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Biomedical subjects

J G Reves

Publications and source records attributed to J G Reves.

At least 181 records · Page 10Linked to original sources
PubMed1983

Inotropic and anesthetic potencies of etomidate and thiopental in dogs.

The effects of etomidate and thiopental on myocardial contractility were compared in 10 experiments on isolated papillary muscle preparation perfused by a conscious donor dog. Equianesthetic doses of etomidate (1.4 mg/kg) and thiopental (15.5 mg/kg) were determined separately in conscious dogs. Tension developed by the papillary muscle decreased significantly less after etomidate (17 +/- 2%) than after thiopental (33 +/- 3%) (P less than 0.002) when injected intravenously in equianesthetic doses in donor dogs. When added to arterial blood perfusing the papillary muscle, etomidate had 4-5 times more negative inotropic effect than thiopental. At the same time, the anesthetic potency of etomidate was approximately 11 times greater than that of thiopental. We conclude that both etomidate and thiopental produce a dose-dependent direct negative inotropic effect but that in equianesthetic doses, etomidate causes less pronounced depression of myocardial contractility than thiopental.

Anesthetics↗
PubMed1983

Regional blood flow during cross-clamping of the thoracic aorta and infusion of sodium nitroprusside.

Labeled microspheres, 15 microns in diameter, were used to determine cardiac output and regional blood flow response to cross-clamping of the midthoracic aorta and subsequent sodium nitroprusside (SNP) infusion in 11 dogs. During aortic cross-clamping, mean arterial pressure above the occlusion (MAPa) increased 30% to 35%, mean arterial pressure below the occlusion (MAPb) decreased 87%, cardiac index decreased 12% to 14%, left atrial pressure (LAP) doubled, and renal and spinal cord (lower part) blood flows decreased substantially (85% to 94%). SNP infusion returned MAPa to baseline values, decreased MAPb by half, and substantially and further decreased renal blood flow (to 3% to 5% of baseline values). Myocardial and cerebral blood flows increased substantially (up to 250% to 400%). An increase in preload (fluid load) was accompanied by an increase in LAP, cardiac index, and myocardial blood flow only but not in renal or spinal cord flow. There was a strong association between cortical renal blood flow and MAPb (r2 = 0.92; p less than 0.0001), which suggests that blood flow through organs and tissues below the occlusion is pressure dependent. The data show that SNP infusion during thoracic aortic cross-clamping improves systemic and regional circulation above the occlusion but decreases MAPb and therefore blood flow below the occlusion. SNP infusion should be used with caution during aortic cross-clamping, since arterial hypotension of any degree may be deleterious to organs below the cross-clamp.

Animals↗
PubMed1983

Circulatory responses to midazolam anesthesia: emphasis on canine splanchnic circulation.

Experiments were performed on nine dogs instrumented with pulmonary artery Swan-Ganz catheters and catheters placed into the distal aorta and posterior caval vein. Electromagnetic flowmeter probes were placed around the portal vein and hepatic artery, and the portal vein was cannulated. A week later, systemic and splanchnic circulatory variables were studied before and after 10 mg/kg of midazolam given intravenously. Three minutes after injection, heart rate increased 26% (P less than 0.006), cardiac index decreased 15% (P less than 0.001), portal flow increased 19% (P greater than 0.05), and hepatic arterial flow decreased slightly (P less than 0.002). Later, portal blood flow decreased 17% below baseline values (P less than 0.006). The biphasic response of portal blood flow to midazolam is probably related to redistribution of blood within the splanchnic system (blood mobilization from spleen and intestine). It is suggested that because maintenance of cardiac output during midazolam anesthesia depends on compensatory mechanisms, failure to increase cardiac output with compensatory increases in heart rate, contractility, and blood volume mobilization from the splanchnic circulation could result in decreased cardiac output.

Anesthesia, Intravenous↗
PubMed1983

Midazolam.

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Anesthetics↗
PubMed1982

Detection of myocardial injury after coronary artery bypass grafting using a hypothermic, cardioplegic technique.

Fifty patients undergoing isolated coronary artery bypass grafting procedures using a clear, cold cardioplegic solution, topical hypothermia, and reduced systemic flow for intraoperative myocardial protection were evaluated for myocardial injury by serial plasma creatine kinase-MB isoenzyme (CK-MB) measurements and electrocardiograms. Forty-one (82%) of the patients had three-vessel disease. Preoperative left ventricular contractility determined angiographically was normal in 13 patients (26%), mildly abnormal in 26 (52%), and moderately or severely abnormal in 11 (22%). The number of arteries grafted ranged from 2 to 6 (mean, 3.5). The mean duration of aortic clamping was 38.6 +/- 1.6 minutes. There were no hospital deaths. Enzymatic and electrocardiographic (ECG) evidence of myocardial infarction occurred in 1 patient. Nonspecific ECG changes occurred in 16 patients (32%), and th electrocardiograms were unchanged in the remaining 33 patients (66%). In the 49 patients without ECG evidence of infarction, the mean peak plasma CK-MB value, which occurred 6 hours after the onset of cardiopulmonary bypass, was 7.9 +/- 0.8 IU/L (standard error of the mean) and the mean integrated area 158 +/- 19.5 IU/L X hours. There was no correlation between these CK-MB values and the extent of disease, number of arteries grafted, or the duration of myocardial ischemia. These data document a low incidence of perioperative myocardial injury with this technique, and can serve as a baseline for comparison with other techniques for intraoperative myocardial protection in this setting.

Adult↗
PubMed1982

Neuronal and adrenomedullary catecholamine release in response to cardiopulmonary bypass in man.

Cardiopulmonary bypass (CPB) alters systemic hemodynamics and affects several biochemical systems involved in cardiovascular regulation. We investigated the changes in levels of circulating epinephrine (E) and norepinephrine (NE) and related them to events during CPB. Twenty-eight patients undergoing various surgical procedures were studied. Plasma E and NE were determined by radioenzymatic assay at eight stages of the operation. A ninefold increase in arterial E (from 75 +/- 13 to 708 +/- 117.3 pg/ml) occurred from prebypass (stage 1) measurements to the end of aortic cross-clamping (stage 4). The values at stage 4 were significantly higher (p less than 0.05) than at all other stages. E decreased rapidly, to 360 +/- 84.3 pg/ml, after myocardial and pulmonary reperfusion (stage 5). Arterial NE increased twofold from stage 1 to stage 4 (from 426 +/- 66.9 to 825 +/- 84.2, p less than 0.05). The increase in NE from initial CPB values (stage 2) to 30 minutes of aortic cross-clamping (stage 3) was associated with an increase in mean blood pressure (r = 0.51, p = 0.02). The peak increases in catecholamines occurred when the heart and lungs were excluded from the circulation, which suggests that either or both contributed to the increase. Because the increase in E was markedly greater than that in NE, the predominant humoral response to CPB appears to be adrenomedullary release of E. This significant increase in catecholamines could jeopardize myocardial protective measures during CPB.

Adrenal Medulla↗
PubMed1982

Premedication with intramuscular midazolam: a prospective randomized double-blind controlled study.

One hundred A.S.A. physical status I and II surgical patients were randomized to receive midazolam, 0.07 mg/kg (group M, 31 patients), hydroxyzine, 1.0 mg/kg (group H, 34 patients), or midazolam diluent as a placebo (group P, 35 patients). Drugs were administered in the vastus lateralis muscle 60 to 90 minutes before anesthesia induction. Anesthesia was induced with thiopental, 3.0 mg/kg, followed by 1.0-mg/kg increments if required. An entry criterion was that patients score greater than or equal to 50% on a subjective Anxiety Visual Analog Test (AVAT). Anxiety was also objectively rated on a six-point scale by a trained observer. Patients and observer were unaware of type of premedication used. Midazolam and hydroxyzine produced significantly (p less than 0.05) greater reduction of anxiety than placebo on both the AVAT and objective anxiety evaluations. Peak onset appeared between 30 and 60 minutes after drug administration. Hemodynamic changes were similar in all groups, and no untoward reactions were encountered before anesthesia. The injection site 24 and 48 hours after administration showed evidence of mild tissue irritation in 68% of patients in group H, 26% of patients in group M, and none of the patients in group P. Midazolam is an efficacious, safe premedicant in relatively healthy patients. It has a prompt onset of action with only minimal tissue irritation.

Anxiety↗
PubMed1981

Effect of halothane on myocardial infarct size in rats.

The effect of halothane on myocardial infarction caused by ligation of the left descending coronary artery was studied in rats. The extent of infarction was quantified 48 hours after ligation of the artery by planimetric measurement of left ventricular slices stained with nitrobluetetrazolium. Animals exposed to halothane one per cent for three hours after the coronary ligation were compared with a control group which received halothane for only 5-7 minutes during surgery. It was found that halothane caused a small increase in infarction size (31.3 +/- 1.5 per cent of the left ventricle compared to 25.7 +/- 2.3 per cent, p less than 0.05). This effect was accompanied by a decrease in systolic blood pressure (91 +/- 2 mmHg compared to 113 +/- 3 mmHg, p less than 0.001). Heart rate did not change significantly. Analysis of our results in comparison to previously reported data on the effect of halothane on myocardial ischaemia in different experimental conditions shows that halothane may produce beneficial as well as detrimental effect on ischaemic injury to the myocardium. The latter can result when the drug causes marked hypotension in the absence of a significant decrease in heart rate.

Animals↗
PubMed1981

Influence of serum protein, serum albumin concentrations and dose on midazolam anaesthesia induction times.

Individual variation occurs in time to induction of anaesthesia with intravenous drugs. Less free drug is available to cross the blood-brain barrier when the drug is highly protein bound. Since this may prolong time to sleep, we correlated the induction time, serum albumin and total protein concentrations, and doses of midazolam, which is a highly protein bound intravenous anaesthetic. There is a poor correlation (r = 0.062) between induction time and serum protein, a weak (r = 0.542) but statistically significant (p = 0.026) correlation between induction time and serum albumin, and a highly significant (p = 0.003) negative correlation (r = 0.579) between drug dose and induction time. The administration of the appropriate dose of midazolam for induction, therefore, appears to affect induction time more significantly than does the serum albumin concentration.

Anesthesia, Intravenous↗
PubMed1981

Hemodynamic responses to anesthetic induction with midazolam or diazepam in patients with ischemic heart disease.

Hemodynamic responses to induction of anesthesia with midazolam maleate and diazepam were compared in patients with ischemic heart disease. While breathing 100% oxygen, 10 patients (group M) received midazolam maleate, 0.2 mg/kg, and 10 patients (group D) received diazepam, 0.5 mg/kg. In addition, 10 patients (group MN) breathing 50% nitrous oxide in oxygen received midazolam, 0.2 mg/kg. Patients in group M had a small but statistically significant (p less than 0.05) decrease (vs awake control values) in systemic and pulmonary arterial blood pressure, pulmonary arterial occluded pressure, stroke index, and left and right ventricular stroke work indices. Patients in group D experienced statistically significant decreases in systemic blood pressure. The only statistically significant differences between groups M and D occurred 5 minutes followed drug administration: heart rates were higher and systemic pressures and left ventricular stroke work indices were lower following midazolam. Hemodynamic changes following midazolam and nitrous oxide were similar to those observed in patients given midazolam and 100% oxygen. Patients in all three groups responded to endotracheal intubation with transient increases in blood pressure, heart rate, and systemic vascular resistance, but the hemodynamic values spontaneously returned toward control levels within 2 to 5 minutes. Although differing somewhat, midazolam, like diazepam, provided rapid, hemodynamically stable induction of anesthesia in patients with ischemic heart disease.

Anesthetics↗
PubMed1981

Midazolam versus diazepam: different effects on systemic vascular resistance. A randomized study utilizing cardiopulmonary bypass constant flow.

In 43 patients electively scheduled for myocardial revascularization surgery, a hemodynamic comparison of 8-chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4] benzodiazepine (midazolam, Ro 21-3981, Dormicum) and 7-chloro-1,3-dihydro-1-methyl-5-phenyl-(2H)1,4-benzodiazepin-2-one (diazepam) was made during cardiopulmonary bypass. Midazolam and diazepam were compared in patients with ischemic heart disease to determine the effects of the drugs on systemic vascular resistance at constant flow (cardiac output) and temperature. Diazepam (0.3 mg/kg) produced significantly greater decreases in perfusion pressure, systemic vascular resistance, and venous reservoir volume than did midazolam (0.2 mg/kg). It was concluded that there are subtle differences in the pharmacologic actions of both midazolam and diazepam. When used with constant flow on cardiopulmonary bypass, diazepam causes more pronounced arterial and venous dilation. These data are at variance with the findings in intact man.

Anesthetics↗
PubMed1980

Pathogenesis of paroxysmal hypertension developing during and after coronary bypass surgery: a study of hemodynamic and humoral factors.

A prospective study of hypertension first appearing during and after saphenous vein bypass coronary surgery was performed in 28 patients to examine the incidence, hemodynamics and mechanism of this problem. In 15 patients (54 percent) new hypertension developed (mean arterial pressure greater than 107 mm Hg), characterized by increased peripheral vascular resistance and unchanged cardiac output within 1 hour after surgery. These 15 patients had a longer history of angina of greater severity, but also had relatively well preserved ventricular myocardium. Because plasma renin activity was depressed in patients in the hypertensive group, activation of the renin-angiotensin system was not important in the pathogenesis of this postoperative hypertension. The expected decrease in total peripheral resistance at the onset of cardiopulmonary bypass was observed in all patients, but later during bypass the peripheral resistance increased in all patients in association with a rise in plasma epinephrine levels. Patients who had hypertension postoperatively had a greater increase in arterial pressure and total peripheral resistance during cardiopulmonary bypass than did those with normal postoperative blood pressure. An elevation in plasma epinephrine and norepinephrine concentration, suggesting enhanced sympathoadrenal responsiveness to the challenge of cardiopulmonary bypass, was characteristic of the hypertensive group. This evidence of enhanced sympathetic activity during surgery may be a useful predictor of the development of postoperative hypertension.

Blood Pressure↗