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Biomedical subjects

J E Greenleaf

Publications and source records attributed to J E Greenleaf.

At least 91 records · Page 5Linked to original sources
PubMed1985

Hypothalamic, rectal, and muscle temperatures in exercising dogs: effect of cooling.

To investigate mechanisms that may be involved in the prolongation of exercise performance with body cooling hypothalamic (Thy), rectal (Tre), and exercising muscle (Tm) temperatures, as well as the heart rate, respiratory rate, blood lactic acid concentration ( [LA] ), and plasma osmolality (Osm) were measured in five dogs during exhaustive treadmill exercise at an ambient temperature (Ta) of 22 +/- 1 degree C without cooling (control) and with external cooling by use of ice packs. In both series of experiments, dehydration of animals was prevented. Compared with exercise with noncooling, exercise with cooling resulted in 1) increased exercise duration from 90 +/- 14 to 145 +/- 15 min (62%, P less than 0.05); 2) attenuated increases in Thy, Tre, and Tm; 3) decreased respiratory and heart rates; and 4) lowered LA. Significant negative correlations were found between both Tm and delta Tm attained at 60 min of the run and time of exercise until exhaustion (r = -0.72 and -0.74, respectively; P less than 0.02). This work failed to differentiate clearly changes or equilibrium levels of brain, core, or muscle temperature as separate factors affecting work tolerance. However, the inverse relationship between Tm reached at 60 min of the run (in both experiments) and the total duration of exercise indicates that sustained muscle hyperthermia may largely contribute to limitation of working ability.

Animals↗
PubMed1985

Exercise hyperthermia as a factor limiting physical performance: temperature effect on muscle metabolism.

The muscle contents of high-energy phosphates and their derivatives [ATP, ADP, AMP, creatine phosphate (CrP), and creatine], glycogen, some glycolytic intermediates, pyruvate, and lactate were compared in 11 dogs performing prolonged heavy exercise until exhaustion (at ambient temperature 20.0 +/- 1.0 degrees C) without and with trunk cooling using ice packs. Without cooling, dogs were able to run for 57 +/- 8 min, and their rectal (Tre) and muscle (Tm) temperatures increased to 41.8 +/- 0.2 and 43.0 +/- 0.2 degrees C, respectively. Compared with noncooling, duration of exercise with cooling was longer by approximately 45% while Tre and Tm at the time corresponding to the end of exercise without cooling were lower by 1.1 +/- 0.2 and 1.2 +/- 0.2 degrees C, respectively. The muscle contents of high-energy phosphates (ATP + CrP) decreased less, the rate of glycogen depletion was lower, and the increases in the contents of AMP, pyruvate, and lactate as well as in the muscle-to-blood lactate ratio were smaller. The muscle content of lactate was positively correlated with Tm. The data indicate that with higher body temperature equilibrium between high-energy phosphate breakdown and resynthesis was shifted to the lower values of ATP and CrP and glycolysis was accelerated. The results suggest that hyperthermia developing during prolonged muscular work exerts an adverse effect on muscle metabolism that may be relevant to limitation of endurance.

Adenine Nucleotides↗
PubMed1985

Blood pressure and plasma renin activity as predictors of orthostatic intolerance.

Some physiological responses to head-up tilt and 3 h standing were evaluated in 13 dehydrated subjects. Seven of the subjects proved to be orthostatically intolerant (INT), exhibiting presyncopal symptoms. Before the symptoms manifest themselves the INT subjects had consistently lower (p less than 0.05) systolic blood pressures, generally lower diastolic and pulse pressures, and elevated (p less than 0.05) plasma renin activity (PRA) compared to the tolerant (TOL) subjects. Plasma vasopressin usually increased more in the INT subjects, but appeared to be related to the severity of presyncopal symptoms rather than to the upright posture per se. It is concluded that systolic and pulse pressures, with PRA, may allow discrimination between TOL, and potentially INT individuals; i.e., predict orthostatic intolerance. It is suggested that dehydration could provide a valuable physiological model for elucidating the causes of orthostatic intolerance.

Adult↗
PubMed1985

Exercise thermoregulation in men after 6 hours of immersion.

Rectal (Tre) and mean skin (Tsk) temperature, skin heat conductance (Ksk), heart rate, and total body sweat rate were measured in 6 men (20-35 years) during 70 min of supine leg exercise (Ta = 23.5 degrees C, rh = 40%) at 50% of their peak O2 uptake (VO2 peak); these data were taken after a 6-h control (C) period in air and after immersion to the neck (NI) in water (34.5 degrees C) for 6 h after overnight food and fluid restriction. After NI mean (+/- S.E.) water balance was -1,285 +/- 104 ml for the 6 h and plasma volume (delta Hb and Hct) decreased by 5.2%. End exercise heart rates after C (141 +/- 3 b X min-1) increased to 148 +/- 3 b X min-1 (p less than 0.05) after NI while Vo2 were both 2.2 L X min-1 Tre increased by 0.5 C degrees (p less than 0.05) between the end of NI and the start of exercise. During exercise following C and NI, delta Tre were +1.0 degrees C and +0.9 degrees C (NS), Ksk were 44 +/- 2 and 43 +/- 1 kcal X m-2 X hr-1 X degrees C-1 (NS), while sweat rates increased from 248 +/- 19 to 366 +/- 52 g X h-1 (p less than 0.05), respectively. Both the total integrated Tre and Tsk curves after NI were higher (p less than 0.05) than for C. These results suggest that, compared with control responses, the equilibrium level of core temperature during submaximal exercise is regulated at a higher level after immersion.

Adult↗
PubMed1985

Effect of physical training in cool and hot environments on +Gz acceleration tolerance in women.

Rectal temperature (Tre), sweat rate, plasma volume (PV), peak oxygen uptake (peak VO2), and relaxed +Gz acceleration tolerance (0.5 G X min-1 linear to grayout) were measured in 15 healthy women 21-41 years old before and after submaximal isotonic exercise training for 2 h X d-1 on a cycle ergometer. The women had 2 weeks of acceleration runs and Vo2 testing, followed by 8 d of exercise training, post-training acceleration runs on day 9, and peak Vo2 tests on day 10. They were divided into three groups: an exercise (heat) group, ambient temperature (Ta) 40.6 degrees C, relative humidity (rh) 42%, and a peak Vo2 of 52%; an exercise (cool) group, Ta = 18.7 degrees, rh = 48%, and Vo2 peak = 55%; and a sedentary control (cool) group. There was no change in peak ventilation, peak heart rate (HR), peak Vo2, or in resting PV in any group after training. Heart rate and Tre were significantly lower after training in both cool and hot environments; HR by 17 b X min-1 (p less than 0.05) and 27 b X min-1 (p less than 0.05), respectively, and Tre by 0.4 degrees C (p less than 0.05) and 0.4 degrees C (p less than 0.05), respectively. Sweat rates were not different in any group. In all groups, acceleration tolerances were not different after training; they ranged from 3.5 to 3.8 G (373 - 410 s). The loss (shift) in PV during acceleration ranged from -5.8% to -10.3% (nonsignificant).(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1985

Plasma lactic dehydrogenase activities in men during bed rest with exercise training.

Peak oxygen uptake (peak VO2) and basal total activity of lactic dehydrogenase (LDH-T) and its five isoenzymes were measured in seven men, 19-21 years old, before, during, and after three 2-week bed rest (BR) periods, each separated by 3-week recovery periods. For 1 h X d-1 during BR, they performed isometric (250 kcal X -1) leg exercise, or no exercise. LDH-T was reduced (p less than 0.05) with all three regimens by day 10 of BR, but the decrease occurred at different rates. The earliest significant (p less than 0.05) reduction in LDH-T with the no-exercise regimen was associated with the greatest decrease in peak VO2 of 12.3%; isotonic exercise was next with a peak VO2 decrease of 9.2%; finally, isometric exercise had the least decrease in peak VO2 at 4.8%. Irrespective of the exercise regimen during BR, the increases in isoenzyme activities occurred mainly in LDH-1 and LDH-2 (heart subunits). Isometric (aerobic) muscular strength training appears to maintain skeletal muscle integrity and, perhaps, oxygen uptake capacity better during bed rest than isotonic exercise training. Reduced hydrostatic pressure during bed rest, however, ultimately overrides effects of both moderate isometric and isotonic exercise training (metabolism) in the resulting decrease in LDH-T.

Adult↗
PubMed1985

Effects of exercise-heat acclimation on fluid, electrolyte, and endocrine responses during tilt and +Gz acceleration in women and men.

Plasma fluid, electrolyte, protein, renin, and vasoactive hormone (epinephrine, norepinephrine, vasopressin) responses were measured in six women (21-23 yr) and four men (21-38 yr) before and immediately following an orthostatic tolerance test (70 degrees head-up tilt) and a +Gz (head-to-foot) acceleration tolerance test (0.5 G X min-1 linear ramp to grayout). These tests were conducted before and after 12 consecutive days of exercise-heat acclimation when the subjects exercised on a cycle ergometer at a relative oxygen uptake of 44% to 49% peak oxygen uptake in a hot environment (Ta = 40 degrees C, 42% rh). During acclimation plasma volume increased by 10.6% (p less than 0.05) in the women and by 11.9% (p less than 0.05) in the men; in both groups exercise heart rate decreased significantly. After acclimation, acceleration tolerance was unchanged in both groups (range 3.1 to 3.4 G); the women's tilt tolerance was unchanged (range 33.6 to 39.5 min), but the men's tilt tolerance increased from 30.4 min before to 58.3 min (delta = 91%, p less than 0.05) after acclimation. Since the pattern of fluid, electrolyte, and protein shifts and acceleration tolerances in the women and men were virtually the same, the hormone responses were highly variable, and the men's tilt tolerance increased significantly after acclimation, it is clear that responses to tilting cannot be used to predict responses to acceleration. Analysis of data from the present study and the literature suggests that current exercise training regimes should be unrestricted for astronauts who have not previously been highly endurance trained.(ABSTRACT TRUNCATED AT 250 WORDS)

Acceleration↗
PubMed1984

Clonidine antagonism of angiotensin-related drinking: a central site of action.

Administration of either isoproterenol (25 micrograms/kg, s.c.) or angiotensin II (200 micrograms/kg, s.c.) induces drinking in rats within 0.5-1 h. This drinking was inhibited by prior administration of the presynaptic alpha-adrenergic agonist clonidine (12 micrograms/kg, i.p.). Urine output was enhanced by clonidine in the angiotensin II-, but not the isoproterenol-treated group. Drinking in response to peripheral administration of either angiotensin II or isoproterenol was also inhibited by intracerebroventricular (i.v.t.) administration of clonidine (8 micrograms/kg). This dose of clonidine also enhanced the urine output after angiotensin II. Further, the drinking induced by i.v.t. administration of angiotensin II, at 4 but not 20 ng/kg was inhibited by peripheral administration of clonidine (12 micrograms/kg, i.p.). When clonidine was administered i.v.t. prior to i.v.t. injection of either angiotensin II (20 ng/kg) or carbachol (1.2 micrograms/kg), the drinking response to these dipsogens was attenuated. These results suggest that clonidine may act centrally to attenuate drinking at a site, possibly in the nucleus tractus solitarius, that may be considered a final common pathway for this response.

Angiotensin II↗
PubMed1984

A role for presynaptic alpha 2-adrenoceptors in angiotensin II-induced drinking in rats.

Studies from this laboratory have shown that either central or peripheral administration of clonidine, the alpha 2-adrenoceptor agonist, can attenuate a variety of dipsogenic stimuli in rats. Further, yohimbine and tolazoline, alpha 2-adrenoceptor antagonists, augment the drinking response to both peripherally administered isoproterenol and angiotensin II. Studies reported here establish a dose-inhibition relationship between the dose of clonidine administered (2 to 32 micrograms/kg) intracerebroventricularly (IVT) and inhibition of the drinking response to peripherally administered angiotensin II (200 micrograms/kg. SC). DI50 was approximately 4 micrograms/kg. Yohimbine (300 micrograms/kg, SC) reversed the antidipsogenic effect of centrally administered clonidine (32 micrograms/kg, IVT) on angiotensin II-induced (200 micrograms/kg, SC) water intake. Phenylephrine, an alpha 2-adrenoceptor agonist, administered IVT (40 and 80 micrograms/kg) also inhibited angiotensin II-induced drinking in a dose-related fashion. The antidipsogenic effect of phenylephrine (80 micrograms/kg) was blocked by administration of yohimbine (300 micrograms/kg. SC). Thus, this effect of phenylephrine most likely occurs by way of alpha 2-adrenoceptors. These results support a role for the pre-synaptic alpha 2-adrenoceptor in the mediation of drinking in rats. Activation of alpha 2-adrenoceptors is accompanied by reduced water intake while inhibition of these receptors enhances water intake.

Angiotensin II↗
PubMed1984

Effect of intracerebroventricularly administered octopamines and synephrines on angiotensin II-induced water intake in rats.

Recent studies from this laboratory showed that l-m-synephrine (phenylephrine), a metabolite of l-m-octapamine, inhibited the drinking response of rats to peripherally administered angiotensin II. The objective of this investigation was to determine whether the isomers of both octapamine and synephrine could inhibit angiotensin II-induced dipsogenesis in the rat. Of the isomers tested, only d,l-m-octopamine and l-m-synephrine blocked the dipsogenic response to administration of angiotensin II (200 micrograms/kg, SC). The antidipsogenic effect of both d,l-m-octopamine and l-m-synephrine could be blocked by concurrent administration of yohimbine (300 micrograms/kg, IP), an alpha 2-adrenoceptor antagonist. The results indicate that m-octopamine and m-synephrine exert their antidipsogenic effect via alpha 2-adrenoceptors. These studies add to a growing body of data suggesting that activation of alpha 2-adrenoceptors inhibits, while blockade of these receptors enhances, angiotensin II-induced drinking.

2-Hydroxyphenethylamine↗
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

Immersion diuresis without expected suppression of vasopressin.

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20-35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersion experiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at the end of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed when there is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.

Adult↗
PubMed1984

Physiological responses to prolonged bed rest and fluid immersion in humans.

Rest in bed and immersion in water have been used for centuries by physicians and healers in treating injury and disease. The qualitative similarity of acute and chronic responses to bed rest, immersion, and weightlessness has sparked renewed interest in and a resultant greater understanding of the mechanisms of disuse deconditioning. Some combination of changes in hydrostatic pressure, reduced total metabolism (exercise), compression force on weight-bearing bones, as well as psychological factors associated with prolonged confinement in a new environment probably comprise the major input stimuli for the adaptive responses. Virtually every physiological system is affected. Early responses involve the fluid, electrolyte, and blood pressure control systems with significant muscular atrophy and decreases in bone density occurring over weeks and months. Much effort has been expended to describe the various responses to bed rest and immersion with understandably less effort devoted to research during weightlessness. Future research should be directed mainly toward an understanding of the mechanisms of these adaptive responses. Additional work is especially needed to elucidate the effects of deconditioning on drug metabolism, functioning of the immune system, carbohydrate metabolism, protein and peptide metabolism in muscle, and calcium metabolism as it affects integrity of bone.

Adaptation, Physiological↗
PubMed1984

Cardiovascular responses during orthostasis: effect of an increase in VO2max.

Cardiovascular responses to orthostasis were assessed in eight men (18-29 years old) before and after an 8-d cycle ergometer exercise training (E) regimen for 2 h . d-1 at 65% maximal O2 uptake (VO2 max). Each subject underwent 60 degrees head-up tilt (60 min max) before (T1) and after (T2) E. Heart rate (HR), systolic (SBP), and diastolic (DBP) pressures were measured each min before, during, and after tilt; pulse pressure (PP), mean arterial pressure (MAP), and rate-pressure-product (RPP) were calculated. Changes in plasma renin activity (PRA), vasopressin (pVP), hematocrit, hemoglobin, and plasma volume (PV, T-1824) were measured from venous blood samples taken pre- and immediately post-tilt. Following E, VO2 max increased by 8.3% (p less than 0.05), resting HR decreased by 8.1% (p less than 0.05), and PV increased by 430 ml (12.2%, p less than 0.05). Mean (+/- S.E.) tilt duration went from 40.0 +/- 5.1 min during T1 to 46.7 +/- 3.4 min during T2 (NS); mean tilt HR decreased from 86 +/- 4 bpm to 77 +/- 3 bpm (p less than 0.05), RPP decreased from 10,320 +/- 390 to 9,317 +/- 310 mm Hg . bpm (p less than 0.05), while mean SBP, DBP, PP, and MAP were unchanged. Plasma volume decreased during tilt by 479 ml in T1 compared to 544 ml in T2 (p less than 0.05), while % delta PV were similar: -13.6% and -13.9%, respectively. Peak fluid-accumulation in the calf and total leg during tilt increased (p less than 0.05) following E.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Physiology of fluid and electrolyte responses during inactivity: water immersion and bed rest.

This manuscript emphasizes the physiology of fluid-electrolyte-hormonal responses during the prolonged inactivity of bed rest and water immersion. An understanding of the total mechanism of adaptation (deconditioning) should provide more insight into the conditioning process. Findings that need to be confirmed during bed rest and immersion are: 1) the volume and tissues of origin of fluid shifted to the thorax and head; 2) interstitial fluid pressure changes in muscle and subcutaneous tissue, particularly during immersion; and 3) the composition of the incoming presumably interstitial fluid that contributes to the early hypervolemia. Better resolution of the time course and source of the diuretic fluid is needed. Important data will be forthcoming when hypotheses are tested involving the probable action of the emerging diuretic and natriuretic hormones, between themselves and among vasopressin and aldosterone, on diuresis and blood pressure control.

Bed Rest↗
PubMed1983

On the mechanism of serotonin-induced dipsogenesis in the rat.

Subcutaneous administration of l-5-hydroxytryptophan (5-HTP), the precursor of serotonin, to female rats induces copious drinking accompanied by activation of the renin-angiotensin system. Neither a reduction in blood pressure nor body temperature accompanied administration of 5-HTP. The objective of the present study was to determine whether serotonin-induced dipsogenesis, like that of 5-HTP, is mediated via the renin-angiotensin system. Serotonin (2 mg/kg, SC)-induced drinking was inhibited by the dopaminergic antagonist, haloperidol (150 micrograms/kg, IP), which also inhibits angiotensin II-induced drinking. Both captopril (35 mg/kg, IP), an angiotensin converting enzyme inhibitor, and propranolol (6 mg/kg, IP), a beta-adrenergic antagonist, blocked serotonin-induced dipsogenesis. The alpha 2-adrenergic agonist, clonidine (6.25 micrograms/kg, SC), which suppresses renin release from the kidney, attenuated serotonin-induced water intake. The dipsogenic responses to submaximal concentrations of both serotonin (1 mg/kg, SC) and isoproterenol (8 micrograms/kg, SC) were additive rather than interactive suggesting that similar pathways mediate both responses. The serotonergic receptor antagonist, methysergide (3 mg/kg, IP), inhibited serotonin-induced drinking but had no effect on isoproterenol (25 micrograms/kg, SC)-induced dipsogenesis. However, neither serotonin (2 mg/kg, SC) nor isoproterenol (25 micrograms/kg, SC)-induced drinking was inhibited by cinanserin (25 micrograms/kg, IP). These data indicate that serotonin induces drinking in rats via the renin-angiotensin system. However, the results of the studies using methysergide suggest that serotonin appears to act at a point prior to activation of beta-adrenoceptors in the pathway leading to release of renin from the kidneys.

Animals↗
PubMed1983

Effects of yohimbine and tolazoline on isoproterenol and angiotensin II-induced water intake in rats.

Subcutaneous administration of the alpha 2-adrenoreceptor antagonists, yohimbine and tolazoline, at doses up to 1000 micrograms/kg, had no effect on water intake of female rats. However, when these compounds were administered SC in combination with either the beta-adrenoreceptor agonist, isoproterenol (10 to 25 micrograms/kg, SC), or with angiotensin II (200 micrograms/kg, SC), water intake was enhanced. In contrast, intraventricular administration of either tolazoline (10 and 20 micrograms/kg) or yohimbine (300 micrograms/kg) failed to augment the dipsogenic response to angiotensin II (150 micrograms/kg, SC). Thus, the enhancing effect of these alpha 2-adrenoreceptor antagonists on isoproterenol- and angiotensin II-induced water intakes appears to be manifested peripherally, rather than centrally. In view of the fact that clonidine, an alpha 2-adrenoreceptor agonist, has been shown to inhibit water intake induced by both isoproterenol and angiotensin II, the results suggest that the alpha 2-adrenoreceptor may play a role in modulating water intake induced by these two dipsogenic agents.

Angiotensin II↗