Monitoring urine oxygen tension during acute change in cardiac output in dogs

To evaluate whether renal blood flow (RBF) can be monitored during acute change in cardiac index, ureter urine oxygen tension (PuO2) and bladder urine oxygen tension (PbO2) were measured in six mongrel dogs. PuO2, cardiac index, and RBF increased after dobutamine infusion and decreased after propranolol infusion. PuO2 had an excellent correlation with RBF (r = 0.94) and a fair correlation with cardiac index (r = 0.50) and mean blood pressure (r = 0.56); RBF had a fair correlation with mean blood pressure (r = 0.52, P < 0.05) but was not related to cardiac index. With multiple-regression analysis, PuO2 was found to be the significant factor related to RBF. PbO2 had a good correlation with PuO2 (r = 0.94) at control levels. Furthermore, when two dogs were added to evaluate relationships among PbO2, PuO2, and RBF, PbO2 had an excellent correlation with PuO2 (r = 0.92) and RBF (r = 0.91). These data indicate that PuO2 is a more sensitive predictor of RBF than cardiac index and mean blood pressure and that PbO2 can be a noninvasive indicator reflecting RBF during acute circulatory change in dogs.

Origin and evolution of plateau waves

✓ Laboratory observations made in cats with fluid-percussion head injuries have suggested that plateau waves or Lundberg “A-waves” are not independent of systemic circulatory events. Four distinct phases in the evolution of the plateau wave have been identified, and each related to a circulatory change in a causal manner. The first phase is the premonitory drift phase where intracranial pressure (ICP) gradually increases prior to the plateau proper. This phase is caused by a slow gradual decline in systemic arterial blood pressure (SABP) which increases ICP by autoregulatory vasodilation and reduces cerebral perfusion pressure (CPP) to a range of 70 to 80 mm Hg. The second phase is the plateau phase initiated at a CPP of about 70 to 80 mm Hg, and is characterized by a rapid increase in ICP as CPP falls further to 40 to 50 mm Hg. The plateau lasts as long as the CPP remains stable and above ischemic levels. The third phase is the ischemic response, characterized by CPP being returned toward normal by increases in SABP in response to very low CPP's. The fourth phase is the resolution, characterized by a rapid decline in the ICP to baseline levels with stabilization of the SABP and CPP, and is best explained by autoregulatory vasoconstriction. Plateau waves appear to occur as the result of intact or mostly intact autoregulation responding to changes in CPP. The series of events that follow are best explained by what is known of normal autoregulation; the various properties of plateau waves are viewed and explained as the expected and logical consequences of an unstable CPP acting upon a generally intact cerebrovascular bed in the face of elevated ICP and decreased compliance.

Physiological evidence for the occurrence of pathways shunting blood away from the secondary lamellae of eel gills

1. Several cardiovascular and respiratory measurements have been performed in eels before and after intravenous injections of adrenaline. These experiments have allowed a comparison to be made of values for the cardiac output determined directly (Q) and using the Fick principle (QF) on individual fish under these two conditions. 2. Under control conditions it was shown that QF/Q = 0.72, indicating that about 30% of the mixed venous blood afferent to the gills is returned directly to the heart and bypasses the lamellar circulation via veno-venous anastomoses between the afferent filament arteries and the central venous space of the gill filaments. 3. Adrenaline, which during winter only has its action due to stimulation of alpha-adrenoreceptors, induced a hypoventilation but no changes in cardiac output in spite of a bradycardia. The oxygen content of the mixed venous blood was markedly increased whereas Ca,O2 remained unchanged as did the percentage utilization of oxygen from the water as it passed over the gills. The efferent blood flow from the gills after injection of adrenaline was almost equal to the total cardiac output. It is suggested that such a circulatory change was due to adrenaline-mediated constriction of veno-venous anastomoses in the gills of the eel.