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Biomedical subjects

B Silke

Publications and source records attributed to B Silke.

At least 145 records · Page 8Linked to original sources
PubMed1984

Haemodynamic effects of intravenous nicardipine during upright exercise in patients with stable angina pectoris.

The immediate haemodynamic effects, at rest and during exercise, of 2.5 and 10mg intravenous nicardipine were measured in 20 male patients with uncomplicated angina pectoris due to angiographically confirmed coronary artery disease. At rest, both doses of nicardipine resulted in reductions in the systemic arterial pressure and vascular resistance and increases in heart rate and cardiac output. The changes were greater after the larger than after the smaller dose of nicardipine. During exercise, neither dose of nicardipine resulted in a substantial change in the haemodynamic profile, except that after the larger dose heart rate and cardiac output were higher than in the control study. These results indicate that the major overall haemodynamic effect of intravenous nicardipine is dilatation of the systemic arteriolar resistance vessels associated with reflex increase in cardiac pumping activity.

Adult↗
PubMed1984

Haemodynamic effects of nicardipine in acute myocardial infarction.

The haemodynamic dose-response effects of the slow-calcium channel blocker nicardipine were evaluated in fifteen male patients with uncomplicated acute myocardial infarction. Following a 1 hr control period, during which the stability of base-line control haemodynamic variables was confirmed, four i.v. boluses of 1.25, 1.25, 2.5 and 5.0 mg of the drug (cumulative dosage 1.25, 2.5, 5.0 and 10.0 mg) were administered at 15 min intervals. The plasma concentrations achieved are within the previously described therapeutic range (greater than 20 micrograms/l). Nicardipine resulted in linear reductions in systemic arterial pressure and vascular resistance, and dose-related increases in heart rate, cardiac and stroke output without change in the left heart filling pressure. Intravenous nicardipine did not induce any depression of left ventricular pumping performance in our patients in the early stages of uncomplicated myocardial infarction.

Blood Pressure↗
PubMed1983

Hemodynamic comparison of primary venous or arteriolar dilatation and the subsequent effect of furosemide in left ventricular failure after acute myocardial infarction.

The hemodynamic effect of venous dilatation (intravenous isosorbide dinitrate [ISDN]) and arteriolar dilatation (intravenous hydralazine), both as firstline treatment and then combined with intravenous furosemide, were evaluated in a randomized, between-group comparison in 20 men with severe acute left-sided cardiac failure after myocardial infarction (MI). Both ISDN (50 to 200 micrograms/kg/hour) (Group 1) and hydralazine (0.15 mg/kg) (Group 2) reduced systemic arterial pressure (p less than 0.05) and vascular resistance (p less than 0.05). Pulmonary artery occluded pressure was reduced (p less than 0.01) only by ISDN, whereas heart rate (p less than 0.01), cardiac output (p less than 0.01) and stroke volume (p less than 0.05) were increased only after hydralazine. After ISDN, furosemide (1 mg/kg) decreased left-sided cardiac filling pressure by 1 mm Hg (p greater than 0.05), whereas after hydralazine, furosemide in a similar dose reduced pulmonary artery occluded pressure by 5 mm Hg (p less than 0.01). In both groups of patients, furosemide transiently increased systemic arterial pressure (p less than 0.05). Cardiac output was reduced (p less than 0.05) and systemic vascular resistance increased (p less than 0.05) in Group 1 patients after furosemide. Similar changes in both variables in Group 2 patients did not attain statistical significance. In conclusion, ISDN-induced venous dilatation is preferable to primary arteriolar dilatation by hydralazine as first-line treatment in acute left-sided cardiac failure. However, hydralazine and furosemide in combination were equally effective in reducing pulmonary artery occluded pressure and increasing cardiac output. The influences of each regimen on prognosis await further investigation.

Adult↗
PubMed1983

Haemodynamic advantages of isosorbide dinitrate over frusemide in acute heart-failure following myocardial infarction.

The immediate haemodynamic effects of intravenous frusemide (1 mg/kg) and intravenous isosorbide dinitrate (50-200 micrograms/kg/h) were compared in a prospective, randomised, between-group study in 28 men with radiographic and haemodynamic evidence of left ventricular failure following acute myocardial infarction. The diuresis induced by frusemide reduced the left heart filling pressure and cardiac output and transiently raised systemic blood-pressure. In contrast, isosorbide dinitrate was accompanied by a reduction in systemic blood-pressure and peripheral resistance with the result that the cardiac output was not decreased despite a large fall in the pulmonary vascular and left heart filling pressures. These results indicate that reduction of excessive preload by venodilatation may be haemodynamically superior to that induced by diuresis in terms of both reducing myocardial oxygen consumption and maintaining peripheral perfusion. The influence of these contrasting treatments on the prognosis of these high-risk patients warrants further study.

Acute Disease↗
PubMed1983

Comparative haemodynamic dose-response effects of intravenous propranolol and pindolol in patients with coronary heart disease.

To determine whether the depression of left ventricular pumping activity associated with beta-blockade alone could be offset by a substantial degree of partial agonist activity, the haemodynamic dose-response effects of intravenous propranolol and pindolol were compared in a randomised between-group saline controlled study in twenty patients with angiographically proven coronary artery disease. The intravenous doses of propranolol (2-16 mg) and pindolol (0.2-1.6 mg) used were selected on the basis of published reports of equivalence in terms of exercise blockade of chronotropic beta-adrenoceptors. Following four intravenous boluses of each drug, administered according to a cumulative log-dosage schedule, there was a log-linear increase in the plasma concentrations of each drug. The range of plasma concentrations achieved were those which have been shown to be associated with substantial attenuation of sympathetic stimulation of cardiac beta-adrenoceptors. At rest propranolol resulted in dose-related linear reductions in heart rate and cardiac output and linear increases in left heart filling pressure and systemic vascular resistance compared with saline-controlled measurements. The only statistically significant change at rest after pindolol was a small increase in the left heart filling pressure. The calculated systemic vascular resistance was increased after propranolol but unchanged after pindolol. During supine bicycle exercise the systolic blood pressure increased less after propranolol than after saline or pindolol. The increments in all other measured haemodynamic variables during exercise were equally influenced by the two drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Haemodynamic effects of frusemide and its influence on repetitive rapid volume loading in acute myocardial infarction.

The haemodynamic effects of intravenous frusemide (1 mg/kg) were studied in 22 male patients with left ventricular failure following acute myocardial infarction. Radiographic pulmonary oedema was present in all patients and their average left heart filling pressure was 20 mmHg. Bolus injection of the drug was followed by immediate increases in systemic arterial pressure (P less than 0.05) and heart rate (less than 0.05); these declined to pre-injection values after 60 min. Following frusemide there were progressive reductions in left heart filling pressure (P less than 0.01), thermodilution cardiac output (P less than 0.01) and stroke volume (P less than 0.05) and a progressive increase in the derived systemic vascular resistance (P less than 0.05). There was an average diuresis of 860 ml during the 90 min following the frusemide injection. The influence of frusemide on left ventricular performance was studied by comparing the circulatory effects of passive leg raising in the control period with those at 30, 60 and 90 min after the drug. In the control period this manoeuvre increased left heart filling pressure, but not heart rate, cardiac output, stroke volume or systemic vascular resistance. Ninety minutes after frusemide, but not before, passive leg raising resulted in a significant increase in cardiac output (P less than 0.01) and stroke volume at a similar increment in filling pressure and a significant reduction in the systemic vascular resistance (P less than 0.05). These circulatory actions of intravenous frusemide are compatible with initial arteriolar constriction and venodilatation followed by depletion of blood volume with subsequent change in left ventricular pumping performance.

Adult↗
PubMed1983

Observations on the mechanism underlying the differences in exercise and isoprenaline tachycardia after cardioselective and non-selective beta-adrenoceptor antagonists.

1 Differences in ability to attenuate isoprenaline tachycardia between the cardioselective beta-adrenoceptor antagonist atenolol and the non-selective drug propranolol, when administered in equivalent anti-exercise tachycardia oral doses, were measured in four normal volunteers. 2 Propranolol at all dose comparisons showed a greater potency in antagonism of isoprenaline tachycardia than atenolol; this ranged from 6 at the lowest doses (40 and 50 mg respectively) to 13 at the highest doses (320 and 400 mg respectively). 3 After doses of each drug which produced equal inhibition of exercise tachycardia, isoprenaline induced a greater increase in heart rate and greater decrease in diastolic blood pressure after pre-treatment with atenolol than after propranolol. 4 The contribution of this isoprenaline induced vasodilatation to the reduced tachycardia response, 1 h after 25 mg oral atenolol, was measured in the same four subjects by correction of the hypotension with an intravenous angiotensin infusion. Reversal by angiotensin of the 17 mm Hg average fall in diastolic blood pressure during the sustained isoprenaline infusion did not reduce the tachycardia. 5 The hypotension that results from isoprenaline stimulation of unblocked vasodilator beta 2-adrenoceptors in normal subjects pre-treated with atenolol appears to make a negligible contribution to the tachycardia response and does not explain the different abilities of cardioselective and non-selective beta-adrenoceptor blocking drugs to antagonise isoprenaline tachycardia. Our results are compatible with the presence of beta 2-adrenoceptors in human atria.

Adult↗
PubMed1983

Haemodynamic dose-response effects of i.v. penbutolol in angina pectoris.

The haemodynamic dose-response effects of intravenous penbutolol, a newer beta-adrenoceptor antagonist with intrinsic sympathomimetic activity but without cardioselectivity, were evaluated in 10 patients with angiographically documented coronary artery disease. Following four logarithmetically cumulative i.v. boluses (0.5-4 mg dosage range) there was a log linear increase in plasma penbutolol concentration; the levels achieved (51 +/- 8 to 219 +/- 19 ng/ml) were in the therapeutic range (12 to 250 ng/ml). Penbutolol resulted in a linear decrease in heart rate (maximum delta HR - 4 beats/min; P less than 0.01); there was a small increase in pulmonary artery occluded pressure which reached its maximum at the lower doses (maximum delta PAOP + 1 mm Hg; P less than 0.01). The resting cardiac output, blood pressure and calculated systemic vascular resistance were unchanged. During 4 min steady-state supine bicycle exercise there was attenuation of exercise cardiac output (delta C.I. - 0.6 1 min-1 m-2; P less than 0.01) and systolic pressor response (delta SBP - 13 mm Hg; P less than 0.01) compared with control observations without change in other measured or derived variables. The haemodynamic profile of penbutolol compared favourably with other beta-adrenoceptor antagonists previously evaluated under similar conditions in patients with ischaemic heart disease. Over the i.v. dose-range evaluated penbutolol attenuated exercise-induced angina with a relatively modest depression of cardiac performance; the small change induced in resting haemodynamic variables may, in part, have been contributed to by the intrinsic sympathomimetic activity of penbutolol.

Adult↗
PubMed1983

Haemodynamic effects of intravenous beta-blocking drugs in coronary heart disease.

Intravenous beta-blocking drugs are being increasingly used in early myocardial infarction but little is known of the comparative haemodynamic effects of drugs with different ancillary pharmacological properties. In patients with stable coronary heart disease all intravenous beta-blocking drugs reduce left ventricular pumping function in a dose-response fashion. The reduction in cardiac mechanical activity is directly related to the dose and inversely related to the degree of intrinsic sympathomimetic activity possessed by each drug; it is independent of the property of 'cardioselectivity'. The lesser depression of left ventricular pumping performance after beta-blocking drugs with intrinsic sympathomimetic activity is probably due to two primary pharmacodynamic effects: a) increased myocardial contractile activity due to stimulation of post-synaptic beta 1- and presynaptic beta 2-adrenoceptors in the sinus node and ventricular myocardium; b) reduction in left ventricular afterload consequent upon the fall in systemic vascular resistance resulting from stimulation of vasodilator beta 2-adrenoceptors in peripheral resistance vessels. A similar but less marked haemodynamic separation of beta-blocking drugs with and without intrinsic sympathomimetic activity is observed in patients with acute myocardial infarction. The quantitative difference in the haemodynamic effects of intravenous beta-blocking drugs in angina pectoris compared to their effects in acute myocardial infarction is probably due to the higher level of sympathetic stimulation and sensitivity to beta-blockade in the latter. It has yet to be shown by formal clinical trial that the haemodynamic advantages attributable to the possession of intrinsic sympathomimetic activity by a beta-blocking drug are translated into clinical benefit.

Adrenergic beta-Antagonists↗
PubMed1983

Beta-blockade in ischaemic heart disease--influence of concomitant ISA or alpha-blockade on haemodynamic profile.

To test the hypothesis that the depression of cardiac performance induced by competitive blockade of sympathetic stimulation at beta-adrenoceptors could be attenuated by the addition of a high level of intrinsic sympathomimetic activity (ISA) or concomitant alpha- and beta-blockade, the haemodynamic dose-response effects of propranolol (non-cardioselective, no ISA), pindolol (non-cardioselective, high ISA) and labetalol (non-cardioselective, alpha-blocker) were compared in a randomized study of 30 patients with stable coronary artery disease. Following 4 intravenous (i.v.) doses of each drug given according to a logarithmic cumulative dosage schedule, changes in circulatory variables were measured 2-4 min following each i.v. bolus and during bicycle exercise following the maximum dose of each drug. At rest propranolol induced dose-related reductions in heart rate, cardiac output and increases in pulmonary artery occluded pressure and systemic vascular resistance. The only change in resting haemodynamic variables following pindolol was a small dose-related increase in pulmonary artery occluded pressure. Labetalol induced dose-related falls in systemic blood pressure and vascular resistance with linear increase in cardiac output and pulmonary artery occluded pressure. During exercise the depression of cardiac output and increase in pulmonary artery occluded pressure which occurred in patients randomized to propranolol was effectively attenuated in the pindolol and labetalol groups. These observations on cardiac performance following beta-blockade in ischaemic heart disease suggest a rational basis for the use of compounds with added vasodilator or intrinsic sympathomimetic properties.

Adult↗
PubMed1983

Haemodynamic dose-response effects of intravenous labetalol in acute myocardial infarction.

The haemodynamic consequences of combined alpha- and beta-adrenoceptor blockade with intravenous labetalol were evaluated in 21 males with either high (n = 6), normal (n = 9) or low (n = 6) systemic arterial pressure, 4-17 hours after acute myocardial infarction without heart failure. Labetalol 190 +/- 18 mg (range 62-300 mg) infusion resulted in dose-related falls in systolic (P less than 0.01) and diastolic (P less than 0.05) arterial pressure in all patients. The rate of pressure reduction per mg of infused labetalol was directly proportional to the control systolic arterial pressure. Cardiac output (thermodilution) was reduced (P less than 0.05) with low dose labetalol (39 +/- 5 mg) without change on continued infusion. Left heart filling pressure (pulmonary artery occluded pressure) was unchanged throughout infusion in all patients. In conclusion, the vasodilating properties of labetalol appeared to offset the beta-blocker induced depression of cardiac function. The increased sensitivity to the effects of labetalol in those patients with hypertension may be related to excessive alpha-adrenoceptor mediated vasoconstriction in this patient group.

Dose-Response Relationship, Drug↗
PubMed1983

Management of acute heart failure following myocardial infarction: hemodynamic advantages of isosorbide dinitrate over frusemide.

The immediate hemodynamic effects of intravenous frusemide (1 mg/kg) and intravenous isosorbide dinitrate (50-200 micrograms/kg/h) were compared in a prospective, randomized, between-group study in 28 men with radiographic and hemodynamic evidence of left ventricular failure following acute myocardial infarction. The diuresis induced by frusemide reduced the left-heart filling pressure and cardiac output and transiently raised systemic blood pressure. In contrast, isosorbide dinitrate was accompanied by a reduction in systemic blood pressure and peripheral resistance, with the result that the cardiac output was not decreased despite a large fall in the pulmonary vascular and left-heart filling pressures. The results indicate that reduction of excessive preload by venodilatation may be hemodynamically superior to that induced by diuresis in terms of both reducing myocardial oxygen consumption and maintaining peripheral perfusion. The influence of these contrasting treatments on the prognosis of these high-risk patients warrants further study.

Adult↗
PubMed1982

A long-term prevention study with oxprenolol in coronary heart disease.

We carried out a randomized double-blind controlled secondary-prevention trial of oxprenolol over seven years. Forty milligrams of oxprenolol or placebo was given twice daily to 1103 men 35 to 65 years old who had an acute myocardial infarction between 1 and 90 months previously. Overall, there was no difference in mortality or cardiac events between the placebo and oxprenolol groups. The major influence on prognosis was the time at which treatment was started after infarction. In 417 patients in whom treatment was started within four months of infarction oxprenolol increased the six-year cumulative survival rate from 77 to 95 per cent (P less than 0.001). In 274 patients with treatment starting between 5 and 12 months of infarction the survival rate was similar in the two groups, but in 412 patients entered between 1 and 7 1/2 years after their first infarction oxprenolol reduced the six-year survival rate from 92 to 79 per cent (P = 0.002). The increased mortality in this latter group mainly occurred late after withdrawal from active treatment. The value of low-dose oxprenolol in secondary prevention appears to be confined to patients treated relatively soon after myocardial infarction.

Adult↗
PubMed1982

Haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone in patients with coronary heart disease.

The acute haemodynamic effects of beta-blockade with propranolol and combined alpha-blockade and beta-blockade with labetalol were compared in a randomised study in 12 patients with coronary artery disease proved by angiography. Propranolol induced significantly greater depression of left ventricular function both at rest and during exercise than labetalol. This difference was probably attributable to the vasodilator activity of labetalol and the associated reduction in afterload offsetting the haemodynamic disadvantages of blockade of cardiac beta-adrenoceptors alone. The haemodynamic advantages of combined alpha-blockade and beta-blockade over beta-blockade alone may thus have therapeutic implications for the use of these treatments in patients with coronary heart disease.

Adult↗