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S Dohi

Publications and source records attributed to S Dohi.

At least 19 recordsLinked to original sources
PubMed2006

Modified nasal cannula for simultaneous oxygen delivery and end-tidal CO2 monitoring during spontaneous breathing.

BACKGROUND AND OBJECTIVES: Supplemental oxygen is commonly given via nasal cannulae in spontaneously breathing patients. Our modified nasal cannula with a clamp between the nasal prongs can provide O2 via one nostril and CO2 can be sampled through the other one. We have studied whether this cannula can provide oxygenation similar to a standard cannula without affecting end-tidal CO2 monitoring. METHODS: Eighty-six patients were studied during spinal anaesthesia and sedation. In 15 patients, arterial blood was sampled while O2 was delivered at flow rates of 0, 2 and 4 L min(-1), with or without clamping between the prongs of our modified nasal cannula. In the remaining 71 patients, arterial O2 was measured while using our modified nasal cannula with the clamp applied. End-tidal CO2 was recorded on a capnograph and the correlation between end-tidal and arterial values with our modified nasal cannula was investigated. RESULTS: No end-tidal CO2 waveforms were found with oxygen flow greater than 2L min(-1) without clamping between the prongs. With clamping there was a significant correlation (r = 0.83) between arterial and end-tidal CO2. A Bland-Altman analysis revealed a bias of 0.49 kPa with precision of +/-0.76 kPa. Arterial oxygenation was not affected by our modified nasal prongs with clamp as compared to the standard cannula. CONCLUSION: Our modified nasal cannula can provide continuous monitoring of end-tidal CO2 without affecting oxygen delivery in sedated, spontaneously breathing patients.

Aged↗
PubMed2004

Epidural oxycodone or morphine following gynaecological surgery.

BACKGROUND: The analgesic action of oxycodone is of rapid onset, in contrast to morphine, and is mediated by kappa-opioid receptors of the spinal cord. We compared analgesia and side-effects of epidural oxycodone with those of morphine after gynaecological surgery. METHODS: We studied prospectively in 75 women in a double-blind, randomized manner: epidural morphine 6 mg day(-1) (n=25), epidural oxycodone 6 mg day(-1) (n=25) and epidural oxycodone 12 mg day(-1) (n=25). All patients underwent gynaecological surgery under general (isoflurane and nitrous oxide) and epidural anaesthesia. Visual analogue scale (VAS) pain scores at rest and on coughing, verbal descriptive scale (VDS) satisfaction scores, sedation scores, pruritus scores and nausea/vomiting scores were recorded for 3 days after surgery. RESULTS: VAS pain scores at rest in patients who received oxycodone 6 mg day(-1) were higher than in patients who received morphine 6 mg day(-1) at 6 h and on the first postoperative day and were significantly higher than in patients who received oxycodone 12 mg day(-1) on the first postoperative day. Scores for nausea, vomiting and pruritus in patients who received oxycodone 6 mg day(-1) and 12 mg day(-1) were lower than those in patients who received morphine. No significant differences were seen in VAS at cough and VDS satisfaction scores between the three groups. CONCLUSION: Epidural oxycodone was as effective as morphine at the doses investigated, with fewer side-effects.

Adult↗
PubMed2003

Anesthesia-related mortality and morbidity over a 5-year period in 2,363,038 patients in Japan.

BACKGROUND: Statistical data of mortality and morbidity related to anesthesia have not been reported in Japan since World War II. The need to comprehensively examine the events of cardiac arrest as well as mortality prompted the first national study in Japan. METHODS: Confidential questionnaires were sent to all Japan Society of Anesthesiologists Certified Training Hospitals every year from 1994 through 1998. Collected data were analyzed for incidence of cardiac arrest and other critical events during anesthesia and surgery, and their outcomes within 7 postoperative days. The principal causes of the critical incidents were also analyzed. RESULTS: With an average response rate of 39.9%, a total of 2,363,038 cases were documented over 5 years. The average incidence per year of cardiac arrest during surgery due to all etiologies and that totally attributable to anesthesia was 7.12 [95%CI: 6.30,7.94] and 1.00 [0.88, 1.12]) per 10,000 cases, respectively. The average mortality per year in the operating room or within 7 postoperative days due to all etiologies and that totally attributable to anesthesia was 7.18 [6.22, 8.13] and 0.21 [0.15, 0.27] per 10,000 cases, respectively. The two principal causes of cardiac arrest during anesthesia and surgery due to all etiologies were massive hemorrhage (31.9%) and surgery (30.2%), and those totally attributable to anesthesia were drug overdose or selection error (15.3%) and serious arrhythmia (13.9%). Preventable human errors caused 53.2% of cardiac arrest and 22.2% of deaths in the operating room totally attributable to anesthesia. CONCLUSIONS: The rates in Japan of cardiac arrest and death during anesthesia and surgery due to all etiologies as well as those totally attributable to anesthesia are comparable to those of other developed countries.

Anesthesia↗
PubMed2003

Changes in calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide in patients undergoing coronary artery bypass grafting.

The initiation of cardiopulmonary bypass creates significant derangements in cardiovascular volume status and both endocrine and autonomic nervous system function. To examine whether such derangements might differ in patients with different pre-operative physical status scores, we measured the plasma concentrations of calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide, catecholamines and antidiuretic hormone, as well as haemodynamic variables, during and after cardiopulmonary bypass in 27 consecutive patients undergoing coronary artery bypass grafting. The pre-operative levels of atrial natriuretic peptide and brain natriuretic peptide differed significantly between ASA II patients and III and IV patients [mean (SD) brain natriuretic peptide levels = 14 (8.2) vs. 129 (51) pg.ml-1]. Plasma calcitonin gene-related peptide increased significantly in both groups after the initiation of cardiopulmonary bypass, and remained increased throughout cardiopulmonary bypass. The changes in plasma epinephrine, norepinephrine and antidiuretic hormone were similar to those reported previously. The changes in plasma calcitonin gene-related peptide, atrial natriuretic peptide and brain natriuretic peptide did not correlate with any changes in haemodynamic variables before or after cardiopulmonary bypass. Measurement of plasma brain natriuretic peptide might usefully be included in the pre-operative evaluation of patients with cardiac disease.

Atrial Natriuretic Factor↗
PubMed2002

Epidural morphine injection after combined spinal and epidural anaesthesia.

BACKGROUND AND OBJECTIVE: Although combined spinal and epidural anaesthesia is efficient and easy to perform, the technique can be a double-edged sword having the potential risk that an increased flux of drugs across the meninges through the hole made in it may lead to severe adverse effects. The aim was to compare the incidence of adverse events when an epidural injection of morphine was given after combined spinal and epidural anaesthesia or after epidural anaesthesia. METHODS: Fifteen patients had an epidural catheter inserted at the L2-3 interspace, and then a spinal block administered via the L3-4 interspace. Another 15 patients only had an epidural catheter inserted. After the onset of spinal or epidural anaesthesia had been confirmed, morphine 2 mg was injected into the epidural space, and a continuous epidural infusion of morphine was started. At the end of the operation and at 4, 8 and 12 h after the administration of epidural morphine and on the next day, the following variables were examined: blood pressure, heart rate, respiratory rate, arterial blood-gas analysis, visual analogue scale pain scores, nausea/vomiting scores, and pruritus scores. RESULTS: In the study population, the epidural injection of morphine was not associated with a significantly higher incidence of adverse events when given after spinal anaesthesia than after epidural anaesthesia. CONCLUSIONS: The adverse effects associated with epidural morphine given after spinal anaesthesia did not increase significantly when a 27-G Whitacre needle was used. Thus, the morphine flux through the meningeal hole into the cerebrospinal fluid was trivial.

Aged↗
PubMed2001

Involvement of p38 MAP kinase in TGF-beta-stimulated VEGF synthesis in aortic smooth muscle cells.

Although it is known that transforming growth factor (TGF)-beta induces vascular endothelial growth factor (VEGF) synthesis in vascular smooth muscle cells, the underlying mechanisms are still poorly understood. In the present study, we examined whether the mitogen-activated protein (MAP) kinase superfamily is involved in TGF-beta-stimulated VEGF synthesis in aortic smooth muscle A10 cells. TGF-beta stimulated the phosphorylation of p42/p44 MAP kinase and p38 MAP kinase, but not that of SAPK (stress-activated protein kinase)/JNK (c-Jun N-terminal kinase). The VEGF synthesis induced by TGF-beta was not affected by PD98059 or U0126, specific inhibitors of the upstream kinase that activates p42/p44 MAP kinase. We confirmed that PD98059 or U0126 did actually suppress the phosphorylation of p42/p44 MAP kinase by TGF-beta in our preparations. PD169316 and SB203580, specific inhibitors of p38 MAP kinase, significantly reduced the TGF-beta-stimulated synthesis of VEGF (each in a dose-dependent manner). PD169316 or SB203580 attenuated the TGF-beta-induced phosphorylation of p38 MAP kinase. These results strongly suggest that p38 MAP kinase plays a part in the pathway by which TGF-beta stimulates the synthesis of VEGF in aortic smooth muscle cells.

Animals↗
PubMed2001

Contrasting effects of midazolam on induction of heat shock protein 27 by vasopressin and heat in aortic smooth muscle cells.

We previously showed that vasopressin stimulates the induction of heat shock protein (HSP) 27, a low molecular-weight HSP, through protein kinase C activation in aortic smooth muscle A10 cells. In the present study, we examined the effects of midazolam, an intravenous anesthetic, on the HSP27 induction stimulated by vasopressin, heat, or sodium arsenite (arsenite) in A10 cells. Midazolam inhibited the accumulation of HSP27 induced by vasopressin or 12-O-tetradecanoylphorbol 13-acetate (TPA), a direct activator of protein kinase C. Midazolam also reduced the vasopressin-induced level of the mRNA for HSP27. In contrast, midazolam enhanced the HSP27-accumulation induced by heat or arsenite. Midazolam also enhanced the heat-increased level of the mRNA for HSP27. However, midazolam had no effect on the dissociation of the aggregated form of HSP27 following stimulation by vasopressin, heat, or arsenite. These results suggest that midazolam suppresses vasopressin-stimulated HSP27 induction in vascular smooth muscle cells, and that this inhibitory effect is exerted at a point downstream from protein kinase C. In contrast, midazolam enhanced heat- or arsenite-stimulated HSP27 induction. Thus, midazolam has dual effects on the HSP27 induction stimulated by various stresses in vascular smooth muscle cells.

Anesthetics, Intravenous↗
PubMed2001

Hemodynamic stability during induction of anesthesia and tracheal intubation with propofol plus fentanyl, ketamine, and fentanyl-ketamine.

PURPOSE: This study was conducted to investigate hemodynamic and cardiac stability during anesthesia induction and intubation, using propofol plus fentanyl, propofol plus ketamine, and propofol plus fentanyl and ketamine. METHODS: Forty-five adult patients were randomly allocated to one of three groups according to the agents used for induction: propofol (2 mg/kg) plus fentanyl (3 microg/kg) (PF), propofol (2 mg/kg) plus ketamine (0.1 mg/kg) (PK), and propofol (2 mg/kg) plus fentanyl (3 microg/kg) plus ketamine (0.1 mg/kg) (PFK). Hemodynamic responses were assessed by measuring changes in blood pressure (BP), heart rate (HR), and cardiac output (CO; using dye dilution combined with pulse dye densitometry [PDD]). RESULTS: BP and HR changes during the induction of anesthesia tended to be greater in the PK group than in the PF and PFK groups. After the injection of propofol, the cardiac index (CI) fell significantly below baseline values in the PF and PFK groups, but remained unchanged in the PK group. After tracheal intubation, BP and HR increased significantly only in the PF and PK groups, and reached a level significantly above baseline values only in the PK group. The CO responses to tracheal intubation were: PK group > PF group > PFK group. CONCLUSION: A combination of propofol plus fentanyl plus ketamine would provide greater reduction of fluctuations in hemodynamic variables associated with induction of anesthesia and tracheal intubation than combinations of propofol plus fentanyl or propofol plus ketamine.

Clinical Trial↗
PubMed2001

Aortic and mitral valve replacement in a patient with acute febrile neutrophilic dermatosis (Sweet's syndrome): report of a case.

A 29-year-old woman was admitted to our hospital with severe orthopnea, fever, and acute dermatosis. She had a 5-year history of episodic acute neutrophilic dermatosis and peripheral leukocytosis following a high fever, which were symptoms consistent with a diagnosis of Sweet's syndrome. Echocardiography revealed remarkable dysfunction of the left ventricle due to severe aortic regurgitation, which had not been present at a previous admission when mild mitral regurgitation was detected. The aortic and mitral valves were replaced with prosthetic valves on an emergency basis. The leaflets of the aortic valve were very thin and appeared fragile. The anterior leaflet of the mitral valve showed severe prolapse due to the torn chordae and hypoplasia of the posterior strut chordae. Her postoperative course was uneventful. Microscopic examination revealed fibrosal degeneration and the infiltration of lymphocytes and macrophages into both heart valves. This may be the first case report of valvulitis and Sweet's syndrome occurring simultaneously.

Adult↗
PubMed2001

Ketamine, not propofol, attenuates cerebrovascular response to carbon dioxide in humans with isoflurane anesthesia.

STUDY OBJECTIVES: To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO(2)) in humans during isoflurane anesthesia. DESIGN: Randomized clinical investigation. SETTINGS: University hospital of a medical school. PATIENTS: 30 ASA physical status I and II adult, elective surgical patients. INTERVENTIONS AND MEASUREMENTS: With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artery (Vmca) and pulsatility index were measured using the transcranial Doppler method under hypocapnic [arterial CO(2)tension (PaCO(2)) 28-32 mmHg], normocapnic (PaCO(2) 38-42 mmHg), and hypercapnic conditions (PaCO(2) 48-52 mmHg). PaCO(2) was altered by supplementing the inspired gas with CO(2) without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg. kg(-1) or propofol (2 mg. kg(-1)followed by an infusion of 6-10 mg. kg(-1). hr(-1)) (n = 15 for each drug), and the measurements were repeated. MAIN RESULTS: Ketamine reduced both absolute and relative cerebrovascular reactivity to CO(2) significantly [2.9 +/- 0.8 (control) vs. 2.6 +/- 1.0 (ketamine) cm. sec(-1). mmHg(-1): p < 0.05; and 3.5 +/- 0.7 (control) vs. 2.8 +/- 0.9 (ketamine) %. mmHg(-1): p < 0.01, respectively]. However, ketamine did not reduce Vmca during hypercapnic conditions (117 +/- 29 cm. sec(-1)) compared with controls (120 +/- 28 cm. sec(-1)). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO(2) reactivity [2.5 +/- 0.8 (control) vs. 2.5 +/- 1.0 (propofol) cm. sec(-1). mmHg(-1), and 3.3 +/- 1.3 (control) vs. 4.1 +/- 1.0 (propofol) %. mmHg(-1), respectively]. CONCLUSIONS: In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO(2), but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO(2).

Adult↗
PubMed2001

The antinociceptive and sedative effects of carbachol and oxycodone administered into brainstem pontine reticular formation and spinal subarachnoid space in rats.

UNLABELLED: To clarify the supraspinal and spinal actions of a cholinergic agonist, carbachol, and an opioid, oxycodone, we studied their antinociceptive and behavioral effects when administered into brainstem medial pontine reticular formation (mPRF) or spinal subarachnoid space with or without pretreatment of muscarinic receptor subtype antagonist. Sprague-Dawley rats were implanted with a 24-gauge stainless steel guide cannula into the mPRF and chronically implanted with a lumbar intrathecal catheter. Antinociception was tested using tail flick latency, motor coordination was evaluated by the rotarod test, and overt sedation was assessed using a behavioral checklist. Carbachol (0.5-4.0 microg) administered into the mPRF produced significant dose- and time-dependent antinociception, sedation, and motor dysfunction. These were completely blocked by pretreatment with atropine and the M(2) muscarinic antagonist, methoctramine, and partially blocked by pretreatment with M(1) pirenzepine but not with M(3) p-fHHSID: Oxycodone administered into the mPRF did not produce such effects. Spinal carbachol and oxycodone produced antinociception without any behavioral effects; their antinociceptive effects were completely blocked by pretreatment with atropine and M(2) antagonist. These results suggest that the antinociceptive action of carbachol is mediated by muscarinic cholinergic receptor activation, especially by M(2) receptor subtype in mPRF and spinal cord, and that although oxycodone seems unlikely to affect the cholinergic transmission of mPRF, spinal oxycodone-induced analgesia is at least partly mediated via the activation of M(2) receptor subtype at the spinal cord. IMPLICATIONS: Carbachol-induced antinociception and sedation is mediated with the activation of M(2) muscarinic receptors. Oxycodone administered into brainstem medial pontine reticular formation did not cause any antinociceptive or behavioral effects, but its spinal administration produced a significant antinociception via M(2) muscarinic receptor activation

Analgesics, Non-Narcotic↗
PubMed2001

The effects of alpha-human atrial natriuretic peptide and milrinone on pial vessels during blood-brain barrier disruption in rabbits.

UNLABELLED: The effects of alpha-human atrial natriuretic peptide (HANP) and milrinone on cerebral pial vessels, especially during blood-brain barrier (BBB) disruption, are not clear. We studied topical HANP (10(-14), 10(-12), and 10(-10) M) or milrinone (10(-7), 10(-5), and 10(-3) M), and IV HANP (0.1, 0.2, and 1.0 microg. kg(-1). min(-1)) or milrinone (0.5, 5.0, and 20.0 microg. kg(-1). min(-1)) with or without hyperosmolar BBB disruption, using a rabbit cranial window preparation. At 10(-12) and 10(-10) M topical HANP produced significant arteriolar (16%, 20%, respectively), but no venular dilation. Topical milrinone (10(-3) M) produced significant arteriolar and venular dilation (21%, 8%, respectively). IV HANP produced no arteriolar or venular changes at any dose except during BBB disruption, when it caused a significant arteriolar (16%, 16%, and 17%, respectively), but no venular dilation. In contrast, IV milrinone caused small but significant arteriolar and venular dilation without BBB disruption (arterioles, 6%, 7% and 8%, respectively; venules, 6% at 20.0 microg. kg(-1). min(-1)). During BBB disruption, these responses to milrinone were similar. Although HANP and milrinone each have a direct vasodilator effect on arterioles, their systemic administration at clinical doses could induce different effects. BBB disruptive conditions could increase the response of pial vessels to systemically administered HANP. IMPLICATIONS: Although alpha-human atrial natriuretic peptide (HANP) and milrinone each have a direct vasodilator effect on cerebral pial arterioles, their systemic administration at clinical doses could have different effects and blood-brain-barrier disruptive conditions could alter the response of pial vessels to HANP, but not to milrinone.

Animals↗
PubMed2001

The effects of topical and intravenous ketamine on cerebral arterioles in dogs receiving pentobarbital or isoflurane anesthesia.

To evaluate the effects of ketamine on cerebral arterioles, we used a closed cranial window technique in mechanically ventilated, anesthetized dogs. Fourteen dogs were assigned to one of the following two basal-anesthesia groups: pentobarbital 2 mg. kg(-1). h(-1) or isoflurane 0.5 MAC (n = 7 each). We administered three different concentrations of ketamine (10(-7), 10(-5), and 10(-3) M) under the window and measured arteriolar diameters. For comparison, in another 14 dogs we examined the effect of systemic (IV) ketamine (1 mg/kg and 5 mg/kg) using the same two basal anesthetics. We measured diameters before and after ketamine administration, and we evaluated the effect of ketamine on CO(2) reactivity of the cerebral arterioles. Neither topical nor systemic ketamine dilated pial arterioles in either basal-anesthesia group. CO(2) reactivity of pial arterioles was reduced under systemic ketamine in both basal-anesthesia groups. The results indicate that although ketamine does not dilate pial arteriolar diameters when topically or IV administered, IV ketamine does attenuate hypercapnic vasodilation in dogs under basal pentobarbital or isoflurane anesthesia. These results provide some insight that ketamine is suitable for supplementary neurosurgical anesthesia.

Adjuvants, Anesthesia↗
PubMed2001

The anxiolytic effects of the 5-hydroxytryptamine-1A agonist tandospirone before otolaryngologic surgery.

UNLABELLED: We studied 160 ASA I or II patients undergoing elective otolaryngologic surgery in order to compare the anxiolytic effects of a novel 5-hydroxytryptamine-1A agonist, tandospirone, with diazepam. To monitor preoperative anxiety, the following variables were used: systolic and diastolic arterial pressure, heart rate, and the state anxiety score yielded by the Spielberger State-Trait Anxiety Inventory. We performed pretreatment evaluation on the day before surgery and posttreatment examination immediately after entry into the operating room. In a double-blinded, randomized design, four groups of 40 patients each received one of the following oral medications 90 min before entry into the operating room: 1) tandospirone 10 mg (T10 group); 2) tandospirone 30 mg (T30 group); 3) diazepam 10 mg (D group); or 4) placebo (P group). After premedication, the State-Trait Anxiety Inventory state anxiety decreased in the T10 (P < 0.02), T30 (P < 0.02), and D groups (P < 0.001), but it increased in the P group (P < 0.001). Tandospirone, 10 and 30 mg, safely reduced preoperative anxiety to a similar extent as oral diazepam 10 mg in patients undergoing elective otolaryngologic surgery. IMPLICATIONS: Oral tandospirone reduces preoperative anxiety to a similar extent as oral diazepam in patients undergoing elective otolaryngologic surgery. This finding implies that tandospirone can be used as an oral premedicant drug for relieving anxiety before surgery.

Adolescent↗