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Biomedical subjects

C E Wade

Publications and source records attributed to C E Wade.

At least 127 records · Page 7Linked to original sources
PubMed1986

Effect of antigravity suit inflation on cardiovascular, PRA, and PVP responses in humans.

Blood pressure, pulse rate (PR), serum osmolality and electrolytes, as well as plasma vasopressin (PVP) and plasma renin activity (PRA), were measured in five men and two women [mean age 38.6 +/- 3.9 (SE) yr] before, during, and after inflation of an antigravity suit that covered the legs and abdomen. After 24 h of fluid deprivation the subjects stood quietly for 3 h: the 1st h without inflation, the 2nd with inflation to 60 Torr, and the 3rd without inflation. A similar control noninflation experiment was conducted 10 mo after the inflation experiment using five of the seven subjects except that the suit was not inflated during the 3-h period. Mean arterial pressure increased by 14 +/- 4 (SE) Torr (P less than 0.05) with inflation and decreased by 15 +/- 5 Torr (P less than 0.05) after deflation. Pulse pressure (PP) increased by 7 +/- 2 Torr (P less than 0.05) with inflation and PR decreased by 11 +/- 5 beats/min (P less than 0.05); PP and PR returned to preinflation levels after deflation. Plasma volume decreased by 6.1 +/- 1.5% and 5.3 +/- 1.6% (P less than 0.05) during hours 1 and 3, respectively, and returned to base line during inflation. Inflation decreased PVP from 6.8 +/- 1.1 to 5.6 +/- 1.4 pg/ml (P less than 0.05) and abolished the significant rise in PRA during hour 1. Both PVP and PRA increased significantly after deflation: delta = 18.0 +/- 5.1 pg/ml and 4.34 +/- 1.71 ng angiotensin I X ml-1 X h-1, respectively. Serum osmolality and Na+ and K+ concentrations were unchanged during the 3 h of standing.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Centrally administered inhibitors of the generation and action of angiotensin II do not attenuate the increase in ACTH secretion produced by ether stress in rats.

The role of the brain renin-angiotensin system in the ACTH response to ether stress in rats was investigated by injecting the angiotensin II receptor blocking drug saralasin, the angiotensin II converting enzyme inhibitors enalaprilat and captopril, and the renin inhibitor L 363714 intraventricularly and measuring the ACTH and corticosterone concentration in plasma 10 min after ether stress. ACTH and corticosterone were elevated to at least the same level in rats treated with the inhibitors as they were in rats treated with the corresponding vehicles; indeed, ACTH values were somewhat greater in stressed rats treated with the converting enzyme inhibitors and the renin inhibitor. ACTH values in the absence of ether were not affected by saralasin, enalaprilat, and captopril and were increased by L 363714. The data do not support the hypothesis that the brain renin-angiotensin system is involved in the maintenance of ACTH secretion or that it mediates the increase produced by ether stress.

Adrenocorticotropic Hormone↗
PubMed1986

Heat-denatured albumin-coated Dacron vascular grafts: physical characteristics and in vivo performance.

Dacron fabrics with a wide range of porosities were autoclaved for 3 minutes after being soaked in serum, 5% albumin, or 25% albumin. Porosity of compound Dacron grafts made with 25% albumin was less than 1 ml/min/cm2 regardless of the fabric base, whereas porosity of grafts made with serum or 5% albumin was proportional to the porosity of the base fabric. Porosity of the compound grafts remained stable for more than 48 hours and to pressure greater than 450 mm Hg, if the grafts were kept moist. Tubes of Marlex mesh coated with heat-denatured albumin, implanted as infrarenal aortic replacements in dogs, showed complete albumin absorption by 3 weeks. However, perigraft tissue reaction and graft incorporation were minimal and extensive false aneurysm formation resulted. Knitted filamentous Dacron 6 mm tubes coated with heat-denatured albumin were implanted as iliofemoral bypass grafts in 12 dogs, with blood-preclotted knitted filamentous Dacron grafts implanted as contralateral control grafts. Comparison of the albumin-coated grafts with the blood-preclotted control grafts showed no differences in healing or patency at 4 to 6 months. Heat-denatured 25% albumin forms a strong and hemostatic coating regardless of fabric base. Albumin-Dacron compound grafts are easily and rapidly made in the operating room, handle well, and are suitable for large and medium-sized arterial replacements without changes in healing or patency. Because of slow tissue incorporation, however, albumin-coated knitted Dacron grafts should be avoided in patients who require long-term anticoagulation therapy.

Albumins↗
PubMed1985

Plasma aldosterone and renal function in runners during a 20-day road race.

To evaluate the effects that repeated long-distance running has on plasma aldosterone concentration and urinary excretion of solutes, fifteen male runners were studied during a 20-day, 500-km road race. Venous blood samples were taken on day 1 prior to running, on day 11 after 10 days of running, on day 13 after a 70-h rest, and on day 18 after an additional five days of running. Overnight urine samples were obtained on day 10 before and after running and on days 11, 12, and 13 during the 70-h rest period. Plasma sodium concentrations on days 13 and 18 and plasma potassium concentrations on days 11 and 13 were decreased (P less than 0.05). Plasma aldosterone levels were increased on days 11 and 18 after running and returned to pre-race levels on day 13 after 70 h of rest. Plasma cortisol concentrations were not altered. The urinary excretion rates of sodium were elevated and of aldosterone were decreased after 70 h of rest. Increase in excretion rate of urinary sodium correlated with decrease in concentration of plasma aldosterone. These findings show that plasma aldosterone levels are chronically elevated with repeated long-distance running, resulting in a decrease in urinary excretion rate of sodium.

Adult↗
PubMed1985

Pituitary and adrenal hormone responses to naloxone in euhydrated and dehydrated dogs.

To assess the role of endogenous opioids in the secretion of pituitary and adrenal hormones, we injected intravenously the antagonist naloxone (1 mg/kg) into six dogs, euhydrated or dehydrated. Plasma renin activity (PRA), osmolality, and concentrations of adrenocorticotropic hormone (ACTH), cortisol, aldosterone, vasopressin, Na+, and K+ were measured. Dehydration elevated (P less than 0.05) PRA, vasopressin, osmolality, and Na+. Thirty minutes after injection of naloxone, osmolality, Na+, K+, hematocrit, and plasma protein were not altered. Naloxone-induced elevations of ACTH (25 +/- 10 and 22 +/- 4 pg/ml) and cortisol (4.8 +/- 1.0 and 5.1 +/- 1.0 micrograms/dl) were similar during euhydration and dehydration, respectively. The increase in aldosterone due to naloxone was greater after euhydration (7.7 +/- 3 ng/dl) than during dehydration (2.3 +/- 0.8 ng/dl). Naloxone increased vasopressin by (5.3 +/- 2.8 microU/ml) during dehydration but not during euhydration. Intravenous hypertonic saline infusions showed that naloxone potentiates the osmotic release of vasopressin. Our results indicated that dehydration did not alter the inhibitory role of opioids in regulation of ACTH and cortisol but suppressed the inhibition of aldosterone secretion. Our findings also showed that opioids inhibit secretion of vasopressin during dehydration by decreased responsiveness to osmotic stimulation.

Adrenocorticotropic Hormone↗
PubMed1985

Acute volume expansion decreases adrenocortical sensitivity to ACTH and angiotensin II.

This study examined the plasma aldosterone and corticosteroid responses to a 60-min infusion of adrenocorticotropin (ACTH) or angiotensin (ANG) II started immediately after an acute isotonic saline volume expansion (0.5 ml . kg-1 . min-1 for 30 min). Five conscious dogs of either sex with exteriorized carotid loops were used in this repeated-design study. Volume expansion per se caused a 10% decrease in hematocrit, a 12.5% decrease in plasma protein, and a 2.7-mmHg increase in central venous pressure with no change in mean arterial pressure, heart rate, or plasma sodium. Volume expansion per se also resulted in significant reductions in vasopressin, plasma renin activity, ACTH, aldosterone, and corticosteroid levels. The aldosterone responses to ACTH and ANG II were significantly inhibited (46-71%) by acute volume expansion. The corticosteroid response to ACTH was 19-29% inhibited by volume expansion. We conclude that acute volume expansion significantly inhibits the adrenocortical sensitivity to its tropic hormones probably via alterations of synergistic factors.

Adrenal Cortex↗
PubMed1984

Sodium balance and aldosterone during dehydration and rehydration in the dog.

The regulation of sodium metabolism and the renin-angiotensin-aldosterone system was evaluated during 24 h of water, but not food, deprivation and during rehydration in the dog. Dehydration caused increases in plasma concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl), vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion increased significantly, leading to a negative sodium balance (1.9 +/- 0.2 meq/kg). Sodium retention was observed after rehydration and sodium balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA) returned turned to control levels after the 1st day of recovery. However, plasma aldosterone was slightly elevated at this time, returning to control after the 2nd day of recovery. The dehydration-induced natriuresis could not be accounted for by a fall in plasma aldosterone. However, sodium retention following rehydration could be aldosterone dependent, because additional studies showed a threefold rise in plasma levels of the hormone 1 h after drinking. The acute rise in aldosterone correlated closely (r = 0.82) with the fall in plasma sodium after drinking but not with changes in adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded that natriuresis is a homeostatic response to dehydration as a means of ameliorating the rise in body fluid osmolality.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1984

Inhibition of plasma vasopressin after drinking in dehydrated humans.

To study the effects of nonosmotic and nonvolumetric factors that may influence secretion of vasopressin, serum Na+, K+, and osmolality (Osm), hemoglobin, hematocrit, plasma arginine vasopressin (AVP), aldosterone (PA), and renin activity (PRA) were measured in five men and three women (26-50 yr, 73 +/- 4 kg) before and after 24 h of mild dehydration (food but no fluid) and seven times during the 1st h after rehydration with 10 ml/kg of tap water (17.5 +/- 0.5 degrees C) consumed in 105 s (range 35-240 s). Dehydration increased mean serum Na+ 3.7 +/- 0.7 meq/l (P less than 0.05), osmolality 9.1 +/- 1.1 mosmol/kg (P less than 0.05), and AVP from a hydrated level of 1.7 +/- 0.2 to 3.3 +/- 0.5 pg/ml (delta = 1.6 pg/ml, P less than 0.05). After rehydration AVP fell to 2.4 +/- 0.3 pg/ml (P less than 0.05) within 3 min and reached the water-replete level of 1.8 +/- 0.3 pg/ml 9 min after drinking started. Serum Na+ and Osm did not change until 30-60 min after drinking. No significant changes occurred in PRA, hemogloblin, hematocrit, or calculated delta in plasma volume, but PA increased from 11.1 +/- 1.5 ng/dl after dehydration to 15.6 +/- 2.6 ng/dl (P less than 0.05) between 30 and 60 min after drinking. The rapid fall in plasma AVP after rehydration took place in the absence of the expected changes in the primary regulators of plasma AVP (i.e., osmolality and plasma volume), with no change in blood pressure. The results suggest that oropharyngeal factors, alone or combined with gastric stimuli, are implicated.

Adult↗
PubMed1984

Response, regulation, and actions of vasopressin during exercise: a review.

Plasma concentrations of vasopressin (antidiuretic hormone), a powerful pressor agent and primary regulator of body fluid homeostasis, are elevated in a dose-related fashion to increases in exercise intensity. The response of plasma vasopressin levels to exercise is not modified by gender, but is reduced with training at absolute submaximal exercise intensities. However, the duration of the exercise and hydration status of the subject alters the observed increase. The increase in plasma vasopressin concentrations during exercise may be mediated by a variety of factors: plasma osmolality, blood pressure, blood volume, plasma concentrations of angiotensin II, psychological variables, and peripheral nerve stimulation. Furthermore, decreases in the metabolism of vasopressin, due to alterations in renal and hepatic blood flow during exercise, may contribute to the increase in plasma concentrations. Although plasma vasopressin concentrations are elevated during exercise, there is no definitive effect during exercise, as the excretion rate of free water is increased, sweat rate and composition are not changed, and a role in plasma volume regulation is dubious. Thus, the function of the elevation in plasma vasopressin levels during exercise is unclear at the present time.

Angiotensin II↗
PubMed1983

Conversion of progesterone to deoxycorticosterone in guinea pig spleen: an animal model for the study of steroid 21-hydroxylase activity in extra adrenal sites.

Steroid 21-hydroxylase activity has been demonstrated, previously, in microsome-enriched fractions prepared from a number of human fetal tissues. The finding that this enzyme activity was present in thymus and spleen is suggestive of the possibility that deoxycorticosterone is important in regulation of immunological processes. In the present investigation, we characterized steroid 21-hydroxylase activity in microsome-enriched preparations of guinea pig spleen. The activity of the enzyme was linear with time for 40 min and with protein concentrations up to 4.8 mg X ml-1 incubation mixture. The apparent Km of the enzyme for progesterone was 0.405 microM. Thus, the potential exists for the biosynthesis of DOC from progesterone in the spleen of the guinea pig as well as in the spleen of the human fetus. Therefore, the guinea pig may be an appropriate animal model for the study of the regulation of steroid 21-hydroxylase activity in the spleen as well as a model for the study of the role of this enzyme in immunologic processes.

Animals↗
PubMed1983

Inappropriate drinking and secretion of vasopressin after caval constriction in dogs.

The object of this study was to determine if chronic thoracic vena caval constriction affected mechanisms regulating water balance, independent of known changes in sodium metabolism in the dog. Fluid and electrolyte balances were determined for 5 days before and 14 days after constriction of the vena cava (n = 5) and in a separate population of time controls (n = 4). Cardiac output was reduced and heart rate was increased in response to chronic caval constriction although blood pressure was maintained at control levels. Water intake and plasma arginine vasopressin (AVP) increased from 31 +/- 4 ml/kg and 1.3 +/- 0.2 pg/ml during the control period to 81 +/- 6 ml/kg and 3.4 +/- 0.6 pg/ml during the period of caval constriction. The caval dogs developed a positive water balance, which preceded the development of a positive sodium balance. This led to a significant fall in plasma osmolality from a control mean of 296 +/- 1 to 284 +/- 4 mosmol/kg during caval constriction and dilutional hyponatremia. Plasma and blood volume increased significantly in response to constriction and were accompanied by formation of 123 +/- 10 ml/kg of ascitic fluid. These results show that water intake and plasma levels of AVP were increased in spite of a fall in plasma osmolality and an increase in vascular volume. These responses cannot be secondary to sodium retention because water was retained in excess of sodium hence hyponatremia. Therefore, chronic caval constriction causes a profound primary disturbance in mechanisms regulating water balance, which may contribute to the formation of edema fluid.

Adrenocorticotropic Hormone↗
PubMed1983

Role of volume and osmolality in the control of plasma vasopressin in dehydrated dogs.

Plasma vasopressin concentrations (pAVP) are elevated during dehydration due to alterations in extracellular fluid (ECF) volume and tonicity. The contributions of the reduction in volume and increase in plasma osmolality to the rise in pAVP were assessed in 6 dogs with bilateral carotid loops following 24 h of fluid, but not food, deprivation. Dehydration significantly (p less than 0.05) increased plasma osmolality from 297 +/- 1 to 315 +/- 2 mosm/kg), decreased body weight from 20.8 +/- 1.2 to 20.3 +/- 1.2 kg, and elevated pAVP from 1.4 +/- 0.2 to 5.3 +/- 0.6 pg/ml. The effect of extracellular fluid volume reduction was tested by reexpanding this compartment in dehydrated dogs with 0.15 M NaCl. Plasma vasopressin concentration was significantly reduced by 1.3 +/- 0.2 pg/ml (33 +/- 4%) and plasma osmolality unchanged following volume replacement. The contribution of the increase in plasma osmolality was assessed by bilateral intracarotid infusions of water at 0.6 ml/min/artery which lowered jugular venous plasma osmolality to euhydrated values (296 +/- 4 mosm/kg), but did not significantly reduce systemic plasma osmolality. Plasma vasopressin levels were significantly reduced 3.2 +/- 1.1 pg/ml (70 +/- 5%). Thus, following 24 h of fluid deprivation in dogs, the rise in pAVP is due to changes in both ECF volume and tonicity. The increase in tonicity plays a greater role in the elevation of pAVP, than the reduction in volume.

Animals↗
PubMed1982

High-density lipoprotein-cholesterol in marathon runners during a 20-day road race.

Plasma high-density lipoprotein (HDL)-cholesterol and lipid levels were measured in 12 male marathon runners (mean age, 40 years) who ran an average of 28 km/day for ten days, rested 70 hours, then continued to run for eight more days, covering a total distance for both running periods of 500 km. Blood samples were obtained on eight mornings. After one week of running, HDL-cholesterol levels increased 18% and triglyceride levels decreased 22%. However, the three-day rest period reversed these changes. As running resumed, HDL-cholesterol levels again increased and triglyceride levels decreased. There were no significant changes in total cholesterol, body weight, or skinfold thickness despite an average caloric intake of 4,800 kcal/day. Heavy beer drinking had no discernible effect on HDL-cholesterol levels, but may have caused mild hepatic injury as suggested by significantly increased serum alanine transferase and gamma-glutamyl transferase values. This study demonstrates that HDL-cholesterol levels increase with higher running mileage and decrease within days of stopping exercise when caloric and alcohol intake remain elevated.

Adult↗
PubMed1982

Osmotic control of plasma vasopressin in the dog.

Seven dogs prepared with carotid loops were used to evaluate the responsiveness of the cerebral osmoreceptors regulating plasma vasopressin concentration (pAVP). Intracarotid and intravenous infusions of hypo- and hypertonic solutions were used to alter cerebral plasma osmolality. Bilateral intracarotid infusion of hypertonic saline (0.90 mmol NaCl kg-1 . min-1 . artery-1) significantly elevated jugular vein plasma osmolality (pOsm) in the first minute (P less than 0.05). Systemic values, determined from saphenous vein samples, were increased after 6 min. After 4 min of infusion, systemic pAVP was significantly increased, attaining a constant level at 6 min. Subsequent experiments with infusions 6 min in duration demonstrated that hypertonic saline infused intracarotidly significantly increased pAVP in a dose-related fashion, whereas similar solutions administered intravenously did not alter pAVP. Hypotonic infusions (intravenous or intracarotid) did not change pAVP consistently. The lack of a depression in pAVP during hypotonic infusions is consistent with the argument that jugular pOsm must be elevated above a threshold to stimulate the release of vasopressin. Linear relationships were demonstrated for jugular pNa+ and pOsm to pAVP employing the threshold model. Cerebral osmoreceptors that regulate plasma vasopressin concentration respond linearly to increasing tonicity above a threshold stimulating the release of vasopressin.

Animals↗
PubMed1982

Effect of hypertonic intracarotid infusions on plasma vasopressin concentration.

The effect of short-term bilateral intracarotid infusions of hypertonic saline on plasma vasopressin concentration (pAVP) was evaluated in five dogs. Intracarotid infusion of saline at 90 mumol . kg-1 . min-1 . artery-1 significantly (P less than 0.05) increased jugular vein osmolality (pOsm) and sodium concentration (pNa+) within 2 min. Saphenous vein pOsm was not altered during the 6 min of infusion, whereas pNa+ was increased (P less than 0.05) from 0.8 +/- 0.1 to 2.3 +/- 0.3 pg/ml. Subsequent experiments using hypertonic saline infusions of 90 and 180 mumol . kg-1 . min-1 administered intracarotidly and intravenously for 6 min were performed. Intracarotid isotonic infusions and intravenous hypertonic infusions did not significantly alter pAVP. Hypertonic intracarotid saline increased jugular vein pOsm and pNa+ in a dose-related fashion, whereas saphenous vein pOsm and pNa+ were not significantly changed after 6 min of infusion. Plasma vasopressin, compared with the isotonic intracarotid infusion (1.5 +/- 0.3 pg/ml), was increased (P less than 0.05) after hypertonic saline to 3.2 +/- 0.6 and 4.8 +/- 0.2 pg/ml for the 90 and 180 mumol . kg-1 . min-1 infusions, respectively. The cerebral osmolality indicated by jugular vein pOsm was therefore increased in the absence of changes in systemic pOsm during intracarotid hypertonic infusions. The increase in pAVP in response to these changes in pOsm supports the presence of central osmoreceptors regulating vasopressin release in the area of distribution of the common carotid arteries.

Adrenocorticotropic Hormone↗
PubMed1982

Antidiuretic hormone responses to eucapnic and hypocapnic hypoxia in humans.

Urinary excretion rate of antidiuretic hormone (UADHV) was studied in male volunteers in response to hypobaric hypoxia. The first series consisted of three groups. The chamber was decompressed to 465, 495, and 438 Torr during high-altitude (HA) exposure for groups I (n = 5), II (n = 5), and III (n = 4), respectively. In group I, the chamber air contained 3.77% CO2 to prevent alkalosis. The level of hypoxemia was similar in groups I and II. Mean 24-h UADHV was unchanged in group I, but increased 96% (P less than 0.05) and 180% (P less than 0.05) in groups II and III, respectively, on day 1 at HA and was normal during subsequent days at HA regardless of symptoms of acute mountain sickness. Shorter sampling intervals employed in a second series of experiments conducted at 495 Torr revealed a twofold increase in UADHV (P less than 0.05) 8-12 h after ascent in eight asymptomatic subjects; UADHV returned to base line within 9 h and remained low. The symptomatic subjects both had increased UADHV (3- and 8-fold from base line) between 2 and 4 h after ascent. Increased UADHV in asymptomatic subjects may be a result of the concomitant decrease in plasma volume, both of which appeared to be eliminated by CO2 supplementation.

Adult↗