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B C Wang

Publications and source records attributed to B C Wang.

At least 145 records · Page 8Linked to original sources
PubMed1983

Effect of body temperature on salicylate-induced hyperventilation.

Hyperventilation and hyperpyrexia occur simultaneously during acute salicylate intoxication. The present experiments were designed to investigate the stimulatory effect of increased body temperature on respiration in this pathological state. Acute salicylate intoxication was produced in mongrel dogs by intravenous infusion of 200 mg sodium salicylate/kg body weight, and the effect of body temperature on salicylate-induced hyperventilation was studied by comparing the respiration of hyperthermic animals with the respiration of animals maintained normothermic during acute salicylate intoxication by bathing them in cold water. The minute volume of ventilation increased greatly over control levels in both normothermic and hyperthermic animals, but this increment was much larger in hyperthermic animals. The increase in ventilation of normothermic animals can be explained as a rise in alveolar ventilation which results in hypocapnia despite large increases in carbon dioxide production and oxygen consumption during acute salicylate intoxication. The further augmentation of ventilation in hyperthermic animals can be explained as a rise in deadspace ventilation in response to increased body temperature during acute salicylate intoxication.

Animals↗
PubMed1983

Effect of intracarotid administration of morphine and naloxone on plasma vasopressin levels and blood pressure in the dog.

The effects of intracarotid injection of morphine and naloxone on plasma vasopressin levels and arterial blood pressure were examined in pentobarbital-anesthetized dogs. Morphine administration decreased blood pressure in a dose-dependent fashion with a threshold between 10 and 50 micrograms/kg. Plasma levels of vasopressin rose in parallel with the decrease in blood pressure and were significantly elevated after doses of 50 and 100 micrograms/kg of morphine. Intracarotid injection of the opioid antagonist naloxone (1 mg/kg) increased blood pressure slightly, but significantly, and increased plasma concentrations of vasopressin approximately 60%. Pretreatment with naloxone did not blunt the hypotensive effect of morphine at a dose of 50 micrograms/kg, but enhanced the secretion of vasopressin in response to the morphine stimulus; plasma vasopressin levels were 5-fold greater than those found in animals given morphine but not pretreated with naloxone. Pretreatment with the histamine receptor blockers chlorpheniramine and cimetidine blunted morphine-induced (50 micrograms/kg) hypotension by about 50% and prevented a significant increase in the plasma vasopressin concentration. The data are consistent with the hypothesis that stimulation of vasopressin secretion by systemically administered morphine is secondary to the blood pressure fall. However, it also appears that, in the pentobarbital-anesthetized dog, naloxone-sensitive systems exert a tonic inhibitory influence over both vasopressin secretion and blood pressure.

Animals↗
PubMed1982

Central infusion of vasopressin decreased plasma vasopressin concentration in dogs.

The effects of increasing the cerebrospinal fluid (CSF) vasopressin concentration (CSFADH) by intracerebroventricular infusion of vasopressin on the plasma vasopressin concentration (PADH) were studied in four groups of anesthetized dogs. One group received an intracerebroventricular infusion of artificial CSF (ACSF) alone for 90 min; the other groups were infused intracerebroventricularly with vasopressin at rates of 10, 20, or 50 microunits/min for 90 min. Arterial blood and CSF samples were taken just before infusion and at 30-min intervals for 210 min. Vasopressin infused intracerebroventricularly at 10, 20, and 50 microunits/min resulted in peak CSFADH of 32.2 +/- 5.3, 82.6 +/- 4.5, and 131.4 +/- 12.5 microunits/ml and reductions in PADH of 32, 47, and 51%, respectively. Only the latter two responses were significant (P less than 0.5-0.01). Because the peak increases in CSFADH after intracerebroventricular infusion of vasopressin ranged from values that were similar to or five times higher than those seen after severe hemorrhage or intracerebroventricular hypertonic saline infusion, we suggest that centrally acting vasopressin may play a physiological role in control of vasopressin secretion.

Animals↗
PubMed1982

Effect of intravenous and intracerebroventricular infusion of hypertonic solutions on plasma and cerebrospinal fluid vasopressin concentrations.

In the anesthetized dog, intravenous infusion of 2.5 M saline (40 microliters/kg . min) increased plasma and cerebrospinal fluid (CSF) osmolality and the plasma vasopressin (ADH) concentration, but did not increase the CSF ADH concentration. The increase in the plasma ADH concentration coincided with the increase in plasma osmolality, but preceded the increase in CSF osmolality. Intracerebroventricular infusion of hypertonic artificial CSF (2,000 mosm/kg . H2O, 10 microliters/min) increased CSF osmolality and plasma CSF ADH concentrations; plasma osmolality did not increase. Thus, receptors which sense changes in plasma osmolality appear to be outside the blood-brain barrier; different receptors may sense changes in CSF osmolality.

Animals↗
PubMed1981

Changes in vasopressin concentration in plasma and cerebrospinal fluid in response to hemorrhage in anesthetized dogs.

In the anesthetized dog, the concentrations of vasopressin (ADH) in plasma and cerebrospinal fluid (CSF) were similar under basal conditions, and there was a highly significant positive correlation between them (r = 0.71, p less than 0.01). Although hemorrhage was capable of increasing the ADH concentration in both plasma and CSF, the threshold for the increase in plasma ADH was much lower than for the increase in the concentration of ADH in CSF. In addition, the magnitude of the increase in the concentration of ADH in plasma was considerably greater than that in CSF at a comparable degree of hemorrhage. Our results suggest that ADH released into CSF during hemorrhage may have a different origin from that released into blood.

Animals↗
PubMed1981

Central effects of dopamine and bromocriptine on vasopressin release and blood pressure.

In order to investigate the role of central dopaminergic receptors in the control of vasopressin release and in cardiovascular regulation, the effects of intracerebroventricular administration of dopamine (DA) and bromocriptine (BC), a specific DA agonist, were compared in the anesthetized dog. The drugs were infused over a 20-min period into a lateral ventricle. DA brought about a transient decrease in mean arterial blood pressure, a slight increase in heart rate toward the end of the experiment, and a suppression of vasopressin release. BC increased heart rate and decreased blood pressure to a greater extent than did DA, and doubled the plasma vasopressin concentration. The increase in vasopressin secretion preceded the fall in blood pressure, ans was, therefore, due to a direct central action of BC. Although in these circumstances it is difficult to determine the role of dopaminergic neurons in the control of vasopressin release, there is some reason to believe that this role may be expressed by the actions of BC under the present experimental conditions.

Animals↗
PubMed1981

The role of central adrenoreceptors in the control of vasopressin release and blood pressure.

In order to investigate the role of central noradrenergic neurons in the control of vasopressin (ADH) release and cardiovascular regulation, norepinephrine (1.4 microgram/kg), clonidine (0.1 microgram/kg), and isoproterenol (1.4 microgram/kg were infused into the lateral cerebral ventricle of the anesthetized dog. The drugs were given over a 20-min period, dissolved in 0.9% saline at a volume rate of 10 microliter/min. Both norepinephrine and clonidine markedly reduced ADH release and lowered arterial blood pressure and heart rate. Isoproterenol had no effect on ADH release and produced a slight reduction in arterial pressure and a large increase in heart rate. Pretreatment with phenoxybenzamine (100 microgram/kg, iv) completely blocked the effects of norepinephrine on blood pressure and heart rate but only partially (about 50%) inhibited the norepinephrine effect on ADH release. Intravenous isoproterenol lowered blood pressure and increased ADH release and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality or plasma sodium and potassium concentrations. It is concluded that, in the anesthetized dog, intraventricular norepinephrine and clonidine decreased ADH release, blood pressure, and heart rate by stimulating alpha-adrenoreceptors. The increased release of ADH after peripheral administration of isoproterenol was presumably due to the reduction in blood pressure and decreased baroreceptor inhibition of ADH release.

Animals↗
PubMed1981

Vasopressin secretion in the New Zealand genetically hypertensive rat.

A study was undertaken to evaluate the role of vasopressin in the pathogenesis of hypertension in New Zealand genetically hypertensive (NZGH) rats. During the course of development of hypertension in NZGH rats from 4 to 11 weeks of age, the 24 h urinary excretion of vasopressin did not differ from that of the New Zealand normotensive control rats (NZNR). Furthermore, at the conclusion of the study (rats 13 to 14 weeks old), the plasma vasopressin concentrations in NZGH and NZNR rats were not significantly different. Although there was no evidence for a difference in secretion of vasopressin from the neurohypophysis in the NZGH rats, there was a substantially increased pressor responsiveness to vasopressin in these rats. This was not specific since NZGH rats also had an increased pressor responsiveness to angiotensin II. The importance of increased pressor responsiveness to vasopressin in the hypertensive process in the NZGH rat requires further study.

Angiotensin II↗
PubMed1980

Effect of norepinephrine on plasma vasopressin concentration and renal water metabolism.

In the anesthetized, normally hydrated dog, the i. v. infusion of norepinephrine (NE; 0.5 microgram/kg/min) resulted in an increased blood pressure and a marked reduction in the plasma vasopressin (ADH) concentration (2.6 +/- 0.2 to 1.1 +/- 0.2 muU/ml). Urine flow and osmolar clearance, and urine osmolality fell. However, the negative free water clearance (TcH2O) increased, despite the reduction in plasma ADH levels. Thus, the NE-induced diuresis appeared to be due largely to the increased solute excretion, but the reduction in plasma ADH levels may also have been a factor. These data show that change in free water clearance is not a satisfactory index of change in the plasma ADH levels may also have been a factor. These data show that change in free water clearance is not a satisfactory index of change in the plasma ADH concentration when there are acute changes in renal hemodynamics and solute excretion. The norepinephrine-induced reduction in ADH secretion appeared to be due largely to increased activity of the arterial baroreceptors, but a central action cannot be ruled out.

Animals↗
PubMed1979

Computer simulation of flow-dependent absorption in microperfused short Henle's loop of rats.

With computer simulation we examined the extent to which current theories and experimental data explain function of single microperfused superficial Henle's loops in rats. In the model standard phenomenological equations describe transport; two sets of transport parameters labeled rat and rabbit were taken from published experiments; Michaelis-Menten kinetics in the ascending thick limb were adjusted arbitrarily; tubular radius is either constant or depends on luminal pressure with compliance based on experimental observations; the interstitium is an infinite sink with salt and urea concentrations constant in the cortex and exponentially increasing in the outer medulla; concentrations resemble those found in hydropenic or saline diuretic rats. The following predictions were obtained. The model with rabbit parameters does not recirculate urea and will not operate with high medullary urea concentrations; with rat parameters too much urea recirculates an the results of perfusion with equilibrium solution are not reproduced. Using a compromise between rat and rabbit parameters, the model reproduces water absorption, salt reabsorption, and urea recirculation as observed in vivo in rat loops perfused at 5-40 nl/min. It also simulates perfusion with saline, equilibrium solution, saline plus furosemide, and 300 mM mannitol. When the model includes a short early distal segment, effluent salt concentration reaches a minimum at a 15 nl/min perfusion rate as observed in vivo; however, concentration at the macula densa is a monotonically increasing function of flow. When permeation rate is a function of wall surface area and thickness a better fit to experimental results is produced. However, the effect is small: water absorption alters by 4% or less and effluent salt concentration is reduced by up to 10% at low perfusion rates. Comparison of rigid and compliant loops shows no relationship between transit time per se and reabsorption.

Animals↗