Biomedical subjects

K C Kregel

Publications and source records attributed to K C Kregel.

At least 37 records · Page 2Linked to original sources

PubMed1996

Alterations in autonomic adjustments to acute hypoxia in conscious rats with aging.

The experimental objective was to determine whether sympathetic nervous system activity and cardiovascular adjustments to hypoxia are altered with advancing age. Norepinephrine (NE) synthesis was blocked with alpha-methyl-DL-p-tyrosine, and NE turnover rates were determined in the left ventricle of the heart, kidney, liver, and adrenal gland in groups of conscious unrestrained mature (12-mo-old) and senescent (24-mo-old) Fischer 344 rats in conditions of normoxia and acute hypocapnic hypoxia (10% O2-90% N2). Calculated NE turnover rates were similar in all four tissues sampled for both age groups in the normoxic condition. Thirty minutes of hypoxia produced elevations in NE turnover rates in the kidney, liver, and adrenal gland, but not in the heart, for both the mature and senescent groups. However, NE turnover rates were attenuated in the kidney (92 vs. 195%) and liver (119 vs. 190%) of senescent compared with mature rats. Hypoxia produced no change in mean arterial pressure from normoxic levels in the mature rats, whereas older rats had a progressive decline in mean arterial pressure (-24 +/- 3 mmHg from baseline) over the course of the hypoxic exposure. In contrast, heart rate responses were similar in the normoxic and hypoxic conditions for both age groups. These findings indicate that sympathetic nerve activity, as estimated from NE turnover rates, increases in a tissue-specific manner with moderate hypoxia, but this increase is markedly attenuated in the kidney and liver with advancing age. In addition, the ability to maintain MAP during a hypoxic challenge is impaired with aging, perhaps due, in part, to a reduced sympathetic vasoconstriction to selected internal organs.

Acute Disease↗

PubMed1996

Differential effects of exercise and heat stress on liver HSP70 accumulation with aging.

Previous reports have suggested that the heat shock response to passive heating may be blunted by aging. However, during exertional heating, factors in addition to elevated temperature may amplify the degree of stress compared with hyperthermia alone. The purpose of this study was to compare the pattern of accumulation of the highly inducible 72-kDa heat shock protein (HSP72) in liver tissue of mature (12-mo-old) and senescent (24-mo-old) male Fischer 344 rats after either passive or exertional heat stress. A euthermic control group was exposed to an ambient temperature (Ta) of 25 degrees C for 4.5 h. A passive heating (heat) group was exposed to an Ta of 42 degrees C until colonic temperature (Tco) reached 41 degrees C. An exertional heating (exercise) group performed intermittent moderate-intensity treadmill exercise (similar absolute intensities for the two age groups) at an Ta of 32 degrees C until Tco reached 41 degrees C. Heating rates were similar in the heat and exercise groups (approximately 0.08 degrees C/min). Rats in both the heat and exercise groups were maintained at a Tco of 41 degrees C for an additional 30 min and subsequently returned to an Ta of 25 degrees C for 3 h. Liver HSP72 accumulation was increased in mature rats after both the heat (+192% vs. control) and exercise (+292%) protocols. In contrast, the senescent rats demonstrated no significant increase in inducible HSP70 with heating but a large increase with exercise (+232%; P < 0.01 compared with control and heat groups). These data suggest that the blunted heat shock protein response to heating observed with aging is not a result of the inability to produce inducible HSP72 because older rats had an robust response to exertional hyperthermia.

Aging↗

PubMed1995

HSP70 induction during exercise and heat stress in rats: role of internal temperature.

The purpose of this study was to determine if the accumulation of the 72-kDa heat shock protein (HSP70) is elevated in response to a prolonged bout of submaximal exercise in which colonic temperature (Tco) remained at control levels. Sprague-Dawley rats were randomly assigned to one of four testing groups [n = 8 per group; ambient temperatures (Ta) for each condition are included]: 1) control (cool/rest; Ta = 24 degrees C); 2) cool and exercise (cool/exercise; Ta = 14 degrees C); 3) nonexertional heating (heat/rest; Ta = 42 degrees C); 4) heat and exercise (heat/exercise; Ta = 32 degrees C). All interventions were approximately 60 min in duration. An exercise bout consisted of treadmill running at 17 m/min and 0% grade, while the heat/rest and heat/exercise experiments consisted of heat exposure that was terminated when Tco reached 41 degrees C. Baseline Tco was similar for all four groups. In the cool/rest and cool/exercise groups, final Tco was not different from the baseline values, nor was it different between these two groups. In the heat/rest and heat/exercise groups, heating rates were similar. Tissue samples were obtained from the gastrocnemius, soleus, and extensor digitorum longus (EDL) muscles of the left hindlimb and the left ventricle 30 min after a trial was completed. An enzyme-linked immunosorbent assay specific for HSP70 was used to directly quantitate absolute levels of HSP70 in tissues. There were significant main effects of both heating and exercise for HSP70 levels in the gastrocnemius, soleus, and left ventricle (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats.

Recent studies have suggested that the interaction between the sympathetic nervous system and nitric oxide (NO) or nitrosyl factors may be an important means by which arterial blood pressure is regulated. We investigated whether NO synthase (NOS) inhibition modulates basal sympathetic nerve discharge (SND) in baroreceptor-innervated and -denervated, chloralose-anesthetized Sprague-Dawley rats. We recorded mean arterial pressure (MAP), renal SND, and lumbar SND before and after administration of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg iv). Two minutes after L-NAME administration in baroreceptor-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decreased from control levels. These changes persisted for up to 20 min after L-NAME administration. In baroreceptor-denervated rats, L-NAME increased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10% from control at 20 min post-L-NAME). In contrast, renal SND progressively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These results demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nitrosyl factors provide tonic excitation to lumbar SND, whereas they provide a tonic restraint to renal SND.

Animals↗

PubMed1995

Augmented mesenteric and renal vasoconstriction during exercise in senescent Fischer 344 rats.

The purpose of this study was to test the hypothesis that vasoconstriction in the mesenteric and renal circulations is greater at both submaximal and maximal exercise intensities with advancing age. Arterial blood pressure, heart rate, and mesenteric, renal, and iliac (hindlimb) artery blood flow velocities were measured before and during graded treadmill exercise in mature (12 mo) and senescent (24 mo) male Fischer 344 rats. During treadmill running at mild, moderate, and maximal exercise intensities (approximately 45, 70, and 100% of maximal oxygen uptake), the increases in arterial pressure were similar in the mature and senescent animals, whereas heart rate rose less in the older group (P < 0.05). Mesenteric and renal flow velocities declined and vascular resistances increased from resting levels in both groups in response to graded exercise; however, the magnitudes of the increases in both mesenteric and renal vascular resistance were significantly augmented in the older rats at the moderate and maximal workloads. Hindlimb blood flow velocity increased and resistance declined from resting levels at each exercise intensity in both groups. In contrast to the visceral and renal adjustments, the magnitudes of the changes in both hindlimb flow and resistance were similar for the two age groups at all exercise intensities. These findings support the hypothesis that mesenteric and renal vasoconstriction is augmented in senescent Fischer 344 rats during exercise at moderate and maximal intensities but not at mild workloads. Despite these regional differences, the maintenance of arterial pressure is not altered at either submaximal or maximal exercise intensities with advancing age.

Aging↗

PubMed1995

HSP70 accumulation in tissues of heat-stressed rats is blunted with advancing age.

To determine whether aging results in reduced accumulation of the 70-kDa heat shock protein (HSP70) in response to a thermal challenge, experiments were conducted in conscious and freely moving mature (12-mo-old) and senescent (24-mo-old) male Fischer 344 rats. Rats were assigned to a euthermic control group or a nonexertionally heated group that was exposed to an ambient temperature of 42 degrees C until colonic temperature reached 41 degrees C. Samples were subsequently obtained from the liver and myocardium, and absolute levels of both the constitutive and inducible forms of HSP70 were quantitated. Heat-stressed rats had significantly elevated HSP70 levels in the liver compared with the euthermic groups. Post hoc comparisons revealed that heat stress elicited marked elevations in liver HSP70 in mature rats compared with age-matched control animals. In contrast, HSP70 values were unchanged in the senescent heated group vs. the control group. In the myocardium, heat stress produced marked increases in HSP70 levels in both the mature and senescent groups compared with age-matched control animals, with accumulation significantly blunted in the senescent vs. mature rats. Thus the increases in liver and myocardial HSP70 accumulation in response to nonexertional heat stress are attenuated with senescence. Because these proteins are postulated to protect cells from injury and enhance cellular recovery from heat stress, the data suggest that an aging organism has a reduced ability to properly maintain cellular function and integrity after a thermal challenge.

Aging↗

PubMed1994

Modulation of autonomic nervous system adjustments to heat stress by central ANG II receptor antagonism.

The purpose of this study was to determine whether central angiotensin II (ANG II) participates in mediating selected sympathetic nervous system and neuroendocrine adjustments to heat stress in conscious freely moving rats. Mean arterial pressure (MAP), heart rate (HR), splanchnic sympathetic nerve activity (SpNA), plasma arginine vasopressin (AVP) concentration, and colonic temperature were measured before and during whole body heating (42 degrees C ambient temperature). Heating was stopped when a colonic temperature of 41 degrees C was attained. On consecutive days, rats received an intracerebroventricular (icv) injection of saline (0.9%) or 25 micrograms of the ANG II AT1-selective receptor antagonist losartan 20 min before the start of heating. Neither treatment influenced control levels of any parameter. The increase above baseline for MAP at the end of heating was attenuated by > 50% in the losartan, compared with the saline trial (P < 0.05), while HR remained unchanged from control values for both trials. Pretreatment with losartan icv eliminated the increase in SpNA observed during the heating period in the saline trial. Furthermore, the magnitude of change in plasma AVP during heating was significantly elevated in rats after icv administration of saline compared with losartan. These findings indicate that central ANG II receptor antagonism significantly attenuates the heating-induced elevations in MAP, sympathetic neural activity to visceral regions, and plasma AVP and suggest that the central nervous system actions of endogenous ANG II are required for full expression of the sympathoexcitatory, pressor, and neuroendocrine responses associated with nonexertional heat stress in the conscious rat.

Angiotensin II↗

PubMed1994

Influence of aging on tissue-specific noradrenergic activity at rest and during nonexertional heating in rats.

The purpose of this study was to test the hypothesis that sympathetic nervous system (SNS) activity to internal organs during nonexertional heat stress is exaggerated with advancing age. Norepinephrine (NE) synthesis was blocked with alpha-methyl-DL-p-tyrosine, and NE turnover rates were determined in the left ventricle, renal cortex, liver, and adrenal gland in groups of conscious unrestrained mature (12-mo-old) and senescent (24-mo-old) Fischer 344 rats before and after whole body heating. Animals were maintained in thermoneutral control conditions (n = 10 per group) or exposed to an ambient temperature of 42 degrees C until colonic temperature (TCO) reached a designated level (39.5 or 41.0 degrees C; n = 10 per group at both temperature levels). NE turnover rates were similar in all four tissues sampled for both mature and senescent rats in the resting condition. Over the course of the heating period, progressive increases in arterial blood pressure and heart rate were observed, with the magnitudes of the pressor and tachycardic responses similar between age groups. At TCO of 39.5 degrees C, calculated NE turnover rates were unchanged from control levels for the senescent and mature animals, whereas animals heated to 41.0 degrees C demonstrated marked elevations in NE turnover in all four tissues for both age groups. In addition, the increase in NE turnover rate at this TCO was significantly higher for senescent rats compared with their younger counterparts in the renal cortex (410 vs. 278%) and liver (557 vs. 170%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1994

Angiotensin-converting enzyme inhibition in infarct-induced heart failure in rats: bradykinin versus angiotensin II.

BACKGROUND: The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors in the prevention of heart failure following myocardial infarction are widely accepted. However, the underlying mechanisms are still a matter of discussion. We therefore investigated the relative contribution of the breakdown of bradykinin and of the inhibition of angiotensin-II synthesis to the beneficial actions of ACE inhibitors in chronic heart failure following myocardial infarction. METHODS: We compared the effects pretreatment with the ACE inhibitor moexipril with those of the type 1 angiotensin (AT1)-receptor antagonist losartan on structural and functional cardiac parameters after myocardial infarction in rats. In addition, the bradykinin B2-receptor antagonist icatabant was used to investigate the role of bradykinin in the cardioprotective effects of ACE inhibition. Rats underwent a sham operation or surgery to induce myocardial infarction. Treatment was started 1 week before myocardial infarction and continued for another 6 weeks after the procedure. RESULTS: Moexipril reduced infarct size (100 +/- 9mm2 compared with 165 +/- 8mm2), the ratio of total heart weight to body weight (2.6 +/- 0.1 g/kg compared with 2.9 +/- 0.1 g/kg) and end-diastolic pressure (8.2 +/- 1.5 mmHg compared with 14.0 +/- 1.7 mmHg). All of these effects of the ACE inhibitor were blocked by concomitant treatment with icatibant. Losartan did not affect any of these cardiac parameters. CONCLUSION: The cardioprotective effects of the ACE inhibitor moexipril administered before myocardial infarction in the present study were a result of the reduced breakdown of kinins rather than of the reduced synthesis of angiotensin II.

Adrenergic beta-Antagonists↗

PubMed1993

Tissue-specific noradrenergic activity during acute heat stress in rats.

The purpose of this study was to determine whether nonexertional heat stress alters the behavior of internal organ and skeletal muscle sympathetic nervous system (SNS) activity in unrestrained conscious rats. Norepinephrine (NE) synthesis was blocked with alpha-methyl-p-tyrosine, and the rate of decline in tissue NE concentration after synthesis blockade was used to estimate SNS activity in the left ventricle, kidney, liver, adrenal gland, and soleus and extensor digitorum longus muscles of the hindlimb. Male Sprague-Dawley rats (250-320 g) were maintained in thermoneutral control conditions (ambient temperature = 24 degrees C, n = 10) or exposed to an ambient temperature of 42 degrees C until a colonic temperature (Tc) of 39.5 or 41.0 degrees C (n = 10 each) was attained. During heating, as Tc rose from control levels (approximately 38 degrees C) to 41.0 degrees C, mean arterial pressure and heart rate increased from 120 +/- 3 to 141 +/- 3 mmHg and from 381 +/- 4 to 420 +/- 5 beats/min, respectively (P < 0.05). There was a strong trend for increased NE turnover rates in the left ventricle, liver, and adrenal gland in NE synthesis-blocked rats attaining a Tc of 39.5 degrees C compared with the normothermic values, whereas the turnover rate in the kidney was significantly elevated at this level of hyperthermia (126%) vs. the control condition. In animals heated to a Tc of 41.0 degrees C, the NE turnover rate was markedly increased in the left ventricle (590%), kidney (531%), liver (262%), and adrenal gland (602%) compared with normothermic control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Sympathetic nervous system activity during skin cooling in humans: relationship to stimulus intensity and pain sensation.

1. Our aim was to determine the relationship between efferent sympathetic nervous system activity to skeletal muscle (MSNA) and both the dynamics of the stimulus and pain sensation during localized skin cooling in humans. MSNA in the lower leg (peroneal microneurography), heart rate, arterial blood pressure, hand skin and muscle temperatures and perceptions of pain were recorded in ten healthy subjects before, during and after immersion (3 min) of a hand in water of different temperatures ranging from non-noxious to extremely noxious (28, 21, 14, 7 and 0 degrees C). 2. Immersion produced an abrupt, water temperature-dependent fall in hand skin temperature (initial 30 s) followed by a more gradual decline. In contrast, the fall in hand muscle temperature was almost linear during immersion. Throughout immersions at the 28, 21, and 14 degrees C water temperatures and during the initial phase of the 7 degrees C level, sensations ranged from not painful to somewhat painful; however, the latter phase of the 7 degrees C immersion and the entire 0 degrees C level were perceived as intensely painful. 3. During the initial 15-30 s of immersion at the 21-7 degrees C water temperatures, MSNA decreased from control levels in all subjects (47-58% on average, P < 0.05), whereas mean arterial blood pressure did not change. MSNA then returned to and remained at control levels throughout the 28-14 degrees C immersions, although arterial pressure, primarily systolic, rose slightly. 4. After some delay, MSNA increased during immersion at both the 7 degrees C (P < 0.05 at 90 s) and 0 degrees C (P < 0.05 at 60 s) levels in a progressive, water temperature-dependent manner, achieving peak values of approximately 200 and 300% of control, respectively, by 2.0-2.5 min. These elevations in MSNA were associated with parallel increases in arterial pressure. 5. Heart rate rose during the onset of immersion at all water temperatures (P < 0.05), but fell rapidly to control levels after 60-90 s. The increases were small (approximately 5 beats/min) and similar at the 28-7 degrees C levels, but were twice as great at the coldest water temperature.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1991

Effects of exercise training on responses to central injection of CRF and noise stress.

The purpose of this study was to test the hypothesis that the cardiovascular and sympathoadrenal responses to acute environmental stress are attenuated by exercise training. Furthermore, we tested the hypothesis that the cardiovascular and sympathoadrenal responses to intracerebroventricular (ICV) administration of corticotropin-releasing factor (CRF) would be attenuated by training. Conscious, unrestrained, male Sprague-Dawley rats assigned to either a treadmill trained (16-26 m/min, 30-60 min/day, 5 days/week) or nontrained (16-26 m/min, 10 min/day, 1 day/week) group were studied. After 8-10 weeks of training, maximal oxygen uptake was significantly higher in the trained (108 +/- 3 ml/kg/min) vs. the nontrained (94 +/- 4 ml/min/kg) group. There were no significant differences in baseline mean arterial pressure, heart rate and plasma catecholamine levels associated with training. Trained rats exhibited significantly attenuated elevations in arterial pressure (20 +/- 3 vs. 36 +/- 2 mmHg for nontrained) and heart rate (-3 +/- 3 vs. 12 +/- 5 beats/min for nontrained) in response to acute noise stress. Twenty minutes after ICV administration of CRF, blood pressure (trained = 119 +/- 2 mmHg, nontrained = 127 +/- 2 mmHg), heart rate (trained = 408 +/- 8 beats/min, nontrained = 424 +/- 10 beats/min), plasma norepinephrine levels (trained = 757 +/- 54 pg/ml, nontrained = 775 +/- 100 pg/ml) and plasma epinephrine levels (trained = 266 +/- 29 pg/ml, nontrained = 225 +/- 42 pg/ml) were significantly elevated in both trained and nontrained groups. CRF-induced elevations of blood pressure, but not heart rate or plasma catecholamine levels, were significantly attenuated in the trained group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Splanchnic sympathetic nerve activity and circulating catecholamines in the hyperthermic rat.

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (Tc, 37, 39, 41, 43, or 44 degrees C) at death. Heart rate (HR), mean arterial pressure (MAP), and Tc were monitored during heat stress under alpha-chloralose anesthesia (12.5 mg.ml-1.h-1). At each predetermined Tc, an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43 degrees C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and Tc were recorded. Tc was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 degrees C in 70 min by increase of ambient temperature to 38 degrees C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a Tc of 37 degrees C and increased significantly as Tc exceeded 39 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Mechanism for pressor response to nonexertional heating in the conscious rat.

The purpose of this study was to determine the systemic hemodynamic mechanism(s) underlying the pressor response to nonexertional heat stress in the unrestrained conscious rat. After a 60-min control period [ambient temperature (Ta) 24 degrees C], male Sprague-Dawley rats (260-340 g) were exposed to a Ta of 42 degrees C until a colonic temperature (Tc) of 41 degrees C was attained. As Tc rose from control levels (38.1 +/- 0.1 degrees C) to 41 degrees C, mean arterial blood pressure (carotid artery catheter, n = 33) increased from 124 +/- 2 to 151 +/- 2 mmHg (P less than 0.05). During this period, heart rate increased (395 +/- 5 to 430 +/- 6 beats/min, P less than 0.05) and stroke volume remained unchanged. As a result, ascending aorta blood flow velocity (Doppler flow probe, n = 8), used as an index of cardiac output, did not change from control levels during heating, but there was a progressive Tc-dependent increase in systemic vascular resistance (+30% at end heating, P less than 0.05). This systemic vasoconstrictor response was associated with decreases in blood flow (-31 +/- 9 and -21 +/- 5%) and increases in vascular resistance (94 +/- 16 and 53 +/- 8%; all P less than 0.05) in the superior mesenteric and renal arteries (n = 8 each) and increases in plasma norepinephrine (303 +/- 37 to 1,237 +/- 262 pg/ml) and epinephrine (148 +/- 28 to 708 +/- 145 pg/ml) concentrations (n = 12, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Cardiovascular responses to exercise in the rat: role of corticotropin-releasing factor.

The effects of intracerebroventricular (icv) administration of a corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical CRF, on systemic and regional hemodynamic adjustments to exercise were studied in conscious rats. On consecutive days, rats received saline icv, alpha-helical CRF icv, and no treatment 30 min before treadmill exercise (TMX). Increases in heart rate (HR) and mean arterial pressure (MAP) in response to TMX (16.1-28.6 m/min) were similar after icv administration of saline or no treatment. In rats receiving saline icv or no treatment, estimated vascular resistance increased in the mesenteric and renal regions and declined in the iliac (hindlimb) region. After icv administration of alpha-helical CRF9-41, HR and MAP responses during TMX were significantly attenuated. In addition, TMX-induced elevations of estimated mesenteric vascular resistance and iliac blood flow velocity were blunted after CRF receptor blockade. These altered cardiovascular and hemodynamic responses were ultimately reflected in the animals' compromised ability to run. The results suggest that the central nervous system actions of endogenous CRF are necessary for the full expression of the cardiovascular adjustments to TMX in the conscious rat.

Animals↗

PubMed1990

Circulatory responses to vasoconstrictor agents during passive heating in the rat.

The purpose of this study was to determine the actions of several pharmacological agents on the circulatory system, and more specifically on the superior mesenteric vascular bed, in response to environmental heat stress in chloralose-anesthetized rats. Animals were instrumented with Doppler flow probes on the mesenteric and renal arteries and exposed to an ambient temperature of 40 degrees C. Heart rate, mean arterial blood pressure (MAP), and core (Tc) and tail skin temperatures were also monitored. As Tc progressively increased from 37 degrees C during heat exposure, MAP rose to a plateau and then fell precipitously as Tc exceeded 41.5 degrees C. Mesenteric resistance increased throughout the early stages of heating before sharply declining prior to the reduction in MAP. The pressor and mesenteric resistance responses to constant infusions of several adrenergic agonists after MAP began falling (Tc = 41.3 degrees C) were significantly (P less than 0.05) attenuated compared with infusions into normothermic animals. In a second set of experiments, injections of both norepinephrine and angiotensin II were made 30 min before and approximately 10, 30, 50, 70, and 90 min after initiation of heating. These injections increased both MAP and mesenteric resistance; however, at TcS greater than 40 degrees C, the responses to both agonists were progressively and significantly attenuated. In a final group of animals, barium chloride infusions produced similar pressor and regional resistance changes during both normothermia and severe hyperthermia (Tc greater than 42 degrees C). These results indicate that, in the chloralose-anesthetized rat, hyperthermia disrupts adrenoceptor function but does not alter the intrinsic ability of vascular smooth muscle to contract.

Angiotensin II↗

PubMed1990

Thermal adjustments to nonexertional heat stress in mature and senescent Fischer 344 rats.

The purpose of this study was to test the hypothesis that the rise in colonic temperature (Tc) during nonexertional heat stress is exaggerated in senescent (SEN, 24 mo, n = 12) vs. mature (MAT, 12 mo, n = 15) conscious unrestrained Fischer 344 rats. On 2 separate days (48 h apart) each SEN and MAT animal was exposed to an ambient temperature (Ta) of 42 degrees C (relative humidity 20%) until a Tc of 41 degrees C was attained and then cooled at a Ta of 26 degrees C until Tc returned to the initial control level. Control Tc was similar in the two groups for both trials. The rate of Tc change during heating was 63% greater (0.070 +/- 0.005 vs. 0.043 +/- 0.004 degrees C/min, P less than 0.05) and the time to 41 degrees C reduced by 36% (54 +/- 6 vs. 85 +/- 10 min, P less than 0.05) in MAT vs. SEN animals during the first exposure, although the cooling rate was slower in the MAT (0.048 +/- 0.004 degrees C/min) vs. SEN (0.062 +/- 0.006 degrees C/min) animals (P less than 0.05). The heating rate was unchanged in MAT animals between trials 1 and 2. However, SEN animals had a 95% increase in heating rate in trial 2 compared with trial 1 (P less than 0.05), and the corresponding time to 41 degrees C was decreased by 44% (P less than 0.05). As a result, rate of heating and time to 41 degrees C were similar in the two groups during trial 2. The cooling rate was similar between trials within each group.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1990

Cardiovascular-sympathetic adjustments to nonexertional heat stress in mature and senescent Fischer 344 rats.

The purpose of this study was to test the hypothesis that the cardiovascular-sympathetic nervous system adjustments during nonexertional heat stress are exaggerated in senescent (S, 24 mo) vs. mature (M, 12 mo) conscious unrestrained Fischer 344 rats. During two separate trials (48 h apart), each animal was exposed to an ambient temperature (Ta) of 42 degrees C until a colonic temperature (Tco) of 41 degrees C was attained and then cooled at a Ta of 26 degrees C until Tco returned to the initial control level. Trial 1: heart rate (HR), mean arterial blood pressure (MAP), and arterial plasma concentrations of norepinephrine (NE), epinephrine (E), and lactate (La) were similar between the S and M groups during the baseline (control) period. The absolute increases in HR, MAP, NE, and E from the control period to the end of heating were of similar magnitudes between groups; however, La increased more in the S than M animals (P less than 0.05). During recovery, the declines toward control levels for all variables were similar or even more rapid in the S vs. M animals (P less than 0.05). Trial 2: the changes in HR and MAP during heating were similar to those observed in trial 1 in both groups. Generally, NE and E control levels were elevated in both groups compared with those in trial 1. The absolute increases in NE during heating were similar to trial 1 in both groups, whereas E increased to a greater extent than in trial 1 in the S animals (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗