Effect of central thermal stimulation on the thermoregulatory behavior of the pigeon

Pigeons, trained to work for cooling reinforcement under an ambient heat load, were centrally thermostinulated. Warming the spinal cord and/or the rostral brain stem led to an increase in response rate, while cooling produced a reduction in response rate.     

Effect of intracranial acetylcholine injection on thermoregulatory responses in the rat.

In a study with 5 male Sprague-Dawley rats, microinjections of acetylcholine (ACh) into the preoptic-anterior hypothalamic tissue or lateral ventricle led to an immediate increase in tail temperature and decrease in hypothalamic temperature. The decrease in hypothalamic temperature, but not the increase in tail temperature, was obscured if the S was active following the injection. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Respiratory and thermoregulatory responses of rabbits breathing carbon dioxide during heat exposure

1. Rabbits were clipped and exposed in turn to three environmental conditions: control (C), cold exposure (CE) and water deprivation (WD). Following each type of treatment, the rabbits were exposed to an ambient temperature (Ta) of 35 degrees C for 1 hr. Throughout this period they breathed either normal atmospheric air or 6% CO2 in air. 2. During heat exposure, measurements were made of the respiratory responses and of the O2 consumption (Vo2) of the rabbits. Rectal temperature (Tre) was measured immediately before and again immediately after heat exposure. 3. When subjected to cold exposure or water deprivation the rabbits showed an initial decrease in respiratory frequency (RF) and an initial increase in VT when compared with controls. There was no difference in VE. Rabbits breathing 6% CO2 showed an increase in VT and VE and a decrease in RF when compared with rabbits breathing atmospheric air. In all cases a change in VT or RF was associated with a reciprocal change in the other parameter. 4. The respiratory responses to breathing 6% CO2 were essentially similar in treated and control rabbits, from which it is concluded that neither cold exposure nor water deprivation alter the sensitivity of the medullary respiratory centre to the respiratory drive from the central chemosensors. 5. The increase in Tre during heat exposure was significantly less in rabbits breathing 6% CO2 than in rabbits breathing atmospheric air. However, there was no significant over-all difference in VO2 between rabbits breathing CO2 and those breathing air. From this it is concluded that increased ventilation induced by CO2 causes a greater dissipation of heat than does thermally-induced panting. 6. It is concluded that VT is controlled by the level of blood PCO2 whereas RF is controlled by thermoregulatory requirements. It is further concluded that the reciprocal relationship between VT and RF is regulated in such a way as to maintain VE at the appropriate level for effecting gaseous exchange and evaporative heat loss.     

Effects of heat production attributable to forced walking on thermoregulatory physiological responses of chickens in a warm environment

1. To determine the effects of heat production on thermoregulatory physiological responses, 5 chickens were forced to walk to increase heat production. The study consisted of two experiments. One involved 3 walking speeds (8, 16 and 24 m/min) at 25 degrees C ambient temperature. The other involved a single walking speed of 16 m/min at 3 ambient temperatures (20, 25 and 30 degrees C). Heat production, heart rate, abdominal temperature, shank skin temperature and respiration rate were measured before, during and after walking. 2. Heat production, heart rate and respiration rate increased abruptly after the start of walking and with increase in walking speed. At the start of walking, an abrupt increase in abdominal temperature occurred independently of walking speed and environmental temperature; then, as walking continued, abdominal temperature increased further with increasing walking speed and increasing environmental temperature. Shank skin temperature declined at the initiation of walking, then increased. 3. Heat production and heart rate recovered rapidly after walking, while shank skin temperature and respiration rate increased and then recovered, except at 30 degrees C. 4. A proportion, 17% to 35%, of the increased heat production was stored, increasing body temperature during walking. After walking, the stored heat was lost by means of panting until abdominal temperature recovered to 41 degrees C or shank skin temperature recovered to 37 degrees C. 5. These results suggest that the greatly-increased heat production attributable to forced walking leads to abrupt thermoregulatory physiological responses, and the heat stored in the body is actively dissipated by panting until abdominal temperature recovers to the pre-walking level. The chief mode of heat loss of birds changes with deep body temperature.     

Effect of prostaglandins on vascular resistance and adrenergic vasoconstrictor responses in the canine uterus

Prostaglandins appear to play an important role in a number of reproductive processes. The effect of prostaglandins on numerous vascular beds has been extensively studied, but the effects on uterine hemodynamics have not. The present study was designed to determine the effects of prostaglandins of the A and E series on uterine vascular resistance and responses to adrenergic nerve stimulation in the canine uterus. PGE1, PGE2 and PGA1 were found to be potent uterine vasodilators. In addition, these agents were able to modify adrenergic vasoconstrictor responses. These effects on uterine vascular resistance and adrenergic vasoconstrictor responses were separable. The results of these studies suggest that prostaglandins of the A and E series may play an important role in regulating uterine blood flow in the nonpregnant animal.     

Peripheral thermoreceptor control of thermoregulatory responses of the rat.

Describes a study of 60 Long-Evans male rats in which a warm cage floor or localized heaters in the subcutaneous fascia, nasal cavity, pharynx, esophagus, or abdominal cavity consistently elicited the grooming, locomotion, and tail vasodilation components of the S's heat-loss repertoire, but never the prone body extension component. All thresholds were below the cutaneous pain escape threshold, and most were below normal local temperatures during heat stress. Spatial summation was marked. It is concluded that peripheral thermoreceptors do not produce a general "heat drive," but preferentially activate grooming, locomotion, and vasodilation, leaving body extension dependent on central thermoreceptors. Thus, the relative proportions of extension and other responses are adjusted to the distribution of hyperthermia in the body, varying with the acuteness or chronicity, and the exogenous or endogenous origin, of the heat. (20 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Muscarinic modulation of endogenous noradrenaline release from adrenergic terminals in the guinea-pig colon

1 The present study examined the role of muscarinic receptors in the modulation of noradrenaline (NA) release in the guinea-pig isolated distal colon. The spontaneous endogenous NA overflow assayed by HPLC-ED was taken as an index of NA release from enteric noradrenergic nerve terminals. 2 Physostigmine (10 microM) significantly enhanced spontaneous endogenous NA overflow. Hyoscine (muscarinic antagonist), (R)-(-)-trihexyphenidyl and telenzepine (M1-selective antagonists), and 11[[2-[(diethylamino)methyl]-1-piperydil]acetyl]-5,11 -dihydro-6H-pyrido[2,3-b][1,4]benzodiazepine-6-one (AF-DX 116, M2-selective antagonist) inhibited NA overflow in a concentration dependent manner, with the following EC50 values: 131.74 (18.19-953.96), 101.62 (58.83-175.60), 150 (60-330), 30 (5-170) nM, respectively. 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP, M1- and M3-selective antagonist) had no significant effect up to 100 microM. 3 The muscarinic agonist oxotremorine inhibited NA overflow in a concentration dependent manner, with an EC50 value of 0.67 (0.30-1.51) microM. The response to oxotremorine was inhibited by muscarinic antagonists with the following order of potency: hyoscine = (R)-(-)-trihexyphenidyl = telenzepine > 4-DAMP > AF-DX 116. 4 In the presence of 3 microM tetrodotoxin (TTX), the effect of oxotremorine and 4-DAMP was unchanged, while hyoscine, (R)-(-)-trihexyphenidyl, telenzepine and AF-DX 116, instead of inhibiting, significantly enhanced NA overflow. 5 The present results indicate that, in the guinea-pig colon, endogenous acetylcholine sustains spontaneous NA release by activating muscarinic receptors possibly located on interneurones. In addition, inhibitory muscarinic receptors may exist on adrenergic terminals.     

Effects of two kinds of pillow on thermoregulatory responses during night sleep

We compared thermoregulatory responses during night sleep between two kinds of pillow. One has special cool medium consisting of sodium sulfate and ceramic fiber (pillow A) and the other polyester padding (pillow B). The subjects wore 100% cotton thin pajamas with short sleeves and three-quarters trousers for summer use. They lay and slept in bed with cotton sleeping mat and cotton quilt between 10:30 p.m. and 6:30 a.m. in a bed room with an ambient temperature (Ta) of 27 +/- 1 degrees C and a relative humidity of 55 +/- 5%, using either of the pillow A or pillow B. When they awoke, the subjects filled out a questionnaire on how well they slept during sleep. Main results were: 1) Rectal and forehead skin temperatures and heart rate were kept significantly lower in the pillow A during the latter half of the night sleep. 2) Palm and thigh skin temperatures were significantly higher mostly in the pillow A. 3) All the subjects regarded the pillow A better for deeper sleep. It was concluded that slight cooling of the head due to the pillow A during night sleep seemed to be of significance for deep sleep.     

Day-night variations of behavioral and autonomic thermoregulatory responses to lipopolysaccharide in rats

This study investigated the day-night differences in behavioral and autonomic thermoregulatory responses to bacterial lipopolysaccharide (LPS) in rats. Male rats were housed individually in cages with a 12: 12 h light dark cycle at an ambient temperature of 24 degrees C. The rats were placed in a box with a temperature gradient and intraperitoneally injected with LPS (10 micrograms/kg). The preferred ambient temperature (Tpr) was estimated by the location of the rats in the box, and intraperitoneal temperature (Tb) was measured by a biotelemetry system. Measurements were taken during the light and dark phases of the day. LPS produced fever in both phases. The magnitude of rise in Tb did not differ between the two periods. In the dark phase, Tpr significantly increased during the development of fever and decreased during the defervescence, while it did not change throughout the febrile course during the light phase. In a separate experiment, rats were loosely restrained and placed in a direct calorimeter. Their colonic temperature (Tcol), evaporative and nonevaporative heat loss and heat production were measured before and after intraperitoneal injections of LPS (10 micrograms/kg). Measurements were taken during the light and dark phases of the day. LPS induced fever in both phases. The magnitude of change in T col, heat loss, and heat production due to LPS did not differ between the two periods. These results suggest that the fertile response of rats to intraperitoneal LPS is not affected by the time of day. However, it seems that during LPS-induced fever, thermoregulatory behavior is not fully activated during the light phase of the day.     

Effects of supplemental shade on thermoregulatory response of calves to heat challenge in a hutch environment

Holstein (n = 12) and Guernsey (n = 6) calves, housed in hutches, were used to evaluate the complex relationships among external environment, housing microclimate, and thermal status of calves. The study was conducted during the summer; 9 calves were housed in hutches under supplemental shade, and 9 calves were maintained in hutches under direct sunlight. Environmental and calf temperatures were measured twice daily at 0700 and 1500 h, which included determinations of air temperature, inner and outer surface temperatures of the hutch, rectal and skin temperatures of the calf, and respiration rate. Outer and inner surface temperatures of the hutch were lower under supplemental shade. Hutch air temperature was highly correlated with inner surface temperature and therefore was lower in the shaded environment. During the p.m. period, when heat stress was highest, calves housed in a shaded hutch environment had lower skin temperatures and respiration rates than did unshaded calves. Body temperature and respiration rates increased less for calves in shade than for calves in sun. These data define the relationship between the calf and the environment. Supplemental shade diminished the severity of heat stress experienced by calves that were housed in hutches during the summer.     

Effects of local restriction of evaporation and moderate local ventilation on thermoregulatory responses in exercising humans

Ten healthy young men participated in two series of three trials: series 1 (C1) with, or without, local restriction of evaporation (either on the trunk or on the legs) and series 2 (C2) with, or without, local moderate nitrogen ventilation (40 l.min-1) under an impermeable garment (trunk or leg ventilation). After 60-min rest in a thermoneutral environment, the subjects exercised in a warm environment [30 degrees C, 47% relative humidity (rh) during C1 and 29% rh during C2] on a cycle ergometer for 60 min at 70 W during C1 or at 60 W during C2. During C1, local covering with plastic foil did not increase internal temperature, but increased the mean skin temperature with a higher effect in the case of leg restriction. The trunk skin temperature was affected by the leg covering while the leg skin temperature was not changed by the trunk covering. Only the local sweat rate of the trunk was increased by the two restriction conditions. During C2, internal temperature was decreased by local ventilation while mean skin temperature was reduced only by trunk ventilation. The local ventilation affected only trunk skin temperature with a greater decrease during trunk ventilation. Trunk ventilation did not influence the skin temperature of the legs while ventilation of the legs decreased trunk skin temperature. In addition, leg ventilation decreased the sweat rate of the legs. The impermeable suit worn during C2 led to a greater physiological strain compared to the plastic film worn during C1 even with local ventilation under the impermeable garment. As expected, limiting sweat evaporation led to an increase in physiological strain. Microclimate ventilation at a rate of 40 l.min-1 was not sufficient to allow total heat dissipation but allowed 60-min exercise in a warm environment to be completed without excessive heat accumulation. It would appear that ventilation of the trunk locally was the best solution because of the smaller increase in skin temperature and higher sweating capacity of the trunk.     

Effect of nitric oxide donors on neutrophil responses induced by immune complexes

The present study characterizes the effect of two nitric oxide (NO) donors, S-nitrosoglutathione (GSNO) and sodium nitroprusside (SNP), on the ability of neutrophils to perform different responses triggered by immune complexes (IC). Pretreatment of neutrophils with either GSNO or SNP exerted a biphasic action on antibody-dependent cellular cytotoxicity (ADCC) performed against erythrocytes (E) coated with IgG antibodies (IgG-E), depending on the amount of IgG employed. While with high amounts of antibodies ADCC was markedly inhibited, at low amounts of antibodies it was significantly increased. Both effects were prevented by haemoglobin, a NO scavenger. Moreover, these effects were reproduced by the cell-permeable analogue of cGMP, dibutyryl cGMP (Bt2cGMP). Other neutrophil functions triggered by IgG-E were also examined. It was found that NO donors did not affect either the phagocytosis of IgG-E or the emission of chemiluminescence (CL). Finally, neutrophil functions triggered by soluble IC (sIC) and precipitating IC (pIC) were analysed. It was observed that NO donors did not modify either cytotoxicity performed towards non-sensitized target cells or CL emission. The significance of these results is discussed.     

Force-frequency relations in the failing rabbit heart and responses to adrenergic stimulation

Yohimbine, an alpha 2 adrenoreceptor antagonist, enhances norepinephrine (NE) release and increases sympathetic activity. We examined the behavioral, peripheral sympathetic and adrenocortical responses to oral yohimbine in seven healthy controls and 11 patients diagnosed with agoraphobia with panic attacks (PD). Patients did not differ in baseline cardiovascular or neuroendocrine measures from controls despite significantly higher baseline anxiety ratings. Placebo caused no changes in baseline-corrected behavioral, cardiovascular or neurochemical responses in either group. Yohimbine induced a panic episode in six PD patients, but no controls. PD patients had significantly higher severity scores of autonomic anxiety symptoms. Yohimbine significantly raised systolic blood pressure (F = 3.07, P < 0.03), plasma NE levels (F = 12.11, P < 0.00) and cortisol levels (F = 4.82, P < 0.02), but had no effect on epinephrine levels. NE responses were similar in both groups, but patients had higher cortisol responses to yohimbine than controls (F = 7.14, P < 0.01). The correlational pattern between behavioral ratings and neuroendocrine responses in patients was opposite to that observed in controls. Despite similar increases in plasma NE levels between PD patients and healthy controls, PD patients had greater anxiogenic, cardiovascular and cortisol responses to yohimbine. Enhanced post-synaptic adrenoreceptor sensitivity may explain the noradrenergic dysregulation found in panic disorder.     

Neuronal responses across cortical field A1 in plasticity induced by peripheral auditory organ damage

The adult auditory cortex is capable of a plastic reorganization of its tonotopic map after damage to restricted parts of the cochlear sensory epithelium. We examine the precise conditions of cochlear damage required to demonstrate such plasticity in the primary auditory cortex (A1) of the cat and the changes observed in neuronal responses in the A1 which has reorganized in plasticity of the tonotopic map. From these data we attempt to predict the conditions required for similar plasticity to occur in humans after cochlear damage.     

The effects of thermogenic agents on hindlimb oxygen consumption in the dog: ICI D7114 and noradrenaline

OBJECTIVES: The purpose of this study was to test the hypothesis that the diameter of the recipient coronary artery of the well developed collateral circulation in patients with acute myocardial infarction increases because of the augmented intravascular pressure caused by subsequent collateral development. BACKGROUND: It is well known that collateral circulation develops after acute myocardial infarction. However, some patients have a well developed collateral circulation at the onset of infarction, which may limit the angiographic evaluation of further development of collateral circulation. METHODS: We measured the diameter of the donor and recipient arteries of the collateral circulation by means of a computer-assisted analysis system in seven patients with acute myocardial infarction who had a totally occluded infarct-related coronary artery during the acute and chronic stages of infarction. All coronary angiograms were obtained after the administration of sublingual nitroglycerin. The measurement was repeated immediately after (within 6 h) and late after (42 +/- 11 days) the onset of acute myocardial infarction. RESULTS: The diameter of the donor artery remained unchanged (1.32 +/- 0.98 vs. 1.42 +/- 1.12 mm). In contrast, the diameter of the recipient artery increased from 1.25 +/- 0.63 to 1.55 +/- 0.61 mm (p < 0.01). These changes in coronary artery diameter were associated with an improvement in regional myocardial wall motion at rest in infarct areas (6.7 +/- 7.0% vs. 13.6 +/- 10.7%, p < 0.05). CONCLUSIONS: These findings indicate that serial measurement of coronary artery diameter is useful for the evaluation of collateral development after acute myocardial infarction.     

Influence of endothelial nitric oxide on adrenergic contractile responses of human cerebral arteries

The present study was designed to investigate the influence of the endothelium and that of the L-arginine pathway on the contractile responses of isolated human cerebral arteries to electrical field stimulation (EFS) and norepinephrine. Rings of human middle cerebral artery were obtained during autopsy of 19 patients who had died 3-8 h before. EFS (1-8 Hz) induced frequency-dependent contractions that were abolished by tetrodotoxin, prazosin, and guanethidine (all at 10(-6) M). The increases in tension were of greater magnitude in arteries denuded of endothelium. N(G)-monomethyl L-arginine (L-NMMA 10(-4) M) potentiated the contractile response to EFS in artery rings with endothelium but did not influence responses of endothelium-denuded arteries. L-arginine (10(-4) M) reversed the potentiating effects of L-NMMA on EFS-induced contractions. Norepinephrine induced concentration-dependent contractions, which were similar in arteries with and without endothelium or in arteries treated with L-NMMA. Indomethacin (3 x 10(-6) M) had no significant effect on the contractile response to EFS or on the inhibition by L-NMMA of acetylcholine-induced relaxation. These results suggest that the contractile response of human cerebral arteries to EFS is modulated by nitric oxide mainly derived from endothelial cells; although adrenergic nerves appear to be responsible for the contraction, the transmitter involved in the release of nitric oxide does not appear to be norepinephrine. The effects of L-NMMA in this preparation appear to be due to inhibition of nitric oxide formation rather than caused by cyclooxygenase activation.     

Effect of nicotine on the immune system: possible regulation of immune responses by central and peripheral mechanisms

Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation. This ability of nicotine to attenuate an inflammatory response may also be the cause of reduced mortality of chronically nicotine-treated mice from acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti-SRBC AFC responses were also observed after intracerebroventricular (i.c.v.) administration of relatively small concentrations of NT (28 micrograms/day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protein tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+]i. These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions.