Venous waterfalls in coronary circulation

Several studies of flow through collapsible tubing deformed by external pressures have led to a concept known as the "vascular waterfall". One hallmark of this state is a positive zero-flow pressure intercept (Pe) in flow-pressure curves. This intercept is commonly observed in the coronary circulation, but in blood-perfused beating hearts a vascular waterfall is not the only putative cause. To restrict the possibilities, we have measured flow-pressure curves in excised non-beating rabbit hearts in which the coronary arteries were perfused in a non-pulsatile way with a newtonian fluid (Ringers solution) containing potent vasodilator drugs. Under these circumstances, vascular waterfalls are believed to be the only tenable explanation for Pe. In physical terms the waterfall is a region where the vessel is in a state of partial collapse with a stabilized intraluminal fluid pressure (Pw). It is argued that the most probable site of this collapse was the intramural veins just before they reached the epicardial surface. In accord with the waterfall hypothesis, Pe increased as the heart became more edematous, but flow-pressure curves also became flatter, implying multiple waterfalls with differing Pws, leading to complete collapse of some of the venous channels. The principal compressive force is believed to have been the interstitial fluid pressure as registered through a needle (Pn) implanted in the left ventricular wall, but a small additional force (Ps) was probably due to swelling of interstitial gels. A method is presented for estimating Ps and Pw. Unlike rubber tubing, blood vessels are both collapsible and porous. Apparently because of increased capillary filtration, Pn was found to increase linearly with the perfusion pressure. Thus, Pw was not the same at all points on the flow-pressure curve. This finding has interesting implications with respect to the concept of coronary resistance.     

Endothelin in the perinatal circulation

During the fetal period, blood is oxygenated through the placenta, and most of the cardiac output bypasses the lung through the ductus arteriosus. At birth, pulmonary vascular resistance falls with the initiation of ventilation. Coincidentally, the ductus arteriosus constricts. Endothelin-1 (ET-1) appears to play an important role during that transition period and postnatally. ET-1 can dramatically increase resistance in the placental microcirculation and may be involved in blood flow redistribution with hypoxia. At birth, the increase in oxygen tension is important in triggering ductus vasoconstriction. It is proposed that oxygen triggers closure of the ductus arteriosus by activating a specific, cytochrome P450-linked reaction, which in turn stimulates the synthesis of ET-1. On the neonatal heart, ET-1 has a positive chronotropic but negative inotropic effect. In the newborn piglet and the fetal lamb, both term and preterm, ET-1 causes a potent, long-lasting pulmonary vasoconstriction. Furthermore, a transient dilator response has been identified, and it is ascribed to nitric oxide formation. ET receptors are abundant in the piglet pulmonary vasculature. They are predominantly of the ETA constrictor subtype, though ETB2 constrictor receptors may also be present in certain species. The dilator response is linked to the ETB1 receptor, and the number of ETB1 receptors is reduced in hypoxia-induced pulmonary hypertension. ET-1 appears to be a causative agent in the pathogenesis of hypoxia- and hyperoxia-induced pulmonary hypertension as demonstrated by reversal of hemodynamic and morphological changes with treatment with an ETA receptor antagonist. Findings are amenable to practical applications in the management of infants with pulmonary hypertension or requiring persistent patency of the ductus arteriosus.     

Pulmonary circulation in experimental pneumonia

The ultrasonic technique was used in acute experiments on open-chest cats under controlled lung ventilation to test the blood flow in damaged and undamaged lung lobes in experimental pneumonia. It was shown that the absolute values of the linear and volumetric blood flow rate in the lower artery of the damaged lobe were similar to those in the analogous undamaged lobe. The blood flow in the damaged focus seems limited, while the blood volume passed through the vessels of the undamaged lobe is normal. This opinion is confirmed by high blood flow values in the artery supplying the damaged lobe with blood, when compared to the data on the absence of marked arterial hypoxaemia.