Search results for "Coronary perfusion pressure"
showing 3 items of 3 documents
Endothelial kinin B1‐receptors are induced by myocardial ischaemia‐reperfusion in the rabbit
2001
Kinin B1-receptors are induced by various inflammatory stimuli. Since myocardial ischaemia-reperfusion results in inflammation, we questioned whether it could induce B1-receptor-dependent responses to des-Arg9-bradykinin (DBK). Thirty-six rabbits were submitted either to a 30 min coronary occlusion followed by a 3 h reperfusion or to a sham operation. The response to DBK was then tested in vivo on mean arterial pressure (MAP) and in vitro on isolated hearts and arterial rings. DBK induced a dose-dependent decrease in MAP in the ischaemia-reperfusion group (DBK, 10 μg kg−1, intra-arterial: -12 ± 2 vs. -5 ± 2 mmHg in the sham group, P < 0.02), which was significantly antagonised by [Leu8]-des…
The specificity of prostaglandin E2 (PGE2) in reducing coronary vascular resistance: A comparison with adenosine.
1978
Experiments were performed on the isolated, electrically driven guinea-pig heart, perfused at constant rate. All animals were pretreated with reserpine. Myocardial contractile force (MCF), coronary perfusion pressure (CPP) and myocardial oxygen consumption (QO2) were monitored continuously. Both adenosine (ADO) and PGE2 produced a concentration-dependent decrease in the CPP. The ED50 (50% of maximum response) was 2.1 +/- 0.6 X 10(-9)M for PGE2 but 40 +/- 7 X 10(-9)M for ADO (P less than 0.01) at 1.8 mM Ca(e). This coronary vasodilation was independent of the external Ca-concentration, which was varied between 0.55-9.0 mM. PGE2 had no effect on MCF or QO2 and the effect of ADO was only sligh…
Staphylococcal α-toxin provokes coronary vasoconstriction and loss in myocardial contractility in perfused rat hearts: Role of thromboxane generation
2000
Background —Cardiac performance is severely depressed in septic shock. Endotoxin has been implicated as the causative agent in Gram-negative sepsis, but similar abnormalities are encountered in Gram-positive sepsis. We investigated the influence of the major exotoxin of Staphylococcus aureus, staphylococcal α-toxin, in isolated perfused rat hearts. Methods and Results —α-Toxin 0.25 to 1 μg/mL caused a dose-dependent increase in coronary perfusion pressure that more than doubled. In parallel, we noted a decrease in left ventricular developed pressure and the maximum rate of left ventricular pressure rise (dP/dt max ), dropping to a minimum of <60% of control. These changes were accompani…