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At least 1,531 records · Page 85Linked to original sources
PubMed1975

Oxygen demand and collateral vessels of the heart. Factors influencing the severity of myocardial ischaemic injury after experimental coronary artery occlusion.

Epicardial electrocardiographic maps were used to assess the effect of heart rate, myocardial contractility, and oxygen need on the severity of myocardial ischaemic injury after acute coronary artery occlusion in dogs. The experimental data indicate statistically significant dependence of the severity of ischaemia on heart rate, contractility, and oxygen need of the heart. These dependences are highly influenced by the spontaneous collateral vessels of the heart.

Animals↗
PubMed1983

Electrophysiological effects of prenalterol on the cardiac conduction system.

The electrophysiological effects of prenalterol, a new beta-receptor agonist, in a dose of 100 micrograms/kg body weight given intravenously for 5 min, were studied in 13 patients with signs of sinus node dysfunction and/or conduction defects within or distal to the atrioventricular (AV) node. In nine patients with signs of sinus node dysfunction a significant reduction was found in corrected sinus node recovery time, on an average by 1955 +/- 640 ms (-61%, P less than 0.05) and in atrial refractoriness, by 61 +/- 21 ms (-20%, P less than 0.05). Similar but insignificant changes were also seen in the four patients with normal sinus node function. In eight patients with AV nodal dysfunction, a significant increase was found in the Wenckebach point, by 51 +/- 10 b.p.m. (+52%. P less than 0.01) and a decrease in the AH interval, by 23 +/- 9 ms (-14%, P less than 0.05). AV nodal refractoriness tended to decrease by 115 +/- 58 ms (-24%, NS). Similar changes were found in the five patients with normal AV conduction. Heart rate increased in all 13 patients, on an average by 28 +/- 5 b.p.m. (+44%, P less than 0.001) and systolic blood pressure by 18 +/- 8 mmHg (+13% P less than 0.01). In conclusion, prenalterol increased sinus node automaticity and atrial and AV nodal conductivity, but did not improve infranodal conduction. Thus, the drug might be useful in the treatment of patients with sinus node dysfunction as well as in patients with spontaneous or induced atrioventricular conduction abnormalities.

Adult↗
PubMed1983

Prenalterol in primary dilated cardiomyopathy: hemodynamic and angiographic evaluation.

The hemodynamic effects of an acute infusion of prenalterol (PN), a new inotropic beta-adrenoceptor agonist, have been evaluated by cardiac catheterization in 10 patients with primary dilated (congestive) cardiomyopathy. A single dose of 20 micrograms/kg was administered over 5 min after basal hemodynamic and angiographic measurements. The administration of prenalterol caused a significant increase in mean cardiac index, from 2.3 to 3.3 l/min/m2 (P less than 0.01) and mean stroke volume, from 47 to 62 ml (P less than 0.01) without a change in heart rate. Mean left ventricular end-diastolic pressure was reduced from 19 to 13 mm Hg (P less than 0.05) and left ventricular dp/dt rose from 902 to 1089 mm Hg/s (P less than 0.01). Stroke work index increased from 27 to 40 g m/m2 (P less than 0.01) and ejection fraction from 31 to 36% (P less than 0.05). Mean blood pressure did not change and the systemic vascular resistance decreased from 24 to 17 RU (P less than 0.01). The favorable effect of prenalterol on left ventricular relaxation was shown by an increase of peak negative left ventricular dp/dt from 946 to 1159 mm Hg/s and by a decrease of the time constant of left ventricular pressure fall from 49 to 39 s. These results demonstrated a positive inotropic effect of prenalterol on patients with diffuse and severely reduced contractility.

Cardiac Output↗
PubMed1983

Haemodynamic and cardiac metabolic effects of the new beta 1 agonist prenalterol in patients with cardiac failure.

Prenalterol, a beta 1 selective agonist, exerts a positive inotropic action in animal studies as well as in human volunteers and is effective when administered orally. To assess its immediate haemodynamic and myocardial metabolic effects, we studied the response to prenalterol (50 and 100 micrograms kg-1 given intravenously by cardiac catheterization) in 15 patients with congestive heart failure secondary to coronary artery disease or non-ischaemic cardiomyopathy. At peak effect, cardiac index increased from 2.6 +/- 0.5 to 3.2 +/- 0.8 l min-1 m2 (mean +/- S.D.) (P less than 0.001); peak rate of left ventricular pressure development rose from 963 +/- 242 to 1335 +/- 411 mmHg s-1 (P less than 0.001); left ventricular end-diastolic pressure fell from 25 +/- 6 to 17 +/- 7 mgHg (P less than 0.001); coronary sinus blood flow increased from 113 +/- 39 to 148 +/- 55 ml min-1 (P less than 0.01); myocardial oxygen consumption was augmented from 12.7 +/- 3.9 to 16.4 +/- 5.8 ml min-1 (P less than 0.001); and heart rate increased slightly (from 76 +/- 12 to 86 +/- 14 beats min-1; (P less than 0.05)). No significant changes occurred in left ventricular systolic pressure, stroke volume index, myocardial lactate extraction rate and myocardial arteriovenous oxygen difference, and no patients developed angina, ECG changes or ventricular arrhythmias. Infusion of prenalterol effectively improved haemodynamic function and cardiac metabolism in cardiomyopathy. Therefore this agent deserves further investigation to evaluate its possible role for the long-term therapy of patients with chronic heart failure.

Adrenergic beta-Agonists↗
PubMed1983

Effects of intraluminal administration of adrenoceptor agonists on transisthmic flow in the rabbit oviduct.

By perfusing the isthmic segment of the rabbit oviduct in vivo at low hydrostatic pressures with Ringer's solution (+38 degrees C), the resistance of the isthmic segment could be measured quantitatively using a drop-recording system. Transisthmic flow, from mid-tube to the uterine end, was thus studied in 45 animals, 48 h after human chorionic gonadotropin (hCG) injection. Stimulation of alpha-adrenoceptors by administration of norepinephrine or phenylephrine to the perfusate resulted in an immediate reduction or cessation of the basal flow. The duration of this effect varied dose-dependently. The administration of beta-adrenoceptor agonists (isoprenaline, prenalterol or terbutaline) markedly increased transisthmic flow. The beta 2-adrenoceptor agonist terbutaline was considerably more potent than the other beta-agonists. Thus, it seems that the isthmic contraction caused by adrenergic luminal stimulation is mediated via alpha-adrenoceptors, while the isthmic dilation is mediated via beta-adrenoceptors, mainly of the beta 2-type.

Animals↗