The physiological strain index applied to heat-stressed rats.

A physiological strain index (PSI) based on heart rate (HR) and rectal temperature (Tre) was recently suggested to evaluate exercise-heat stress in humans. The purpose of this study was to adjust PSI for rats and to evaluate this index at different levels of heat acclimation and training. The corrections of HR and Tre to modify the index for rats are as follows: PSI = 5 (Tre t - Tre 0). (41.5 - Tre 0)-1 + 5 (HRt - HR0). (550 - HR0)-1, where HRt and Tre t are simultaneous measurements taken at any time during the exposure and HR0 and Tre 0 are the initial measurements. The adjusted PSI was applied to five groups (n = 11-14 per group) of acclimated rats (control and 2, 5, 10, and 30 days) exposed for 70 min to a hot climate [40 degrees C, 20% relative humidity (RH)]. A separate database representing two groups of acclimated or trained rats was also used and involved 20 min of low-intensity exercise (O2 consumption approximately 50 ml. min-1. kg-1) at three different climates: normothermic (24 degrees C, 40% RH), hot-wet (35 degrees C, 70% RH), and hot-dry (40 degrees C, 20% RH). In normothermia, rats also performed moderate exercise (O2 consumption approximately 60 ml. min-1. kg-1). The adjusted PSI differentiated among acclimation levels and significantly discriminated among all exposures during low-intensity exercise (P < 0.05). Furthermore, this index was able to assess the individual roles played by heat acclimation and exercise training.

Carbachol, an acetylcholine receptor agonist, enhances production in rat aorta of 2-arachidonoyl glycerol, a hypotensive endocannabinoid.

The production of 2-arachidonoyl glycerol, an endogenous cannabinoid, is enhanced in normal, but not in endothelium-denuded rat aorta on stimulation with carbachol, an acetylcholine receptor agonist. 2-Arachidonoyl glycerol potently reduces blood pressure in rats and may represent an endothelium-derived hypotensive factor.

Heat acclimation: cardiovascular response to hot/dry and hot/wet heat loads in rats.

Body temperature, blood pressure (BP) and heart rate (HR) of rats before and after acclimation to heat were studied in chronically cannulated sedentary conscious rats in different hot environmental conditions [hot/dry: 40 degrees C, 20% relative humidity (RH) and hot/wet: 35 degrees C, 70% RH]. During exposure to heat stress, acclimated rats showed an attenuated increase in colonic temperature (Tc) compared to non-acclimated rats. Concomitantly, an abrupt decrease in HR, delayed and attenuated elevation in mean arterial BP and improved cardiac efficiency were recorded. Differences were observed upon exposure to the hot/wet and hot/dry climates: the hot/dry climate imposed a greater physiological burden than the hot/wet climate. The data suggest that for sedentary rats dry heat produces a greater load than humid heat. Thus, the conventional heat load indices do not apply universally but have a thermoregulatory pattern specificity.

Mechanism of heat acclimation induced bradycardia in the sand rat.

The effect of heat acclimation on chronotropic response of the heart under normothermic and hyperthermic conditions was studied in the sand rat, Psammomys obesus, a diurnal desert species. All animals were acclimated at 34 degrees C for 0, 5, 14, 30 or 60 days; heat stress was achieved by exposure at 38 degrees C. Continuous measurements of heart rate (HR) were carried out on conscious animals, using chronic subcutaneous electrodes. Atropine (0.1 mg/100 g) and propranolol (1 mg/100 g) were administered to evaluate the para-sympathetic (V) and sympathetic (S) influences on HR. Intrinsic HR (HRi) was measured following administration of both drugs simultaneously. P. obesus developed bradycardia from day 5 of the acclimation. This bradycardia was induced solely by decreased HRi, overriding partial vagal withdrawal. During hyperthermia apparent thermal insensitivity of HR was observed. This was attained by partial sympathetic withdrawal compensating for the increase in HRi due to body temperature rise. It can be concluded that in P. obesus, heat acclimation induced bradycardia is attained by intrinsic changes in the pacing cells. It also emerges that the hyperthermic response is independent of and is not affected by heat acclimation.

Central and peripheral contributions to control of heart rate during heat acclimation.

The contributions of the autonomic nervous system and the cardiac pacing cells in the development of heat-acclimation-induced bradycardia were analyzed, and the effect of heat acclimation on the chronotropic response of the heart to heat stress (40 degrees C) was studied. Rats were acclimated at 34 degrees C for 0, 5, 14, 30 and 60 days. Heart rate (HR) was measured in conscious animals, using chronic subcutaneous electrodes. Sympathetic and parasympathetic influences were studied by IP administration of 0.1 and 1 mg/100 g body weight atropine and propranolol respectively, while intrinsic HR (HRi) was measured following administration of both drugs simultaneously. The effects of carbamylcholine and norepinephrine on the beating rate of isolated rat atria were investigated to study pacemaker responsiveness to neutrotransmitters. Up to day 14 of heat acclimation, bradycardia was attained by tonic parasympathetic acceleration (18%) and temporal sympathetic withdrawal (0.8% on day 14), to compensate for the gradually augmented HRi (2.5% and 8% on days 5 and 14, respectively). Following long-term acclimation HRi declined below pre-acclimation rate. This was associated with resumed sympathetic activity (16% and 10% on days 30 and 60 respectively) while parasympathetic activity continued to be high (18%). Tachycardia, known to occur with severe uncontrolled body hyperthermia, was attenuated following heat acclimation by 42%. It was concluded that during the initial phase of heat acclimation bradycardia is achieved primarily by changes in autonomic influences, while following long-term acclimation, changes in the intrinsic properties of the pacing cells (HRi) and the autonomic system both play a role.

Regulation of submaxillary gland muscarinic receptors during heat acclimation.

Binding properties of submaxillary gland muscarinic receptors and agonist-induced saliva secretion were studied in rats subjected to heat acclimation. The maximal binding capacity for the muscarinic antagonist N-[3H]methyl-4-piperidyl benzilate was increased from control value of 0.21 to 0.40 pmol/mg protein within 1-2 days of heat acclimation. The increase in the number of muscarinic receptors per gland (100%) was by far higher than the increase in tissue weight (20%), indicating higher density of receptors in the acinar cells of the treated rats. High levels of receptors coincided with the appearance of high-affinity binding sites for muscarinic agonists (oxotremorine, pilocarpine and carbamylcholine), and with reduced tissue sensitivity to pilocarpine. After 4-8 weeks of heat acclimation, the number of receptors as well as tissue response to pilocarpine returned to control levels. These results suggest a functional correlation between the transient upregulation muscarinic receptors in the submaxillary gland and the physiological activity in salivary secretion, and indicate that the high-affinity muscarinic receptors may attenuate saliva secretion during the initial phase of heat acclimation.

Altered responsiveness to parasympathetic activation of submaxillary salivary gland in the heat-acclimated rat.

Submaxillary salivary gland responsiveness during the heat acclimation procedure (34 +/- 1 degree C) was studied in the rat. Gland responsiveness was evaluated by measuring saliva flow rate of the anesthetized animals following either parasympathetic nerve stimulation or i.v. application of pilocarpine. A thirty percent decrease in glandular responsiveness for the two modes of stimulation was measured during the first 10 days of acclimation. Following 60 days of acclimation recovery was observed. It is concluded that decreased responsiveness of the heat-acclimated gland is a glandular event. Increased saliva flow occurring at the initial phase of acclimation is apparently due to changes in the thermoregulatory center.

Thermoregulatory activity in the rat: effects of hypohydration, hypovolemia and hypertonicity and their interaction with short-term heat acclimation.

Hypothalamic temperature thresholds to heat-induced (40 degrees C ambient temperature) tail vasodilation (Vth) and salivation (Sth) as well as salivary flow rate and volume were studied in conscious rats, hypohydrated (24 hr water deprivation), hypovolemic (20% dextran sc), hypertonic (1M NaCL po), hypertonic and hypovolemic and heat-acclimated (5 days at 34 degrees C) before and after hypohydration. Sth was elevated in hypohydrated, hypovolemic, hypertonic and heat-acclimated hypohydrated rats concomitantly with a remarkable decrease in saliva volume, flow rate and heat tolerance. Heat acclimation alone resulted in a reduction in Vth, Sth, salivary flow and volume. Vth was not affected by hypohydration, but was elevated following hypovolemia and combined hypovolemia and hypertonicity. It is concluded that alterations in both plasma volume and osmolarity, which may occur during hypohydration, play a major role in the alteration in thermoregulatory responses during hypohydration. Heat acclimation does not improve tolerance during hypohydration. Thus, during hypohydration, the control of body fluids overrides thermoregulation.

The effects of HGCl2 and mersalyl on mechanisms regulating intracellular calcium and transmitter release.

HgCl2 and mersalyl increased and later decreased both the spontaneous and evoked transmitter liberation at the frog neuromuscular junction. Lower concentration of HgCl2 exhibited only an inhibitory effect on transmitter release. These mercurials inhibited calcium transport of mitochondria and synaptosomal vesicles. Lower concentrations of HgCl2 showed a stimulatory effect on mitochondrial calcium uptake. It is suggested that the effect of mercurials on transmitter release is mediated via changes of the intracellular calcium ion concentration.

Adrenergic influences on rabbit oviduct: effect of muscle size and ovarian hormones.

This study attempts to distinguish between a direct action of ovarian steroids on adrenergic neurons in the oviduct and an indirect effect mediated by changes in muscle size. Mature rabbits were treated as follows: group 1, ovariectomized and a polyethylene catheter (1 mm OD) inserted into isthmus of one oviduct (CT) with contralateral oviduct as control (C); group 2, normal, estrous animals with one intubated isthmus (ET) and contralateral control (E). Fourteen days postoperatively, oviducts were removed and muscle-wall thickness, norepinephrine (NE) content, and response to nerve stimulation were measured. Although castration atrophy was prevented in CT, NE content of CT was significantly less than C, 0.032 +/- 0.07 versus 1.09 +/- 0.10 nmol. NE content of ET was also significantly less than E (1.32 +/- 0.03 versus 1.81 +/- 2.0) despite a greater wall thickness of ET. It was concluded that: a) withdrawal of ovarian hormones reduces NE contents by a direct action on nerves; b) moderate stretch, per se, increases muscle size and reduces NE content; c) nerve stimulation induces muscle contraction despite large reduction in transmitter content.

Neuromuscular transmission: inhibition by manganese ions.

Manzganiese ions. are potent blocking argenits of synaptic transmission at the neuromuscular junction in the frog. The main site of action is the presynaptic nerve terminal, where the ions decr-ease the amount of transmitter liberated by a never impulse. The inihibition produced by manganese is reversible.

Activation of transmitter release by strontium and calcium ions at the neuromuscular junction.

1. The interaction between Ca and Sr ions on quantal transmitter release at the frog neuromuscular junction was studied, using conventional electrophysiological techniques.2. While Ca ions always activate transmitter release, the activating action of Sr ions depends on the Ca ion concentration in the medium; at low [Ca], strontium ions enhance the release, but at higher [Ca] they inhibit it. It is postulated that there is a [Ca] at which Sr ions do not affect transmitter liberation.3. When Sr activates release, its effect and the effect of Ca add in a more than linear fashion.4. Magnesium ions inhibit the release induced by Sr.5. The results can be explained by assuming that Ca and Sr act on the same site, at some stage of the process of quantal transmitter release. The affinity of both ions towards the sites is approximately the same, but the effectiveness of Sr is much smaller.