Cardiac and microcirculatory effects of different doses of prostaglandin E1 in man

Abstract

A cumulative dose response to intravenous PGE1 was established in 12 healthy volunteers. Systolic time intervals, including pre-ejection period (PEP), the ventricular ejection time (VET) and the RR-interval, were continuously determined, and transcutaneous oxygen pressure (tcpO2) was recorded. RR-intervals fell in a dose dependent manner, reaching a significantly lower level at 128 ng.kg-1.min-1 of PGE1 (basal value 842 ms falling to 756 ms). PEP decreased from 89 ms to 74 ms and the ratio PEP/VET decreased from 35% to 30%, indicating increased myocardial contractility. The maximal increase in tcpO2 was 125% on the calf and 60% on the foot. The peak tcpO2 was observed at an infusion rate of 16 ng.kg-1.min-1 PGE1. A decline in tcpO2 was seen at infusion rates greater than 64 ng.kg-1.min-1 PGE1 indicating a decrease in skin perfusion. The results indicate that the effects of intravenous PGE1 on skin perfusion occur at a lower threshold than the increase in myocardial contractility. A maximal increase in skin perfusion can be achieved with doses of PGE1 devoid of systemic haemodynamic effects.

Prostaglandin E1 and arterial occlusive disease: pharmacological considerations

“…Intravenous infusion of 2 100 ng kg-' min-I causes I system I flush, increases heart rate and decreases blood pressure and peripheral resistance in healthy subjects [38-401. Conversely, transcutaneous oxygen pressure as a parameter reflecting capillary flow was increased by 125% during an intravenous infusion of PGEl (16 ng kg-I min-I), demonstrating that the effects on local perfusion can be achieved with doses of PGEl devoid of systemic haemodynamic effects [38]. Comparable results were obtained in patients with arterial occlusive disease, during intravenous infusion of PGEl (9.5 ng kg-I min-'), using venous occlusion plethysmography [41].…”

“…PGEl is a potent vasodilator [6,7,37,38] in man. Intravenous infusion of 2 100 ng kg-' min-I causes I system I flush, increases heart rate and decreases blood pressure and peripheral resistance in healthy subjects [38-401. Conversely, transcutaneous oxygen pressure as a parameter reflecting capillary flow was increased by 125% during an intravenous infusion of PGEl (16 ng kg-I min-I), demonstrating that the effects on local perfusion can be achieved with doses of PGEl devoid of systemic haemodynamic effects [38].…”

Effect of the technique for assisting renal blood circulation on ischemic kidney in acute cardiorenal syndrome

“…The rationale for using PGE 1 included its properties as a potent vasodilator and its reported benefit in preventing renal ischemia under hypoperfusion and ischemia [14,15]. The rate of 0.015 lg/kg/min of PGE 1 for a kidney was arbitrarily determined based on data showing that low systemic infusion rates of PGE 1 below 0.032 lg/kg/min do not cause a change in blood pressure or heart rate in healthy humans [16,17]. The renal-selective infusion of PGE 1 with RSP exerted vasodilating effects on the renal vascular system without having a significant effect on the systemic vascular system, which enabled an increase in the RSP flow and resulted in increased oxygen delivery, which should be favorable for treatment of ACRS.…”

Prostaglandin E1in critical limb ischemia transcutaneous PO2: A predictor of efficacy?

“…The principal reactivity and susceptibility to interventions of the cutaneous perfusion might help predict the success of therapy [11]. A number of investigators have reported that tcPO 2 measured at the ischemic extremity rises when PGE 1 is infused intravenously [5,9,18]. In our pilot study we tried to find a parameter that might predict the effectiveness of a conservative approach to a patient with critical limb ischemia.…”