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Biomedical subjects

M Kuro

Publications and source records attributed to M Kuro.

At least 91 records · Page 5Linked to original sources
PubMed1991

Anaesthetic management of phaeochromocytoma associated with tricuspid atresia.

The anaesthetic management of a patient with phaeochromocytoma, tricuspid atresia and pulmonary vascular stenosis is reported. The patient received no preoperative preparation with adrenergic blockers. Anaesthesia was induced and maintained with fentanyl, diazepam and sevoflurane. Intraoperative blood pressure was controlled with sodium nitroprusside, sevoflurane, phentolamine, and propranolol. For hypotension after resection of the tumour norepinephrine was required. This patient did not have a systemic to pulmonary shunt procedure performed, so the maintenance of pulmonary blood flow in the presence of haemodynamic instability during operation for phaeochromocytoma was a major concern. Monitoring of oxyhaemoglobin saturation (SpO2) with a pulse oximeter was considered to be useful because SpO2 may reflect pulmonary flow. During serious haemodynamic disturbances due to the manipulation of the tumour, the heart rate was inversely correlated with SpO2, but the relationship between mean arterial pressure and SpO2 was weak. Therefore, control of heart rate appeared to be more important than control of blood pressure in this case.

Adolescent↗
PubMed1991

Detection of coronary blood flow associated with left main coronary artery stenosis by transesophageal Doppler color flow echocardiography.

Demonstration of disordered blood flow in a coronary artery may be helpful in anticipating the presence of stenosis. To examine the possibility of disordered coronary blood flow associated with left main coronary stenosis, left main coronary flow was visualized by transesophageal Doppler color flow echocardiography in 52 patients undergoing coronary angiography. Twenty patients had significant left main coronary stenosis (Group 1) and 32 patients did not (Group 2). Adequate two-dimensional echocardiographic images of the left main coronary artery were obtained in 17 patients in Group 1 and 30 patients in Group 2. Sixteen patients in Group 1, including five patients in whom the stenosis could not clearly be defined by two-dimensional echocardiography, exhibited the aliased reddish-yellowish elements producing the mosaic pattern at the stenotic or poststenotic segments, or both. In contrast, nonaliased bluish jets, suggesting laminar flow away from the transducer, were seen in echocardiograms from 27 patients in Group 2. This group included four patients with stenosis-like images on two-dimensional echocardiography. The aliased mosaic pattern was found in only three patients in Group 2 (p less than 0.01). Thus, sensitivity to detect the stenosis was improved when Doppler color flow imaging was applied. Flow velocity was significantly higher at the site of stenosis in patients in Group 1 (116 +/- 28 cm/s, n = 10, mean +/- SD) than in Group 2 (29 +/- 12 cm/s, n = 21, p less than 0.01), suggesting that the augmentation of flow velocity with or without turbulence due to the stenosis contributed to the appearance of the mosaic flow images.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1991

Myocardial epinephrine sensitization with subanesthetic concentrations of halothane in dogs.

The authors investigated myocardial epinephrine sensitization by subanesthetic concentrations of halothane. The dose-response relationship for the action of halothane was examined with etomidate plus varying subanesthetic concentrations of halothane in dogs. The arrhythmogenic threshold of epinephrine was decreased in a dose-dependent manner at end-tidal concentrations of halothane between 0.1 and 0.3%. At end-tidal halothane is greater than 0.3%, and no further reduction of arrhythmogenic threshold of epinephrine occurred. The plasma concentrations of epinephrine producing four or more premature ventricular contractions in 15 s were 201.3 +/- 34.3, 98.1 +/- 13.9, 60.3 +/- 8.63, 57.9 +/- 12.8, 54.5 +/- 8.61, and 53.9 +/- 4.86 ng/ml (mean +/- SEM), at 0, 0.1, 0.3, 0.5, 1.0, and 1.5% of halothane at end-tidal concentrations, respectively. The results suggest that in the presence of etomidate, halothane produces myocardial sensitization to epinephrine at subanesthetic concentrations as low as 0.1%. Increasing halothane to 0.3% produces a further reduction in the arrhythmogenic dose of epinephrine.

Anesthesia↗
PubMed1991

Dexmedetomidine prevents epinephrine-induced arrhythmias through stimulation of central alpha 2 adrenoceptors in halothane-anesthetized dogs.

Since alpha 2-adrenergic agonists have important effects on the adrenergic system that have recently been applied to the anesthetic setting, we investigated the effect of stimulation of alpha 2 adrenoceptors on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic threshold for epinephrine was determined during halothane anesthesia in the presence of dexmedetomidine, a selective alpha 2 agonist, and L-medetomidine, a stereoisomer of medetomidine that lacks alpha 2-agonist activity. Dexmedetomidine increased the arrhythmogenic threshold for epinephrine in a dose-dependent manner during halothane anesthesia. At the highest dose of dexmedetomidine, 0.5 microgram.kg-1.min-1, there was a three-fold increase in both the arrhythmogenic dose of epinephrine and the plasma epinephrine concentration that was reached at this dose. On the other hand, L-medetomidine over the same dose range did not effect the arrhythmogenic dose of epinephrine. Atipamezole, a central alpha 2 antagonist that crossed the blood-brain barrier, blocked the antiarrhythmic action of dexmedetomidine. L-659,066 a peripheral alpha 2 antagonist that does not penetrate the blood-brain barrier, did not affect the antiarrhythmic action of dexmedetomidine. Thus, dexmedetomidine's antiarrhythmic effect on epinephrine-induced arrhythmias during halothane anesthesia appears to be mediated at least in part by stimulation of central alpha 2 adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1991

Roles of beta 1- and beta 2-adrenoceptors in the mechanism of halothane myocardial sensitization in dogs.

The authors investigated the comparative roles of beta 1- and beta 2-adrenoceptors in myocardial sensitization by halothane in dogs. The arrhythmogenic dose (AD) of isoproterenol was determined in the presence of various doses of phenylephrine during halothane anesthesia in dogs, and the influences of 1-metoprolol (beta 1-antagonist) and ICI-118,551 (beta 2-antagonist) on the AD were examined. In the presence of 1-metoprolol, the AD of isoproterenol was significantly greater than the control, but in the presence of ICI-118,551, the AD of isoproterenol was lower. Blood pressure during the arrhythmias was higher in the presence of ICI-118,551 than that in controls. In addition, the AD of ritodrine (beta 2-agonist) was also determined at various doses of phenylephrine. The interaction between phenylephrine and ritodrine in inducing arrhythmias showed hyperbolic isoboles. However, 1-metoprolol completely inhibited the occurrence of arrhythmias induced by ritodrine and phenylephrine. The results suggest that myocardial beta 1-adrenoceptors play an essential role in the genesis of arrhythmias during halothane anesthesia in dogs, whereas beta 2-adrenoceptors do not.

Adrenergic beta-Agonists↗
PubMed1991

[Leukocyte removability of a newly developed filter, RC-100, in rapid transfusion].

Leukocyte-depleted blood products are currently a burning issue in transfusion medicine. As methods for depleting leukocytes, the bedside filters are shown to have a high removal rate and several kinds of them are in use. We investigated the leukocytes removal rate of a new filter RC-100 (Pall Co., Glen Cove, NY) under the condition of rapid rate of transfusion during operations. In flow rates of 30, 60, 100 ml.min-1, the removal rate of leukocytes for CRC were 99.9 +/- 0.06, 100.0 +/- 0.00 and 99.4 +/- 0.20% respectively, and for WB 100.0 +/- 0.00, 99.9 +/- 0.10 and 99.1 +/- 0.70%, respectively. The recovery rates of erythrocytes were not significantly decreased for CRC and for WB in all flow rates. These results suggest that RC-100 could be useful either for CRC and for WB even with the rapid flow rate under 100 ml.min-1.

Blood Transfusion↗
PubMed1991

Phenytoin prevents epinephrine-induced arrhythmias through central nervous system in halothane-anesthetized dogs.

The authors investigated the effect of phenytoin through the central nervous system on epinephrine-induced arrhythmias in halothane-anesthetized dogs. The arrhythmogenic dose (AD) of epinephrine during halothane anesthesia was determined in the presence of phenytoin (1 mg/kg), vehicle, and saline, which were administered directly into the cisterna magna. Phenytoin increased the AD of epinephrine as compared with vehicle or saline. The cerebrospinal and plasma concentration of phenytoin during the arrhythmias were 23.6 and less than 0.5 micrograms/ml, respectively. There was no significant difference in AD between the vehicle and saline groups. The same dose of phenytoin (1 mg/kg) administered intravenously did not affect the AD of epinephrine, and the plasma concentration of phenytoin during the arrhythmias was 1.2 micrograms/ml. These findings suggested that phenytoin exerts a protective effect against halothane-epinephrine arrhythmias through a central mechanism and that the central nervous system may be involved, at least in part, in the myocardial sensitization by halothane.

Anesthesia↗
PubMed1991

[The effects of thromboxane receptor antagonist on hemodynamic responses after neutralization of heparin by protamine].

In a double blind test, the effects of ONO 3708, thromboxane A2 (TXA2) receptor antagonist, on hemodynamic responses after neutralization of heparin by protamine, were evaluated in 19 patients undergoing coronary artery bypass graft. Severe circulatory disturbances were not observed in all patients after intravenous administration of protamine (3 mg.kg-1) over 5 minutes, and in particular ONO 3708 (2.5 micrograms.kg-1.min-1 given with continuous infusion) group (n = 10) showed no deleterious hemodynamic responses to protamine. On the other hand, in placebo group (n = 9) the mean pulmonary artery pressure (mPAP) and the mean pulmonary/systemic artery pressure ratio (Pp/Ps) increased significantly, immediately following protamine administration, compared with the baseline values and ONO 3708 group. The results suggest that pulmonary hypertension after protamine is associated with TXA2 release and that ONO 3708 is useful to avoid this reaction.

Aged↗
PubMed1990

[Response to CO2 and autoregulation of cortical cerebral blood flow during isoflurane anesthesia].

Response to CO2 and autoregulation of cortical cerebral blood flow (CBF) during isoflurane anesthesia were studied in 10 patients undergoing neurosurgery. The patients were anesthetized with 0.5 to 1.2% end-tidal isoflurane and 66% nitrous oxide in oxygen. The CBF was measured by thermal diffusion using a flow probe with a Peltier stack. PaCO2 was controlled to produce hypocarbia, normocarbia and hypercarbia by changing tidal volume and respiratory rate. Arterial blood pressure was altered. Hypotension was achieved by intravenous infusion of trimetaphan and hypertension was induced by intravenous administration of metaraminol. During isoflurane anesthesia the response to CO2 of CBF was kept at PaCO2 between 27.8 and 53.9 mmHg. The following relationship was obtained. CBF = 2.54 x PaCO2-53.0, r = 0.59, n = 131 The autoregulation of CBF was evaluated in 7 patients, and in 2 patients, the autoregulation of CBF was abolished.

Anesthesia, Inhalation↗
PubMed1989

[Impaired B lymphocyte function during open heart surgery].

Sequential in vitro lymphocyte function tests in 13 patients undergoing cardiac operation were performed to study B lymphocyte function following operation. Lymphocytes were stimulated with phytohemagglutinin (PHA), pokeweed mitogen (PWM) and Staphylococcus aureus Cowan 1 (SAC). Mitogen responses were measured by 3H-labeled thymidine incorporation. The SAC responses were significantly depressed following operation. Immunoglobulin secreting cells were measured by protein A plaque forming cell assay. The numbers of immunoglobulin secreting cells induced by PWM or SAC decreased remarkably at least as long as 3 day after the operation. The percentage of circulating B lymphocytes increased significantly postoperatively. This indicates that the B lymphocytes remaining after the operation were functionally impaired.

Antibody-Producing Cells↗