogs. The topical application of clonidine constricts pial vessels. This is mediated by the activation of alpha2-adrenoceptors and adenosine triphosphate-sensitive K+-channels. I.v. clonidine constricts only pial small veins.

Adjuvants, Anesthesia↗
PubMed1998

The optimal test dose of epinephrine for epidural injection with lidocaine solution in awake patients premedicated with oral clonidine.

UNLABELLED: We attempted to determine the optimal test dose of epinephrine for use with epidural anesthesia in awake patients premedicated with clonidine. Eighty-eight adult patients were randomized into two groups [oral premedication with clonidine 5 microg/kg (CLON) or no premedication (CONT)]. Before induction of general anesthesia, heart rate (HR) and blood pressure (BP) were measured for 3 min after the i.v. injection of 3 mL of 1.5% lidocaine containing epinephrine (0, 1.25, 2.5, 5, 7.5, or 15 microg) in a randomized, double-blind manner. We calculated 95% confidence intervals for the peak HR and BP increases induced by each dose of epinephrine. At 7.5 microg, epinephrine induced a significantly greater increase in HR and BP in CLON than in CONT. The 95% confidence interval for the HR change induced by 7.5 microg of epinephrine in CLON was nearly the same as the accepted standard dose of epinephrine (15 microg) in CONT. We conclude that premedication with clonidine enhances HR and BP responses to the i.v. administration of epinephrine-containing epidural test solutions. Consequently, 7.5 microg of epinephrine may be sufficient to enable detection of accidental injection into a blood vessel in awake patients premedicated with clonidine 5 microg/kg. IMPLICATIONS: Clonidine, a commonly used preanesthetic medication, alters patients' cardiovascular responses to drugs such as epinephrine. Our randomized, double-blind study suggests that, in awake patients receiving oral clonidine premedication, 7.5 microg of epinephrine (half the usual dose) is adequate as an indicator of accidental injection into the epidural vessels during epidural anesthesia.

Adult↗
PubMed1998

Pulmonary arterial and right ventricular responses to prophylactic albumin administration before aortic unclamping during abdominal aortic aneurysmectomy.

UNLABELLED: During abdominal aortic aneurysmectomy (AAAectomy) and before aortic unclamping (XU), we studied the effects of albumin administration on pulmonary arterial and right ventricular responses in 39 anesthetized patients using a modified thermodilution technique. Group 1 patients (n = 18) were given no extra IV fluids. Group 2 patients (n = 21) were given additional albumin administration (5% albumin at 10 mL/kg) before XU. After XU, mean arterial blood pressure (MAP) decreased significantly in each group, and MAP and stroke volume index (SVI) were not significantly higher in Group 2 than in Group 1. At 5 min after XU, the patients in Group 2 had a higher mean pulmonary arterial pressure and pulmonary vascular resistance index and a lower right ventricular ejection fraction than those in Group 1 (P < 0.05), but their SVIs were well maintained. These results indicate that albumin administration before XU may not always prevent post-XU hypotension. It caused a significant increase in right ventricular afterload and a significant dilation of the right ventricular cavity; however, right ventricular function was almost equally maintained in both groups. However, because SVI did not increase in some patients (Group 2) with the increase in right ventricular end-diastolic volume index after XU, albumin administration should be performed carefully before XU during AAAectomy. IMPLICATIONS: We studied the effects of albumin administration before aortic unclamping on pulmonary arterial and right ventricular responses during abdominal aortic aneurysmectomy using a modified thermodilution technique. Albumin administration before aortic unclamping may not always prevent hypotension, and it may cause a higher pulmonary arterial pressure than in patients without albumin administration.

Aged↗
PubMed1998

Inhibitory effects of propofol on intracellular signaling by endothelin-1 in aortic smooth muscle cells.

BACKGROUND: Blood pressure decreases when propofol is administered. However, the exact mechanism underlying the vascular effects of propofol has not yet been elucidated. Endothelin produced by vascular endothelial cells is a potent vasoactive peptide that elicits prolonged contraction of vascular smooth muscle cells. The effects of propofol on endothelin-1-induced intracellular signaling in an aortic smooth muscle cell line, A10 cells, were examined. METHODS: Cultured A10 cells were pretreated with propofol for 20 min and then stimulated with endothelin-1. The effect of propofol on the endothelin-1-induced Ca2+ influx into A10 cells was evaluated by measuring intracellular 45Ca2+. The effects of propofol on the endothelin-1-induced activation of phosphatidylinositol-hydrolyzing phospholipase C and phosphatidylcholine-hydrolyzing phospholipase D were evaluated by measuring the formation of inositol phosphates and choline, respectively. The effect of propofol on endothelin-1 binding to its receptor was determined by an [125I] endothelin-1-binding assay. RESULTS: Propofol inhibited the endothelin-1-induced Ca2+ influx, but this was significant only at supuraclinical concentrations. The endothelin-1-stimulated formation of inositol phosphates was significantly suppressed by propofol. However, propofol had no effect on the formation of inositol phosphates induced by NaF, an activator of heterotrimeric guanosine triphosphate (GTP)-binding proteins. Propofol inhibited the endothelin-1-induced formation of choline. Propofol had no effect on the binding of endothelin-1 to its receptor. CONCLUSIONS: These results suggest that propofol inhibits endothelin-1-induced intracellular signaling in vascular smooth muscle cells. The inhibitory effect of propofol might be exerted at a point between the endothelin-1 receptor and its GTP-binding protein. However, because all significant effects are observed at high concentrations, clinical relevance is unclear.

Anesthetics, Intravenous↗
PubMed1998

Isoflurane and sevoflurane induce vasodilation of cerebral vessels via ATP-sensitive K+ channel activation.

BACKGROUND: Activation of adenosine triphosphate-sensitive K+ channels causes cerebral vasodilation. To assess their contribution to volatile anesthetic-induced cerebral vasodilation, the effects of glibenclamide, an adenosine triphosphate-sensitive K+ channel blocker, on the cerebral vasodilation induced by isoflurane and sevoflurane were studied. METHODS: Pentobarbital-anesthetized dogs (n = 24) assigned to one of two groups were prepared for measurement of pial vessel diameter using a cranial window preparation. Each dog received three minimum alveolar concentrations (MAC; 0.5, 1, and 1.5 MAC) of either isoflurane or sevoflurane, and the pial arteriolar diameters were measured in the presence or absence of glibenclamide (10(-5) M) infused continuously into the window. Mean arterial pressure was maintained with phenylephrine. Furthermore, to assess the direct effect of isoflurane and sevoflurane on cerebral vessels, artificial cerebrospinal fluid was administered topically by being bubbled with isoflurane or sevoflurane. The blocking effect of glibenclamide on the vasoactive effects of these anesthetics also were evaluated. RESULTS: Isoflurane and sevoflurane both significantly dilated large (> or = 100 microm) and small (< 100 microm) pial arterioles in a concentration-dependent manner (6% and 10%, 3% and 8% for 0.5 MAC; 10% and 19%, 7% and 14% for 1 MAC; 17% and 28%, 13% and 25% for 1.5 MAC). Glibenclamide attenuated the arteriolar dilation induced by these anesthetics (not significant in isoflurane). Topical application of isoflurane or sevoflurane dilated large and small arterioles both in a concentration-dependent manner. Such vasodilation was inhibited completely by glibenclamide. CONCLUSION: The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane appears to be mediated, at least in part, via activation of adenosine triphosphate-sensitive K+ channels.

Adenosine Triphosphate↗
PubMed1998

Mechanisms underlying cerebrovascular effects of cigarette smoking in rats in vivo.

BACKGROUND AND PURPOSE: The effects of acute smoking on cerebral circulation are controversial. This study was designed (1) to clarify any differences between the effects of cigarette smoking and nicotine infusion and between the effects of single- and multiple-cigarette smoking on cerebral vessels and (2) to probe the mechanism(s) underlying the vascular responses. METHODS: In pentobarbital-anesthetized, mechanically ventilated Sprague-Dawley rats, pial vessel diameters were measured with the use of a cranial window preparation. We studied the effects of (1) 60 puffs per minute of mainstream cigarette smoke from cigarettes having 2 nicotine levels (0.1 and 1 mg per cigarette), (2) administration of nicotine (0.05 mg per body IV), and (3) repeated smoking (four 1 mg nicotine-containing cigarettes at 30-minute intervals) (n=6 each). RESULTS: Inhalation of smoke from a 0.1 or 1 mg nicotine-containing cigarette for 1 minute caused pial arterioles to constrict at 30 seconds (7.2% and 7.3%, respectively) and then to dilate (peak at 5 to 10 minutes; 4.6% and 17.9%, respectively). Nicotine infusion caused pial vasodilation (35.7%) without an initial vasoconstriction. Repeated smoking suppressed the pial vasodilation but not the initial vasoconstriction. The vasodilation induced by a single cigarette was greatly inhibited by pretreatment with mecamylamine or glibenclamide and attenuated by propranolol or Nomega-nitro-L-arginine methyl ester; the initial vasoconstriction was inhibited by seratrodast, a thromboxane A2 receptor antagonist (n=6 in each case). CONCLUSIONS: Single-cigarette smoking had a significant biphasic effect on cerebral arteriolar tone. The vasodilation was attenuated by repeated smoking. The vasodilation is most likely an effect of nicotine, at least in part mediated via sympathetic activation, NO production, and K+ channel activation. The vasoconstriction is partially due to thromboxane A2 induced by cigarette smoke.

Animals↗
PubMed1998

[Two elderly patients with thoracic herpetic pain and post herpetic neuralgia treated with continuous thoracic sympathetic ganglion block through a placed catheter].

Epidural block is very useful in the treatment of herpetic pain and post herpetic neuralgia. However, in the elderly patients with cardiac disease or diabetes mellitus, severe cardiovascular changes may occur by epidural block. Epidural block caused severe hypotension in two elderly patients with herpetic pain and post herpetic neuralgia who had diabetes mellitus or hypertension. Continuous thoracic sympathetic ganglion block with local anesthetics through a placed catheter reduced their pain and caused almost no changes in cardiovascular system.

Aged↗
PubMed1998

[Cerebral oxygen saturation and hemoglobin index under separate brain perfusion].

We monitored bilateral cerebral oxygen saturation and hemoglobin index while the brain received separate perfusion for major vascular surgery. Before surgery, left cerebral oxygen saturation and hemoglobin index were within normal limits but right cerebral oxygen saturation and right hemoglobin index were low. At the end of surgery, right cerebral oxygen saturation was elevated and almost equal to left cerebral oxygen saturation, and right hemoglobin index was elevated too but slightly lower than left hemoglobin index. We found that oxygen delivery to the right cerebral hemisphere improved in comparison with presurgical period. No paralysis or any other neurological complications occurred postoperatively. We conclude that such monitoring is useful during and after anesthesia under separate brain perfusion.

Aged↗
PubMed1998

[Anaphylactic shock associated with a central venous catheter impregnated with chlorhexidine and silver sulfadiazine].

A 28 year-old male patient developed anaphylactic shock on separate occasions, possibly due to the contact with a central venous catheter impregnated with chlorhexidine and silver sulfadiazine. He was successfully resuscitated. On the second operation, blood basophils disappeared and plasma histamine level increased extremely up to 80 ng.ml-1 soon after anaphylactic shock. One year after the first shock, he did not develop anaphylactic shock following the insertion of a central venous catheter without the impregnation. Pin prick test and scratch test showed positive reactions only to chlorhexidine. Latex-specific anti-IgE antibody was not detected. Therefore, chlorhexidine was confirmed as the causative agent of anaphylactic shock. Because chlorhexidine is extensively used as an antiseptic drug in emergency rooms and intensive care units, we should be aware of the possibility of chlorhexidine induced anaphylactic reactions.

Adult↗
PubMed1998

[Comparison of pulse dye densitometry and thermodilution method in cardiac output measurement].

We measured cardiac outputs at forty points from five patients by pulse dye densitometry and compared these with those measured by thermodilution method. We obtained a good correlation (y = 1.090 x = . 0.030, n = 40, 5 cases) and small mean bias (0.348 +/- 0.830 l.min-1, n = 40, 5 cases) between the two methods. We suggest that this method of cardiac output measurement by pulse dye densitometry is not invasive and may be more effective than that by thermodilution method.

Cardiac Output↗
PubMed1998

[Difficult tracheal intubation with von Recklinghausen disease].

We experienced a case of difficult tracheal intubation in a 15-year-old boy with von Recklinghausen disease scheduled for resection of a right neck tumor. His scoliosis made it difficult to intubate and to manage airway because he easily developed dyspnea. We tried nasotracheal intubation with the patient awake under sedation using a bronchofiberscope, but we found an unexpected tumor jeopardizing his airway patency near his vocal cord. Preoperative examination of a tumor in the airway is essential in the anesthetic management of the patients with von Recklinghausen disease.

Adolescent↗
PubMed1998

[Pulmonary fat embolism during bipolar hip endoprosthesis].

Two patients had fatal fat pulmonary embolism during bipolar hip endoprosthesis. Two women, 71-year-old and 76-year-old, with femoral neck fracture underwent bipolar hip endoprosthesis under combined lumbar epidural/general anesthesia. Soon after the placement of bone cement and a femoral stem with a bipolar endoprosthesis in the femoral shaft, the patients developed circulatory collapse. Immediate cardiopulmonary resuscitation did not restore adequate circulation and the patients died 3.5 hours and 1 hour thereafter, respectively. Pathological examination revealed the presence of fat particles within the entire pulmonary arteries, arterioles and capillaries. Main cause of the present pulmonary fat embolism may be an increase in the intramedullary pressure during cement pressurization and femoral stem placement. Anesthetists have to be aware of occurrence of this serious syndrome during bipolar hip endoprosthesis. For earlier detection of this serious complication we recommend to monitor central venous pressure and pulmonary artery pressure in patients undergoing bipolar hip endoprosthesis.

Aged↗
PubMed1998

[Hemorrhagic shock during laparoscopic cholecystectomy detected by transesophageal echocardiography].

A 47-year-old man was scheduled for laparoscopic cholecystectomy under general anesthesia supplemented with epidural anesthesia. A direct arterial line and a transesophageal echocardiogram probe were inserted before surgery. Anesthesia was maintained with nitrous oxide and isoflurane but without epidural anesthesia. Severe hypotension occurred about 30 minutes after introducing pneumoperitoneum but surgeons denied massive bleeding in the operative field. Although this made us difficult to diagnose the incident as massive bleeding or pulmonary air embolism (PAE), a collapsed heart was detected by transesophageal echocardiography (TEE). Its end-diastolic diameter of the left ventricle was reduced to 20 mm and left ventricular end-systolic cavity obliteration was demonstrated. We could easily diagnose the decrease of blood volume due to PAE using TEE.

Anesthesia, Epidural↗
PubMed1997

Alteration of redox state of human serum albumin in patients under anesthesia and invasive surgery.

Human serum albumin is a mixture of mercapt- (HMA, reduced form) and nonmercaptalbumin (HNA, oxidized form). We studied the mercapt<-->nonmercapt conversion of human serum albumin, which reflects the redox state of the extracellular fluids, in cardiac and other common surgical_ patients using high-performance liquid chromatography. Mean values of [(HMA)/(HMA+HNA)]+/-standard deviation, fHMA+/-sigma], for patients who received common surgery (group 1) and cardiac surgery (group 2) at the start of anesthesia were 0.636+/-0.050 (n = 83) and 0.615+/-0.062 (n = 14), respectively. fHMA values were markedly lower than those for healthy male adults of 0.750+/-0.028 (n = 28). fHMA values increased at 24 h after the start of anesthesia and decreased on the 4th postoperative day in most of the patients. These postoperative changes were prominent in cardiac surgical patients. Although fHMA values after the 7th postoperative day recovered to those at the start of anesthesia in almost all of common surgical patients, those in cardiac surgical patients never recovered even on the 21st postoperative day.

Adult↗
PubMed1997

Non-GABAergic effects of midazolam, diazepam and flumazenil on voltage-dependent ion currents in NG108-15 cells.

Non-gamma-Aminobutyric acid (GABA)-mediated effects of benzodiazepines (BZs) have not been widely investigated. However, there is significant evidence in the literature to suggest that several experimental and clinical observations are inconsistent with the commonly accepted GABAergic mechanisms of action for these drugs. The purpose of the present study was to explore electrophysiological effects of midazolam, diazepam and a specific BZ antagonist, flumazenil, using patch-clamp techniques in NG108-15 cells which do not express the GABAA receptor. Midazolam and diazepam decreased Na+, K+ and Ca2+ currents in a dose-related manner. Ca2+ currents were reduced more significantly by diazepam than by midazolam. Flumazenil showed no effects on voltage-dependent ion currents. GABA by itself showed neither effects on the membrane potential nor these ion currents. Midazolam and diazepam, but not flumazenil, exhibited effects on voltage-dependent ion currents in cultured neurons.

Animals↗