Biomedical subjects

J Zink

Publications and source records attributed to J Zink.

14 recordsLinked to original sources

PubMed1981

Noradrenergic control of blood vessels in the premature lamb fetus.

Experiments were conducted with fetal lambs of 113-120 days gestation (0.8 term) to assess the integrity of adrenergic neurotransmission at the level of the blood vessels. Regional blood flow and the distribution of blood from the inferior vena cava were compared when the arterial pressure was increased either by an infusion of exogenous noradrenaline or when tyramine was used to evoke a local release of the neurotransmitter. Most vascular beds perfused via the descending aorta were constricted to a similar extent by both drugs although the renal circulation did not respond to tyramine. Noradrenaline increased the distribution of blood from the inferior vena cava to the fetal lungs and both drugs increased placental blood flow. These data indicate that mechanisms for effective adrenergic control of vascular are developed in many organs of the premature lamb fetus by 0.8 of term.

Animals↗

PubMed1978

Relative rates of absorption of fluid and protein from the peritoneal cavity in cats.

The relative rates of fluid and protein absorption from the peritoneal cavity of anesthetized cats were measured over 6 hours at an intraperitoneal pressure of 15 mm Hg and with intraperitoneal protein concentrations from 1-8 g%. The fractional absorption rates of fluid and protein did not change significantly over the 6 hours and were not significantly different from each other within each one hour period. In addition both fractional absorption rates were unaffected by the protein concentration of the fluid within the peritoneal cavity. Although the absolute rate of absorption is greatly increased by elevation of the intraperitoneal pressure, these data indicate that the process remains iso-oncotic as would be expected for lymphatic rather than transcapillary absorption.

Absorption↗

PubMed1977

Intraperitoneal pressure in formation and reabsorption of ascites in cats.

The rate of ascites formation or reabsorption was recorded in anesthetized cats using the technique of intraperitoneal plethysmography. Hepatic venous pressure was increased using an extracorporeal circuit to drain effluent blood from the liver. When the intraperitoneal pressure was set to zero, elevation of hepatic venous pressure increased portal pressure and produced a constant rate of ascites formation. However, equivalent increments of portal pressure without elevation of hepatic venous pressure did not cause ascites formation, indicating that the liver was the source of ascites when hepatic venous pressure was increased. The rate of ascites formation was proportional to hepatic venous pressure, but elevation of the intraperitoneal pressure reduced the transsinusoidal pressure gradient responsible for fluid filtration from the liver. Although this reduced the rate of ascites formation, a secondary effect partly opposed this reduction in filtration rate. From this study and from previous work, there are now quantitative data showing that the intraperitoneal pressure is an important factor which accelerates the rate of reabsorption and decreases the rate of formation of ascites to bring these processes into equilibrium.

Animals↗

PubMed1977

Control of ascites absorption in anesthetized cats: effects of intraperitoneal pressure, protein, and furosemide diuresis.

There is considerable evidence that fluids are removed from the peritoneal cavity by drainage into lymphatics lining the surface of the diaphragm, but there is little quantitative information on the rate of reabsorption as affected by conditions which exist in cirrhotic ascites. In the present study a plethysmographic technique was utilized to record the rate of absorption of fluid from the peritoneal cavity of anesthetized cats. The results of studies in 33 cats showed that the rate of fluid absorption from the peritoneal cavity was directly proportional to the intraperitoneal pressure regardless of whether the intraperitoneal fluid was free from protein or contained a protein concentration equivalent to that of plasma. Fluid was absorbed with a protein concentration equivalent to that present in the peritoneal cavity. Thus it is apparent that the intraperitoneal pressure is an important factor controlling the accumulation of ascitic fluid but the protein concentration of the intraperitoneal fluid does not affect the rate of reabsorption. In addition, marked diuresis induced by intravenous furosemide does not appear to mobilize ascites by an effect on the reabsorption process.

Absorption↗

PubMed1976

Sites of autoregulatory escape of blood flow in the mesenteric vascular bed.

1. Stimulation of the sympathetic nerves to the intestinal vascular bed results in an initial decrease in blood flow followed by a recovery towards the control level. This recovery was termed autoregulatory escape by Folkow and his co-workers and they suggested it was associated with a redistribution of blood flow within the intestinal wall. This theory has been examined in cats anaesthetized with pentobarbitone sodium. 2. The sympathetic nerves to the intestinal vascular bed were stimulated for 4 min periods at a submaximal frequency (4 Hz). The blood flows to individual parts of the superior mesenteric arterial bed (whole intestine, mucosal and submucosal layer, muscle layer of intestine, mesentery and lymph nodes, appendix and colon) were measured using radioactive microspheres before, at the peak of the vasoconstriction (30 sec), after autoregulatory escape had occurred (3-5 min) and during the hyperaemia after cessation of nerve stimulation. 3. All parts of the mesenteric vascular bed showed a significant initial vasoconstriction followed by a recovery in the flow to a level not significantly different from the pre-stimulation control flow. All parts showed a significant hyperaemia after cessation of stimulation. The distribution of the superior mesenteric flow at the peak of the vasoconstriction, after autoregulatory escape had occurred and during the hyperaemia after cessation of nerve stimulation was not significantly different from that during the control period. 4. It is concluded that all parts of the mesenteric vascular bed show autoregulatory escape and that this phenomenon is not associated with a redistribution of blood flow within the intestinal wall. Autoregulatory escape must involve relaxation of the same vessels which were originally constricted and various theories on the mechanism of the escape are discussed.

Animals↗

PubMed1976

An improved plethysmograph with servo control of hydrostatic pressure.

One limitation of the conventional fluid displacement plethysmograph is that the hydrostatic pressure varies as recordings of volume change are obtained. Thus, use of this instrument can lead to inaccuracies that are proportional to the compliance of the biological system under study. This paper describes an improved design which utilizes a servo-control system and an open, mobile reservoir to ensure that the hydrostatic pressure is maintained constant as volume changes are recorded. The result is a device that succeeds in combining stability, sensitivity and accuracy in a fluid displacement plethysmograph.

Compliance↗

PubMed1975

Halothane-epinephrine-induced cardiac arrhythmias and the role of heart rate.

The authors previously showed that cyclopropane-epinephrine-induced bigeminal arrhythmias can best be explained by a re-entrant mechanism. They have now obtained evidence for reentry in bigeminal arrhythmias during infusions of epinephrine (.5-3 mug/kg/min) in dogs anesthetized with .8 per cent halothane. Both a critical level of blood pressure and a critical increase in heart rate were necessary for arrhythmias to be induced in any given animal. Artificial elevation of the blood pressure during infusion of a subthreshold dose of epinephrine could induce bigeminy, and the arrhythmia could be aborted by a sudden reduction of blood pressure. The heart rate accelerated approximately 40 beats/min prior to the onset of bigeminy, and atrial pacing at similarly increased rates during subthreshold infusion of epinephrine could induce bigeminy. Stimulation of the peripheral end of the cut right cervical vagus reduced heart rate and converted bigeminy to sinus rhythm. Bradycardia was not the sole mechanism of the vagal effect since conversion to sinus rhythm could also be achieved with more rapid stimulation of the vagus when the heart rate was maintained constant by atrial pacing. Under these conditions further acceleration of the heart rate could reinstate a bigeminal arrhythmia that was again sensitive to further increases in the frequency of vagal stimulation, and it is concluded that the vagus acts on the spread of the re-entrant impulse. This is best shown with cyclopropane anesthesia, because AV-nodal block occurs more easily with halothane. In addition, very brief periods of increased heart rate caused prolonged periods of bigeminy, which indicates that changes in heart rate may alter the electrophysiology of the halothane-sensitized myocardium to promote bigeminal arrhythmias by a re-entry mechanism.

Anesthesia, Inhalation↗

PubMed1974