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Enhanced haemodynamic effects of propranolol in acute myocardial infarction.
- Source :
- European Heart Journal; May1984, Vol. 5 Issue 5, p366-373, 8p
- Publication Year :
- 1984
-
Abstract
- To evaluate the possible influence of sympathetic activation on the haemodynamic response to intravenous beta-blockade, the dose-response characteristics of three boluses of propranolol were evaluated in 8 patients with uncomplicated infarction and compared in a similar number of patients with stable angina. Following a control period, when haemodynamic stability was confirmed, propranolol 2, 2 and 4 mg (cumulative dosage 2, 4 and 8 mg) was injected into the central circulation at 15 min intervals. Despite close matching in baseline control haemodynamic variables between the groups, in stable angina, pro pranolol resulted in dose-related depression of cardiac output without change in systemic blood pressure, whereas following myocardial infarction the drug induced significantly greater falls in cardiac output (P>0-05) and a dose-related decrease in systemic blood pressure. Despite the greater effects of propranolol on cardiac output following myocardial infarction, the left ventricular filling pressure was increased to a lesser extent compared with stable angina. The explanation for this observation may reside in a greater susceptibility of the left ventricular wall to increase its compliance, under conditions of high sympathetic stimulation, following beta-blockade. These data support experimental and biochemical evidence of sym pathetic activation in myocardial infarction; the hyperadrenergic state conditions an augmented haemody namic response to competitive antagonism of sympathetic stimulation at cardiac beta-adrenocep tors. [ABSTRACT FROM PUBLISHER]
Details
- Language :
- English
- ISSN :
- 0195668X
- Volume :
- 5
- Issue :
- 5
- Database :
- Complementary Index
- Journal :
- European Heart Journal
- Publication Type :
- Academic Journal
- Accession number :
- 55883769
- Full Text :
- https://doi.org/10.1093/oxfordjournals.eurheartj.a061670