Vasopressin and oxytocin responses to acute and chronic osmotic stimuli in man.

The regulation of both arginine vasopressin (AVP) and oxytocin secretion was studied during rapid and prolonged osmotic stimuli in normal adult volunteers. In five subjects given an intravenous infusion of 0.85 mol NaCl at 0.05 ml/kg per min over 2 h there was a significant (P less than 0.05) rise only in plasma AVP, with no significant change in plasma levels of oxytocin. In six further subjects 5 days of restriction to 500 ml fluid daily resulted in significant increases of both plasma and 24-h urinary AVP, whereas there was no change in corresponding oxytocin levels. During another 5-day period in which the same subjects were given an additional 200 mmol sodium as well as having their fluid intake restricted to 1000 ml daily, there were again significant rises in plasma and 24 h urinary AVP with no change in corresponding oxytocin levels. We conclude that, in man, AVP is selectively secreted in response to both dehydration and high sodium intake, whilst even after the stimulus of rapidly increasing plasma osmolality during intravenous infusion of hypertonic saline the rise in oxytocin is not statistically significant. It therefore appears unlikely that oxytocin has a significant role in the physiological control of fluid balance in man.

Elasmobranch pericardial function. 3. The pericardioperitoneal canal in the horn sharkHeterodontus francisci.

The pericardial and peritoneal spaces of elasmobranch fishes are connected by the pericardioperitoneal canal (PPC), which allows pericardial fluid to escape when pressures exceed 0.1-0.3 kPA. Using the horn shark (Heterodontus francisci), we tested the hypothesis that the PPC functions to increase cardiac stroke volume by lowering pericardial pressure during activity. We also assessed the role of the PPC during coughing, feeding, or burst swimming and examined the effects of PPC occlusion. Increases in heart size were not prevented following augmented venous return in sharks with undisturbed or occluded PCP, evidence that argues that pericardial fluid loss through the PPC is a cause of increased cardiac stroke volume and not the result. Coughs, feeding, and burst swimming led to discharge of pericardial fluid. Chronic PPC occlusion resulted in an increased pericardial pressure, fluid volume, and frequency of coughing, and a decreased survival time compared to shams. Thus, in the horn shark the PPC likely compensates for constraints that may be imposed by the pericardium, provides a route for pericardial drainage, and regulates cardiac stroke volume during periods of activity.

Elasmobranch pericardial function 2. The influence of pericardial pressure on cardiac stroke volume in horn sharks and blue sharks.

The importance of negative pericardial pressure to heart function in clasmobranchs has been questioned due to the discovery of positive pericardial pressures in healthy horn sharks (Heterodontus francisci). We therefore implanted electromagnetic flow probes on the ventral aorta of horn sharks and blue sharks (Prionace glauca) and assessed stroke volume and pericardial pressure as pericardial fluid volume (PFV) was varied to test the hypothesis that elasmobranchs are capable of maintaining a relatively large stroke volume at pericardial pressures near and above ambient. Stroke volume was maximum between zero and 25% maximum PFV (maximum PFV: the volume of pericardial fluid required to open the pericardioperitoneal canal), where pericardial pressure was most negative. At 50% maximum PFV (pericardial pressure near or slightly above ambient) stroke volume was 70% and 98% of its maximum in horn sharks and blue sharks, respectively. At a larger PFV, stroke volume declined drastically, reaching zero where both PFV and pericardial pressure were maximum. Thus, at a pericardial pressure apparently associated with resting or mild activity, stroke volume is a relatively large proportion of the apparent maximum. Increased circulatory demands associated with strenuous activity may induce ejection of pericardial fluid through the perieardioperitoneal canal, which then lowers pericardial pressure. The lowered pericardial pressure causes an increase in stroke volume, indicating that control is in part effected by changing pericardial pressure.

Elasmobranch pericardial function. 1. Pericardial pressures are not always negative.

Acute studies have led to the generalization that negative pericardial pressure is necessary for optimal cardiac function in elasmobranchs. We chronically instrumented horn sharks with pericardial catheters to test the hypothesis that ejection of pericardial fluid through the pericardioperitoneal canal (PPC) during routine handling could have accounted in part for previous measurements of exclusively negative pressures (-0.3 to -9.1 cm H2O) in elasmobranchs. Maximum and minimum pericardial pressures measured immediately following routine handling (acute pressures) were more negative than those measured in resting horn sharks at intervals from 1 to 27 days following handling (chronic pressures). Chronic pericardial pulse pressure was less than acute. Entirely positive pericardial pressures were observed on occasion. Handling of chronically catheterized horn sharks resulted in ejection of 21 per cent (range=10-26, n=5) of the initial pericardial fluid volume through the PPC and reduced pericardial pressure. Operating pericardial fluid volume of horn sharks averaged 2.0 ml.kg(-1) (range=1.6-2.6, n=9). The PPC opened after 4.3±0.2 ml.kg(-1) (x±S.E.) of elasmobranch saline had been slowly infused into the pericardium, corresponding to an average pressure of 1.3±0.2 cm H2O (n=10). The presence of the PPC plus a comparatively large pericardial fluid volume allows horn sharks to regulate pericardial pressure. Our analysis of pericardial pulse pressure, which can be an index of cardiac activity, suggests in contrast to previous studies that the elasmobranch heart can have relatively high stroke volumes at pericardial pressures near ambient. Thus, for venous return in resting or even moderately active elasmobranchs, it is more important that pericardial pressure be pulsatile than at a mean level which is negative.

Function of the pericardium and pericardioperitoneal canal in elasmobranch fishes.

Previous studies of cardiac function in elasmobranch fishes have not included the influence of the pericardioperitoneal canal on pericardial pressure and volume and thus on cardiac function. Accordingly, we studied the function of the pericardium and pericardioperitoneal canal in sharks and rays. We found negative pericardial pressure that rose to a plateau of approximately 0 mmHg when fluid was infused into the pericardium with the canal undisturbed. However, this pericardial pressure elevation caused severe cardiac tamponade. After the canal was occluded, the pressure plateau was substituted with an exponential rise. We injected radioisotopes into the pericardial cavity and obtained scintigrams several hours later. The scans and counts of body fluids and tissues indicated absorption, disputing the suggestion that the primary function of the canal may be inadequate absorption of pericardial fluid. We conclude that the pericardioperitoneal canal maintains negative pericardial pressure, which is a prerequisite in elasmobranch fishes and may serve to regulate pericardial pressure level to optimize cardiac function in relation to changes in cardiac size.