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Biomedical subjects

R Krebs

Publications and source records attributed to R Krebs.

At least 55 records · Page 3Linked to original sources
PubMed1976

Increase in the coronary vascular resistance by indomethacin in the isolated guinea pig heart preparation in the absence of changes in mechanical performance and oxygen consumption.

Experiments were performed in isolated guinea pig hearts, perfused at constant volume. Left ventricular pressure, left ventricular dp/dtmax, coronary vascular pressure and coronary venous pO2 were measured continuously. Indomethacin (1.4 X 10(-6) M) increased coronary vascular resistance by 15% over control (p less than 0.01) without altering the myocardial contractile force. When PGE2 (1.4 X10(-8) M) was subsequently added, it abolished the indomethacin action and lowered the coronary vascular resistance below the pre-indomethacin control value. This increase in coronary vascular resistance caused by indomethacin was also seen when the animals were pretreated with reserpine and/or the adrenoceptor blocking agents phenoxybenzamine and propranolol, but was prevented completely by previous addition of PGE2 (1.4 X 10(-7) M). The results provide evidence for possible involvement of endogenous prostaglandin-like substances in the maintenance of coronary vascular resistance in the isolated guinea pig heart.

Animals↗
PubMed1976

Interactions of isoprenaline and prostaglandin E2 with respect to myocardial contractile force, coronary vascular resistance and myocardial oxygen consumption in guinea-pig isolated hearts.

Left ventricular pressure (LVP), left ventricular pressure derivative (LV dp/dtmax), coronary vascular resistance (CVR) and myocardial oxygen consumption (Qo2) were measured simultaneously in isolated, electrically driven hearts of guinea-pigs at constant perfusion rate. 2 LVP, LV dp/dtmax, CVR and Qo2 were greatly decreased by either the addition of prostaglandin E2 (50 ng/ml) to the perfusion fluid or pretreatment of the animals with reserpine. 3 Isoprenaline (0.5 nM to 100 nM) induced increases in LVP, LV dp/dtmax and Qo2. In the presence of prostaglandin E2, there was a parallel shift of the isoprenaline concentration-response curve for LVP and LV dp/dtmax. This effect was not seen, after the animals had been treated with reserpine. 4 Qo2 was also decreased by prostaglandin E2 only in non-reserpine treated animals. 5 CVR was diminished by isoprenaline in the untreated group. However, there was increase in CVR, when isoprenaline was added to either prostaglandin E2 or reserpine-pretreated hearts which was enhanced in the reserpine plus prostaglandin E2-treated group (P less than 0.01). 6 The results give evidence for different actions of prostaglandin E2 on isoprenaline concentration-response curves for LVP, LV dp/dtmax and CVR.

Animals↗
PubMed1975

Actions of prostaglandin E2 on myocardial mechanics, coronary vascular resistance and oxygen consumption in the guinea-pig isolated heat preparation.

1 In isolated, electrically driven (3 Hz) hearts of guinea-pigs the action of prostaglandin E2 on left ventricular pressure (LVP), oxygen consumption (Qo2) and coronary vascular resistance (CVR) was studied by establishing cumulative concentration-response curves. The hearts were perfused at a constant flow (10 ml/min) with Tyrode solution (Ca++ 1.8 mM) at 32 degrees C. 2 Under control conditions prostaglandin E2 (2.86 X10(-11) -1.43 X 10(-7) M) decreased LVP, QO2 and CVR in a concentration-dependent manner by maximally 27, 18 and 38%, respectively (P less than 0.05). 3 After reserpine pretreatment there were lower initial values for all parameters measured. The effect of prostaglandin E2 on LVP and QO2 was abolished, but CVR was further diminished, depending on the concentration. 4 The results seem to support the hypothesis of an interaction of prostaglandin E2 with endogenous catecholamines as far as the effects on LVP and QO2 are concerned. In contrast, prostaglandin E2 seems to have a direct action on CVR, which is independent of the presence of catecholamines.

Animals↗