Biomedical subjects

O Shido

Publications and source records attributed to O Shido.

At least 55 records · Page 3Linked to original sources

PubMed1993

Role of intrapreoptic norepinephrine in endotoxin-induced fever in guinea pigs.

The peripheral administration of pyrogens has been shown previously to affect the activity of central noradrenergic neurons, but the effects have been variable and no consensus has emerged regarding their functional significance. Because norepinephrine (NE) microdialyzed into the preoptic area (PO) of the anterior hypothalamus of conscious guinea pigs is hypothermizing, the possibility was investigated whether NE might be a febrilytic rather than a febrigenic mediator. Intravenous injections of Salmonella enteritidis lipopolysaccharide (2.0 micrograms/kg) evoked a bimodal fever, which was attenuated in a dose-dependent manner by NE microdialyzed (10 or 20 micrograms/microliters at a rate of 2 microliters/min for various durations) into the PO. The alpha 2-adrenergic receptor antagonists rauwolscine (1 or 2 micrograms/microliters) and yohimbine (1 microgram/microliter) microdialyzed intrapreoptically significantly reduced the trough of body (core) temperature (Tc) between the first and second peaks of the bimodal fever and prolonged the overall febrile course. None of these effects was associated with changes in skin temperature. The level of NE (assayed by high-performance liquid chromatography with electrochemical detection) in the preoptic extracellular fluid collected by intracerebral microdialysis was significantly elevated at the end of each rising phase of the bimodal fever, just before or about the time when Tc began to fall, compared with pyrogen-free saline controls at the same times. These results suggest that intrapreoptic NE may have a thermolytic effect on fever by reducing metabolic heat production and may thus play a physiological role in the initiation of febrilysis in guinea pigs.

Animals↗

PubMed1993

Relationship between body core and peripheral temperatures at the onset of thermoregulatory responses in rats.

The relationships between body core temperature and environmental temperature (T(a)) at the onset of tail skin vasodilation, thermally-induced salivary secretion and cold-induced thermogenesis were examined in rats. Hypothalamic temperature (Thy) was measured as an index of body core temperature. Internal body heating and cooling were made using an intravenous thermode chronically implanted in the inferior vena cava at various T(a)s. External heating and cooling were made by changing T(a) at a constant rate, while Thy was controlled at constant levels with the thermode. Internal heating induced tail skin vasodilation but not thermally-induced salivary secretion, and internal cooling induced cold-induced thermogenesis. External warming caused tail skin vasodilation and thermally-induced salivary secretion, but external cooling failed to induce cold-induced thermogenesis. There were significant correlations between Thy and T(a) at the onset of tail skin vasodilation, thermally-induced salivary secretion and cold-induced thermogenesis. When T(a) was taken as an indicator of thermal input from the skin, the ratios of the potency of inputs from the body core and skin were estimated to be between 8:1 and 6:1 at the onset of tail skin vasodilation, 8:1 at the onset of thermally-induced salivary secretion, and 5:1 for the control of cold-induced thermogenesis. These results suggest that, in rats, the contribution of thermal input from the skin to the onset of thermoregulatory responses is relatively small.

Animals↗

PubMed1993

Alteration of nyctohemeral changes in body core temperature by repeated cold exposure given at a fixed time daily in rats [corrected].

The effects of cold exposure for several hours at a fixed time once a day on nyctohemeral variations of hypothalamic temperature (Thy), heat balance, and feeding and locomotor activities were examined in rats. The cold-exposed group was subjected to an ambient temperature of 3 degrees C for about 5 h in the last half of the dark phase daily for 10 or more than 21 consecutive days, while the control rats were kept constant at 24 degrees C. The 10-d cold exposure had little effect on nyctohemeral changes in Thy and locomotor activity. However, after completing a 3- to 4-week cold exposure schedule, the levels of Thy, heat loss, heat production, and feeding and locomotor activities of the cold-exposed rats significantly decreased for 1-2 h during the period of the previous cold exposure time. These decreases lasted for at least 2 d after the end of the cold exposure schedule. These results suggest that the patterns of nyctohemeral changes in body core temperature and feeding and locomotor activities were altered after repeated cold exposure at a fixed time once a day in rats.

Animals↗

PubMed1992

Blood flow through the ophthalmic veins during exercise in humans.

The blood from the face flows into the intracranium through the ophthalmic veins when human subjects become hyperthermic. To investigate a possible mechanism underlying this change in direction of flow, five young men were subjected to either passive body warming or exercise on a cycle ergometer, in a climatic chamber whose air temperature and relative humidity were 28 degrees C and 40%. Tympanic (Tty) and oesophageal temperatures, forehead sweat rate (msw), skin blood flow (Qsk) and blood flow through the ophthalmic vein (Qov) were measured, and the mean skin (Tsk) and mean body (Tb) temperatures were computed. Passive body warming was induced by a box-shaped body warming unit enclosing all but the subject's head. Exercise was performed either at an intensity of 60% maximal oxygen consumption or with the intensity increasing in increments. During both tests, msw and Qsk started to increase shortly after the imposition of the heat load. The Qov began to change with the venous blood flowing from the face into the intracranium and a complete reversal in the direction of Qov (from the face to the intracranium) came significantly later than the increases in msw and Qsk. The Tty at the time of flow reversal was the same in both tests. The Tsk (and hence Tb) at flow reversal was, however, significantly higher during passive body warming than during exercise. The mechanism for switching the direction of Qov appeared to have been triggered by a high temperature in the brain, and not by thermal input from the periphery of the body.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1991

Enhancement of finger blood flow response of postprandial human subjects to the increase in body temperature during exercise.

The present study was performed to investigate the effect of food intake on thermoregulatory vasodilatation in seven healthy male volunteers. The changes in oesophageal (Toes) and mean skin temperatures, finger and forearm blood flows (BF), oxygen consumption (VO2) and heart rate (fc) with and without food intake were measured before and during a 40-min exercise at an intensity of 35% maximal O2 consumption at an ambient temperature of 25 degrees C. Exercise commenced 60 min after food intake. Ingestion of food equivalent to 50.2 kJ.kg body mass-1 elevated mean body temperature, BF, VO2 and fc in 60 min. Four subjects responded to exercise with a marked increase in finger BF and with no sweating (non-sweating group), while the other three responded with perspiration over almost the whole skin area and with little change in finger BF. Further analyses were made mainly in the non-sweating group. The postprandial increases in Toes, BF, VO2 and fc were persistent during exercise. The rate of increase in finger BF with the increase in Toes and mean body temperature was significantly greater with food intake than without. However, there was no difference in the response of forearm BF to exercise between the two conditions. These results suggested that food intake enhanced finger BF response to the increase in deep body temperature during exercise. It was also concluded that there was a regional difference in cutaneous vasomotor response to thermal load in the postprandial subjects.

Adult↗

PubMed1991

Effect of heat acclimation on diurnal changes in body temperature and locomotor activity in rats.

1. The present study was performed to examine the effects of heat exposure hours hours at a fixed time once a day on diurnal variations of deep body temperature, heat balance and locomotor activity in rats. 2. The heat-exposed group (HE) was subjected to an ambient temperature of 33.5 degrees C for about 5 h in the last half of the dark phase daily for at least 10 consecutive days, while the control rats were constantly kept at 24 degrees C. 3. After the completion of the heat exposure schedule, hypothalamic temperature (Thy), heat loss, heat production and locomotor activity of HE rats significantly decreased for 3-4 h during the period of previous heat exposure time and formed a characteristic trough in the dark phase, which was never observed in the control rats or in the HE rats before the start of the heat exposure schedule. 4. The troughs of Thy, heat loss and heat production in the dark phase were persistent for at least 2 days after the end of the heat exposure schedule. The reductions of locomotor activity in this period were, however, observed only on the first day after stopping the heat exposure schedule. 5. These results suggest that the time memory for heat exposure was formed in heat-acclimated rats and was persistent for at least 2 days after the removal of heat exposure. It is also concluded that the reduction in metabolic heat production contributed to the fall of Thy during the period of heat exposure.

Acclimatization↗

PubMed1991

Mechanism of vasoconstriction in the rat's tail when warmed locally.

The vascular response of the tail to local warming was investigated in urethan-anesthetized rats whose colonic temperature was maintained at 39.5 degrees C with an intravenous thermode at an ambient temperature of 23 degrees C. The tail, covered with thin latex tubing, was immersed in temperature-controlled water initially kept at 35 degrees C. The tail was warmed by raising the water bath temperature from 35 to 44 degrees C at a constant rate. Tail blood flow (BF), mean arterial blood pressure (BP), and tail skin temperature (Tsk) were measured before and during the local warming. Tail vascular conductance (VC) was computed as 100 x tail BF/BP. When Tsk exceeded 37 degrees C, tail BF and VC significantly decreased from the levels at Tsk of 35 degrees C, and significant reductions in tail BF and VC occurred until Tsk reached 42 degrees C. Surgical deafferentation of the tail, chemical sympathectomy with 6-hydroxydopamine (100 mg/kg), and alpha-blockade with phentolamine (7 or 40.1-45.5 mg/kg) or phenoxybenzamine (5 mg/kg) failed to stop the decrease in tail BF and VC during the local warming. These results suggest that a reflex via the central nervous system and the alpha-adrenergic sympathetic nervous system is not indispensable for heat-induced vasoconstriction (HIVC). It is therefore assumed that, at least in the rat's tail, HIVC predominantly originates from a local vascular response to high temperature.

Animals↗

PubMed1991

Temperature regulation during acute heat loads in rats after short-term heat exposure.

Eleven rats were kept at an ambient temperature of 33.5 degrees C (HC) for 4-5 consecutive days, 9 additional rats were subjected to 33.5 degrees C for approximately 5 h daily (HI) for the same period, and 12 controls (Cn) were kept at 24 degrees C. After the exposure, the rats were placed in a direct calorimeter, where the wall temperature was set at 24 degrees C, and subjected to direct internal heating (6.2 W.kg-1, 30 min) through an intraperitoneal electric heater. After the first heat load and when thermal equilibrium had been attained again, the rats were subjected to indirect external warming by raising the jacket water temperature surrounding the calorimeter from 24.0 to 38.8 degrees C in 90 min. Hypothalamic (Thy) and colonic temperatures (Tco), evaporative and nonevaporative heat loss, and metabolic heat production (M) before the acute heat loads did not differ among the groups. During heat loads, the latent times for the onsets of the rises in tail skin temperature and evaporation were significantly longer, and Thy and Tco at the start of increases in heat losses tended to be higher, in the HC than in the Cn. M significantly decreased in all groups, but the magnitude and duration of reduction in M were significantly greater in the HC than in the Cn. There were no differences between the thermoregulatory responses to heat loads of the HI and Cn. These results suggest that in HC the threshold core temperature for heat loss response and the upper critical temperature have already shifted to a higher level and that HC respond to heat stress more strongly with the reduction of M than Cn. Short-term intermittent heat exposure had little effect on the thermoregulatory mechanisms in rats.

Acclimatization↗

PubMed1990

Thermoregulatory responses to acute body heating in rats acclimated to continuous heat exposure.

Thermoregulatory responses to an acute heat load with intraperitoneal heating (IH) or indirect external warming (EW) by increasing ambient temperature (Ta) were investigated with direct and indirect calorimetry in rats acclimated to environments of 24.0 degrees C (Cn), 29.4 degrees C (H1), and 32.8 degrees C (H2) for greater than 15 days. The rats were placed in a direct calorimeter where the air temperature was maintained at 24 degrees C for the initial 3 h. IH was then made for 30 min through an electric heater implanted chronically (6.5 W.kg-1) in the peritoneal cavity, and EW was performed by raising the jacket water temperature surrounding the calorimeter from 24 to 39 degrees C (0.19 degrees C.min-1). Hypothalamic (Thy) and colonic temperature immediately before the start of the heat load tended to be higher as the acclimation temperature increased. During IH, the threshold Thy for the tail skin vasodilation (Tth) was significantly higher in H2 than in Cn rats. During EW, however, there was no difference in Tth between the groups. Metabolic heat production (M) was slightly suppressed during IH and significantly depressed only in H2 rats. During EW, M was suppressed in all the groups. The magnitude and duration of suppression were greater in H2 rats than in the other two groups. The responses in nonevaporative heat loss and thermal conductance (C) to the rise in Thy did not differ among the three groups during IH. According to the rise in Thy, however, there was a greater C increase in H2 than in Cn and H1 rats during EW.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1990

Heat loss responses in rats acclimated to heat loaded intermittently.

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1989

Blunted febrile response to intravenous endotoxin in starved rats.

The effects of fasting on the febrile responses to intravenous injection of bacterial lipopolysaccharide (LPS; endotoxin) of Escherichia coli were investigated in rats. Ad libitum-fed rats (C) produced a biphasic fever with an increase in the temperature difference between brown adipose tissue and colon and shivering activity (SA). Measurement by a direct calorimeter showed no particular changes in heat loss. Rats starved for 4 days (F4) responded to intravenous LPS with a monophasic fever accompanied by an increase in SA only. However the maximal rise in colonic temperature (Tco) did not differ from C rats. Subsequent 2-day fasting reduced SA and the maximal fever height. Endogenous pyrogen (EP) injected intravenously produced a prompt rise in Tco followed by prolonged hyperthermia in C rats. In the F4 rats, there was no such sustained rise in Tco as a result of intravenous EP. The response in Tco to intravenous prostaglandin E2 (PGE2) was the same in fed and starved rats. The administration of LPS, EP, and PGE2 into the lateral ventricle evoked a similar extent of hyperthermia in C and F4 rats. Because the second phase of fever has been shown to occur after pyrogens are translated into a febrile stimulus within the blood-brain barrier, it is assumed that the functional changes of the blood-brain barrier such as in the permeability of pyrogens or in the sensitivity of pyrogen receptors resulted in the absence of the second phase of fever in starved rats.

Animals↗

PubMed1989

Changes in body temperature of rats acclimated to heat with different acclimation schedules.

Male Wistar rats, initially maintained at an ambient temperature (Ta) of 23.8 degrees C, were subjected to one of seven different heat acclimation schedules under a 12:12-h light-dark cycle (lights on at 0600 h). Two groups of rats were exposed to Ta of 32.4 degrees C all day for 5 (HC5) or 10 (HC10) days. The other four groups were exposed to Ta of 32.8 degrees C for 5 h/day during the last half of the dark phase for 5 (NI5) or 10 (NI10) consecutive days or during the last half of the light phase for 5 (DI5) or 10 (DI10) consecutive days. Control rats (C) were kept at 23.8 degrees C throughout the experiment. Hypothalamic temperature (Thy) was measured every 5 min with a chronically implanted thermocouple from 1 day before the beginning to 2 days after the end of the heat acclimation periods. During the heat acclimation periods, daily mean Thy rose significantly in HC5 and HC10 rats but decreased significantly in NI5 and NI10 rats. Daily mean Thy did not change in C, DI5, and DI10 rats. Thy in HC10 rats sharply decreased at the end of the heat acclimation periods and remained at low levels for approximately 3 h. On the 2nd postacclimation day, however, mean Thy returned and remained at a significantly higher level. In NI10 rats, the mean Thy in the postacclimation period was significantly lower than the preacclimation values. No such changes in mean Thy were observed in DI10 rats. Five-days of heat exposure had little effect on the postacclimation Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

Acclimatization↗

PubMed1989

Changes in brown adipose tissue metabolism following intraventricular vasoactive intestinal peptide and other gastrointestinal peptides in rats.

The effects of intracerebroventricular (icv) vasoactive intestinal polypeptide (VIP), secretin, glucagon, and cholecystokinin-octapeptide (CCK-8) on the thermoregulatory and cardiovascular systems were studied in conscious rats. The icv injection of VIP at a dose of 10 micrograms produced hyperthermia with an increase in the positive difference between the interscapular brown adipose tissue (BAT) and colonic temperatures (TBAT-Tco), but had little effect on nonevaporative heat loss. Mean arterial blood pressure and heart rate increased following the icv VIP. The results were consistent at ambient temperatures (Ta) of 18, 23, and 28 degrees C. The icv injection of secretin at doses of 1 and 10 micrograms at Ta of 23 degrees C produced hypothermia with a decrease in (TBAT-Tco) and elevated blood pressure without any change in heart rate. The 10 micrograms of icv glucagon had no effect on the thermoregulatory and cardiovascular systems. The large dose of icv CCK-8 (10 micrograms) induced persistent hyperthermia. Nonsulfated-form CCK-8 and CCK-tetrapeptide, however, were ineffective on all variables measured. These results indicate that the central VIP activates BAT thermogenesis and induces hyperthermia, but has a minimum effect on nonevaporative heat loss. Although VIP, secretin, and glucagon have similarities in terms of chemical structure, their effects on body temperature, BAT thermogenesis, and the cardiovascular system are quite different.

Adipose Tissue, Brown↗

PubMed1989

Metabolic and blood pressure response to feeding activity is enhanced in freely moving spontaneously hypertensive rats.

Atrial temperature (Tat), heat production (M), mean arterial blood pressure (BP), and feeding (FA) and locomotor (LA) activities were measured over a 24-h period in spontaneously hypertensive rats (SHR) and their normotensive controls (Wistar Kyoto rats; WKY) at an ambient temperature of 24 degrees C. Clear day-night changes in all variables were observed in both groups except for BP and LA in SHR. During the day (0600-1800 h), SHR moved more frequently and seemed to eat more food than WKY. However, the total amount of food consumed for the 2 consecutive days was the same in both SHR and WKY. Compared with WKY, average M and BP during the day and at night and FA and LA during the day were significantly higher in SHR. The responses of Tat for a 24-h period, M during the day and for a 24-h period, and BP during the day to FA were significantly enhanced in SHR. There were no such significant differences of responses in Tat, M, and BP to LA between SHR and WKY. The results suggest that SHR is hyper-responsive in metabolism and blood pressure to feeding activity, particularly in the daytime, but not to locomotion.

Animal Husbandry↗

PubMed1987

Suppression of brown adipose tissue metabolism following intraventricular bombesin in rats.

The effects of intraventricular bombesin (BS) at doses of 0.1, 1.0, and 10.0 micrograms on thermoregulatory and cardiovascular functions were studied in conscious rats with a direct calorimeter at ambient temperatures (Ta) of 18, 23, and 28 degrees C. At two lower TaS, the central BS produced a profound decrease in colonic temperature (Tcol) with a reduction of the temperature difference between the interscapular brown adipose tissue (BAT) and the colon (TBAT-Tcol). Increases in nonevaporative and evaporative heat losses and mean arterial blood pressure (BP) were consistent following the central BS at any dose tested at any Ta. In the sinoaortic deafferentated rats, a 0.1 microgram of BS produced hypothermia with a significant decrease in (TBAT-Tcol) and heat production (M). Changes in Tcol, (TBAT-Tcol), and M in the denervated rats, however, were not different from those in the sham-operated rats. These results suggest that the central BS suppresses BAT thermogenesis and facilitates heat loss mechanisms. The baroreflex-mediated metabolic reduction is not the case in the BS-induced hypothermia in rats.

Adipose Tissue, Brown↗

PubMed1986

Cardiovascular and thermal responses to intravenous endotoxin in guinea pigs.

Changes in blood pressure, heart rate, and heat balance during febrile response to E. coli endotoxin were studied in unanesthetized guinea pigs at an ambient temperature of 24 degrees C. The heat balance was measured with direct and indirect calorimetry. An intravenous injection of endotoxin (5 micrograms X kg-1) produced characteristic biphasic changes in the intra-aortic temperature (Tar), heat production (M), and heat loss (H). The response of arterial blood pressure (BP) to the endotoxin was monophasic and that of heart rate appeared triphasic. Phenylephrine (PHE: 20 micrograms X kg-1 X min-1) infused intravenously in the two rising phases of fever increased BP to the same extent, but the amount of the reflexive bradycardia seemed to be less during the first rise of Tar. The increased metabolism (shivering and nonshivering thermogenesis) during fever development was suppressed by PHE infusion at the two rising phases. The results conclude that, in guinea pigs, the baroreflexive suppression of metabolism is persistent during fever development, but the reflex sensitivity may be different at different phases of fever.

Animals↗

PubMed1986

Effects of chronic administration of naloxone on wheel running activity in rats under 2-h feeding schedule.

The effects of chronic administration of naloxone (120-150 micrograms X kg-1 X h-1) on the wheel running activity (WR) and on food and water intakes were studied in male Wistar rats subjected to a 2-h restricted feeding (1200-1400 h) schedule at 24 +/- 1 degrees C and LD 12:12 (L: 0600-1800 h) cycle. The restricted feeding significantly increased WR before and after the feeding time. Food and water intakes per day were reduced and body weight gradually decreased for the 2-week food restriction period. Food and water intakes appeared to be suppressed by naloxone, particularly shortly after the administration. The chronically administered naloxone slightly increased the 24-h WR. In the naloxone-treated rats, the fraction of WR before the feeding time (anticipatory activity) was significantly increased compared with saline-treated rats. The fraction of WR after the feeding time (succeeding activity) did not change. These results suggest that the endogenous opioid system may play a role in suppressing the excess increase in the anticipatory locomotor activity in the food restricted rats.

Animals↗

PubMed1985

Effects of intraventricular angiotensin II on heat balance at various ambient temperatures in rats.

Angiotensin II (AII, 5 micrograms) injected into the cerebral ventricles produced hypothermia in conscious rats at ambient temperatures (Ta) of 18, 23, and 28 degrees C. At Ta of 18 and 23 degrees C, AII-induced hypothermia was attributed to both enhancement of heat loss and suppression of metabolic rate. At Ta of 28 degrees C, AII-induced hypothermia seemed to be mainly attributed to increased heat loss.

Angiotensin II↗