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Biomedical subjects

S Reiz

Publications and source records attributed to S Reiz.

83 records · Page 5Linked to original sources
PubMed1981

Hemodynamic and cardiometabolic effects of prenalterol in patients with acute myocardial infarction and shock.

Five patients with acute myocardial infarction and shock were treated with a new, highly selective beta-1-adrenoreceptor agonist, prenalterol. After 1 and 2 mg of the drug, all patients had markedly increased blood pressure and cardiac output, but no changes in heart rate or systemic vascular resistance. Left- and right-sided filling pressures decreased in three of the patients. In two of the patients, however, the increase in contractility and afterload was followed by a marked increase in left- and right-sided filling pressures, and myocardial lactate uptake changes to lactate production. After addition of sodium nitroprusside, blood pressure and filling pressures returned towards normal, and myocardial lactate uptake was restored. As anticipated from the hemodyanamic findings, myocardial oxygen consumption increased after prenalterol. It is suggested that the potent inotropic agent prenalterol may be used with great caution in cardiogenic shock.

Adrenergic beta-Agonists↗
PubMed1981

Myocardial oxygen consumption and coronary haemodynamics during fentanyl-droperidol-nitrous oxide anaesthesia in patients with ischaemic heart disease.

Eight patients with stable ischaemic heart disease were investigated to determine the effects of fentanyl (15 micrograms/kg) - droperidol (150 micrograms/kg) - nitrous oxide (75%) anaesthesia, without concomitant fluid challenge, on myocardial oxygen consumption and lactate uptake, and central and coronary haemodynamics. Anaesthesia induced reductions in mean arterial pressure (--35%, P less than 0.01), systemic vascular resistance (--30%, P less than 0.01), left ventricular stroke work index (--50%, P less than 0.01) and total body oxygen consumption (--23%, P less than 0.01), with no changes in heart rate, cardiac output or mean pulmonary arteriolar occlusion pressure. Mixed venous oxygen content increased (P less than 0.05). Systemic vasodilatation, circulatory adaptation to an overall lower metabolic rate, and clinically negligible cardiodepression are the likely mechanisms behind the central haemodynamic response to this form of anaesthesia. Coronary sinus blood flow (measured by the continuous thermodilution technique) decreased (P less than 0.01) in parallel with the decrease in coronary perfusion pressure. Thus coronary vascular resistance remained unchanged. As expected from the haemodynamic findings, myocardial oxygen consumption decreased (--37%, P less than 0.01). Coronary sinus oxygen content and myocardial oxygen extraction did not change, nor was myocardial lactate uptake affected. No ST-T-segment depressions or dysrhythmias were recorded. These observations indicate that myocardial oxygenation was adequate in spite of the reduction in coronary perfusion pressure. There was poor correlation between changes in myocardial oxygen consumption and rate pressure product (R = 0.455) or triple produce (R - 0.375).

Aged↗
PubMed1981

Invasive analysis of non-invasive indicators of myocardial work and ischaemia during anaesthesia soon after myocardial infarction.

Atrial pacing was used for preoperative evaluation of six patients with recent anterior myocardial infarction (MI) (e.g. within 6 weeks) scheduled for abdominal emergency surgery. Central and coronary haemodynamics were used to compare changes in myocardial work and oxygenation with alternations of the non-invasive variables rate pressure product (RPP) (systolic blood pressure X heart rate), triple product (TP) (systolic blood pressure X heart rate X mean pulmonary arteriolar occlusion pressure) and ST-T segments (lead V5). There was good correlation between myocardial oxygen consumption and rate pressure product and triple product during pacing to stable angina pectoris. ST-T-segment depressions were recorded already at moderate chest discomfort and correlated well with a decrease in coronary vascular resistance. Changes in myocardial oxygen consumption induced by combined thoracic epidural analgesia (T3-4 to L1-2) and light general anaesthesia with nitrous oxide and fentanyl were poorly correlated with changes in rate pressure product or triple product. ST-T-segment depressions were recorded on five occasions in four of the patients, all in association with intubation and/or extubation. Only on one of these occasions could RPP or TP have indicated that myocardial oxygen demand exceeded supply. On the other four occasions, it was probable that myocardial ischaemia was induced by transient arterial hypoxaemia. The V5 ST-T-segment was the most sensitive non-invasive variable to monitor. The anaesthetic method was safe in all patients, as judged by good intraoperative cardiovascular stability, low morbidity and absence of intra- or postoperative reinfarction.

Abdomen↗
PubMed1980

Hemodynamic and cardiometabolic effects of prenalterol in patients with gram negative septic shock.

The hemodynamic effects of prenalterol, a new inotropic agent, were investigated in 10 patients with gram negative septic shock. In four of the patients, coronary sinus blood flow (CSF) and myocardial oxygen and lactate extraction were also determined. After baseline hemodynamic measurements, prenalterol was infused intravenously over a 10-min period to a total dose of 150 micrograms/kg. All patients responded within 15 min after completion of prenalterol infusion by increasing mean arterial pressure from 57 +/- 11 to 75 +/- 20 mmHg (7.58 +/- 46 to 9.97 +/- 2.66 kPa), (+32%), (P less than 0.01) and cardiac index from 2.65 +/- 0.40 to 3.80 +/- 0.47 1.min-1.m-2, (+44%) (P less than 0.001). There was no change in heart rate or systemic vascular resistance, nor were any arrhythmias recorded. The urinary output increased significantly. After prenalterol, CSF increased from 185 +/- 14 to 246 +/- 14 ml.min-1, (+33%), (P less than 0.001) and myocardial oxygen and lactate extraction rose from 19.8 +/- 2.1 to 26.6 +/- 2.1 ml O2.min-1, (+34%) (P less than 0.001) and from 33.2 +/- 2.3 to 44.7 +/- 2.1 mumol.min-1, (+35%), (P less than 0.001), respectively. The total body oxygen consumption increased from 287 +/- 13 to 348 +/- 23 ml O2.min-1, (+21%), (P less than 0.01) and the arterial lactate concentration decreased from 5.61+/- 0.55 to 3.94 +/- 0.16 mmol.l-1, (-30%), (P less than 0.01), suggesting improved tissue perfusion. The results demonstrate that prenalterol is a potent, highly selective inotropic agent inducing the same magnitude of increase in blood pressure and cardiac output as reported for dopamine in septic shock.

Adult↗
PubMed1980

Effects of thoracic epidural block and prenalterol on coronary vascular resistance and myocardial metabolism in patients with coronary artery disease.

A thoracic epidural block from T1 to T12 was performed with plain prilocaine in four patients with coronary artery disease who were scheduled for abdominal aortic aneurysm surgery. The hemodynamic effects of the block consisted of marked reduction in arterial blood pressure due to impairment of cardiac performance and reduction in systemic vascular resistance. The heart rate decreased moderatetly. The epidural block induced a marked reduction in coronary vascular resistance with only a moderate decrease in coronary sinus blood flow. The myocardial oxygen and lactate utilization decreased in parallel to the decrease in cardiac work. In spite of the absence of arrhythmias and ST-T-segment changes following the epidural block, regional myocardial dysoxia could not be ruled out with the present methods. Administration of the cardioselective beta 1-adrenoreceptor agonist prenalterol increased cardiac performance and thereby arterial blood pressure, but did not affect the systemic or coronary vascular resistance.

Aged↗
PubMed1979

Hemodynamic effects of prenalterol, a beta1-adrenoreceptor agonist, in hypotension induced by high thoracic epidural block in man.

The hemodynamic effects of prenalterol, a new beta1-adrenoreceptor agonist, on hypotension induced by a thoracic epidural block extending between T1 and T12 and thereby blocking the cardiac sympathetic supply have been studied in eight patients scheduled for abdominal aortic aneurysm resection. The thoracic epidural block induced a drop in blood pressure, due to a reduction in cardiac output and systemic vascular resistance. Intravenous infusion of 10 mg of prenalterol rapidly and effectively reversed the hypotension by an increase in cardiac output without any effects on systemic vascular resistance or heart rate. The results indicate that prenalterol is a pure beta1 agonist with a marked inotropic but no chronotropic property.

Adrenergic beta-Agonists↗
PubMed1979

Effects of thoracic epidural block and the beta-1-adrenoreceptor agonist prenalterol on the cardiovascular response to infrarenal aortic cross-clamping in man.

Sixteen patients scheduled for abdominal aortic resection and grafting were randomly assigned to two groups to study the cardiovascular effects of infrarenal aortic cross-clamping. The patients in the first group had received a thoracic epidural block followed by intravenous administration of the selective beta-1-adrenoreceptor agonist prenalterol prior to induction of general anaesthesia. The patients in the second group served as controls and received no specific treatment prior to general anaesthesia. In both groups, aortic cross-clamping was followed by an equal rise in pulmonary artery diastolic pressure and mean systemic arterial pressure. There was a significant difference in systemic vascular resistance, as the control group had a 46% increase 30 s after cross-clamping, while the pretreated patients had only a 7% increase at the same time. Moreover, the patients given the thoracic epidural block followed by prenalterol increased their stroke volume and cardiac indices, as compared to the patients in the control group who showed a significant decrease in these parameters. Possible mechanisms for the mode of action of the combined thoracic epidural block and beta-1-adrenoreceptor agonist pretreatment are discussed.

Adrenergic beta-Agonists↗
PubMed1979

Hemodynamic and cardiometabolic effects of infrarenal aortic and common iliac artery declamping in man--an approach to optimal volume loading.

Nineteen patients undergoing abdominal aortic aneurysm surgery were randomly assigned to two groups and investigated to elucidate the mechanisms of declamping hypotension. The control group of nine patients was kept at an average mean pulmonary artery occlusion pressure (MPAOP) of 11 mmHg (1.46 kPa) before declamping. The other group was volume loaded to a MPAOP of 16 mmHg (2.13 kPa) shortly before declamping. Following declamping there was a significantly greater decrease in mean arterial pressure in the control group, with the same reduction of MPAOP in both groups. In parallel, cardiac and stroke volume indices decreased in the control patients, but remained unchanged in the volume-loaded patients. In the control group there was a reduction in myocardial substrate utilization which was not seen in the volume-loaded patients. No signs of myocardial ischemia could be demonstrated in any of the groups. The results indicate that mismatching between intravascular volume and blood volume is the main cause of infrarenal aortic or common iliac artery declamping hypotension. Volume loading before declamping to a slightly elevated MPAOP can effectively prevent hypotension, while a normal MPAOP does not guarantee a stable hemodynamic situation after declamping.

Aged↗
PubMedDate not supplied

Central and renal haemodynamic effects of intravenous infusion of non-ionic and ionic contrast media. An experimental investigation in the pig.

The central and renal haemodynamic effects after intravenous infusion (1 ml/s) of a non-ionic (iohexol) and an ionic (metrizoate) contrast medium were investigated in 16 pigs. The injected contrast media induced marked haemodynamic changes compared with normal saline. However, there were no significant differences between the ionic and the non-ionic media. It was concluded that the effects were only partially caused by an increase in the blood volume due to the injected volume. In addition, the effects related to the viscosity, the osmolality and other not specified pharmacodynamic properties of the media are proposed to be of importance.

Animals↗