Enhanced heat production in physically restrained rats in hypoxia

1981 ◽  
Vol 51 (6) ◽  
pp. 1601-1606 ◽  
Author(s):  
M. Hayashi ◽  
T. Nagasaka

Combined effects of restraint and hypoxia (9.5% O2 in N2) on heat production (M), heat loss (HL), colonic temperature (Tcol), and cardiovascular activity were studied in unanesthetized rats. In freely moving (F) rats, hypoxia decreased M, HL, Tcol, and heart rate (HR). In restrained (R) rats, however, hypoxia increased M, HL, Tcol, and HR. The increase in these parameters was greatest within 30 min of hypoxia, and the peak value of M was 10.4 W X m-2 higher than in normoxia. After chemical sympathectomy with 6-hydroxydopamine hydrobromide, no such increase was observed in R rats. l-Norepinephrine bitartrate (0.4 mg X kg-1) increased M and HR in F rats in hypoxia. The increase in M was, however, 9.5 W X m-2 and significantly less than that observed in normoxia. Hypoxia significantly reduced blood flow to the brown adipose tissues (BAT) in R rats. The BAT may not be responsible for the increased metabolism in restrained hypoxia-exposed rats. Hypoxia significantly increased blood flow to the heart and the diaphragm, and to a lesser extent to the limb muscles. The increased metabolism in the cardiac and respiratory muscles may be a cause of hyper-metabolism in restrained rats. The limb muscles may also play some role in increasing metabolism in these rats.

1979 ◽  
Vol 57 (1) ◽  
pp. 16-23 ◽  
Author(s):  
M. T. Lin

The thermal responses of three groups of control, 6-hydroxydopamine (6-OHDA) treated and 5,7-dihydroxytryptamine (5,7-DHT) treated rabbits to the administration of chlorpromazine (CPZ) were assessed at three different ambient temperatures (Ta: 2, 22, and 32 °C). Depleting catecholamines (CA) in brain with 6-OHDA produced a decrease in metabolic rate, in respiratory evaporative heat loss, and in ear blood flow at both Ta's of 2 and 22 °C, while depleting 5-hydroxytryptamine (5-HT) contents in brain with 5,7-DHT produced the opposite responses at the same Ta's. However, these amine-depleted animals maintained their rectal temperatures within normal limits over a wide range of Ta's tested. Furthermore, intraperitoneal administration of CPZ produced hypothermia at both Ta's of 2 and 22 °C. The major cause of the CPZ-induced hypothermia was an inhibition of metabolic heat production at Ta of 2 °C. At Ta of 22 °C, the CPZ-induced hypothermia was due to both a decrease in heat production and an increase in ear blood flow. However, CPZ hypothermia was attenuated in the CA-depleted animals, but was potentiated in the 5-HT-depleted animals. The data indicate that brain monoamines are involved in the central mechanisms of CPZ-induced hypothermia.


1984 ◽  
Vol 62 (10) ◽  
pp. 1327-1332 ◽  
Author(s):  
Florent Depocas ◽  
David O. Foster ◽  
Gloria Zaror-Behrens ◽  
Suzanne Lacelle ◽  
B. Nadeau

Twenty-four hours after subcutaneous administration of 6-hydroxydopamine (6-OHDA) at a dose of 10 mg/kg body weight in warm-acclimated rats, noradrenaline (NA) content and dopamine β-hydroxylase (DBH) activity of interscapular brown adipose tissue (IBAT) were reduced to about 10 and 35% of control values. Corresponding values for cold-acclimated rats, similarly treated, were 12 and 32%. In both groups of animals, calorigenic function in IBAT assessed by measurement of the effect of cold exposure on rate of blood flow through the tissue was lost almost completely. Twenty-four hours after treatment of rats with various doses of 6-OHDA, calorigenesis in IBAT was directly related to residual NA. Measurements of noradrenaline content and DBH activity from 1 to 10 days after 6-OHDA and the increase in IBAT blood flow of cold-exposed animals from 1 to 7 days after 6-OHDA indicated marked differences in the extent to which each of these indicators of the integrity and function of sympathetic nerve endings recovered with time and with the acclimation temperature of the animals. Regeneration of macromolecuiar components of noradrenergic vesicles in IBAT appeared to occur more rapidly in cold than in warm-acclimated animals. Thus, moderate doses of 6-OHDA may acutely sympathectomize IBAT, but as previously reported for other tissues, full recovery of function of IBAT occurs long before noradrenaline stores are replenished.


1998 ◽  
Vol 275 (1) ◽  
pp. R92-R98 ◽  
Author(s):  
Akiko Kobayashi ◽  
Toshimasa Osaka ◽  
Yoshio Namba ◽  
Shuji Inoue ◽  
Tai Hee Lee ◽  
...  

Subcutaneous administration of capsaicin (5 mg/kg) immediately increased the temperature of the tail skin (Tsk) for 2 h in urethan-anesthetized rats, suggesting an increase in heat loss. O2 consumption, an index of heat production, also immediately increased after the capsaicin injection, and this increase lasted for >10 h. Colonic temperature (Tco) decreased within 1 h after the injection, and this decrease was followed by a long-lasting hyperthermic period. Adrenal demedullation largely attenuated the capsaicin-induced increase in O2consumption, and sympathetic denervation of the interscapular brown adipose tissue partly attenuated the increase in O2 consumption. However, capsaicin-induced heat loss was normal in these rats. In rats with cutaneous vasodilation maximized by warming and administration of hexamethonium, capsaicin did not further increase Tsk but normally induced heat production, and Tco gradually rose without a hypothermic period. Thus capsaicin simultaneously increased heat loss and heat production, and inhibition of one response did not affect the other. These findings suggest that capsaicin simultaneously activates independent networks for heat loss and heat production.


2009 ◽  
Vol 297 (2) ◽  
pp. E490-E494 ◽  
Author(s):  
U. S. Pettersson ◽  
J. Henriksnäs ◽  
L. Jansson

Previous studies have shown that the Goto-Kakizaki (GK) rat, a nonobese type 2 diabetes model, has an increased white adipose tissue (WAT) and islet blood flow when compared with control rats. The aim of the study was to examine if these increased blood flow values in GK rats could be affected by the β3-adrenoceptor antagonist SR-59230A. We measured organ blood flow with a microsphere technique 10 min after administration of SR-59230A (1 mg/kg body wt), or the corresponding volume of 0.9% NaCl solution (1 ml/kg body wt) in rats anaesthetized with thiobutabarbital. The GK rat had an increased blood flow in all intra-abdominal adipose tissue depots except for the sternal fat pad compared with Wistar-Furth (WF) rats. However, no differences were seen in the blood perfusion of subcutaneous white or brown adipose tissue. The blood flow was also increased in both the pancreas and in the islets in the GK rat compared with WF rats. SR-59230A treatment affected neither WAT nor pancreatic blood flow in WF rats. In GK rats, on the other hand, SR-59230A decreased both WAT and islet blood flow values to values similar to those seen in control WF rats. The whole pancreatic blood flow was not affected by SR-59230A administration in GK rats. Interestingly, the brown adipose tissue blood flow in GK rats increased after SR-59230A administration. These results suggest that β3-adrenoceptors are involved in regulation of blood flow both in islet and in adipose tissue.


1988 ◽  
Vol 64 (1) ◽  
pp. 174-180 ◽  
Author(s):  
R. L. Johnson ◽  
M. B. Reid

Sublethal inhibition of citrate metabolism in the tricarboxylic acid (TCA) cycle with monofluoroacetate (MFA) has been shown to cause a fivefold increase in myocardial blood flow without any change in cardiac output, blood pressure, or O2 consumption (C. Liang, J. Clin. Invest. 60: 61-69, 1977); however, blood flow did not increase to any organs examined other than the heart, including resting limb skeletal muscle. Preferential inhibition of glycolysis with iodoacetate (IA) failed to cause similar changes in distribution of blood flow. This unique response of myocardium to TCA cycle inhibition suggested a unique metabolic control of cardiac vasodilation. An alternate explanation is that MFA is preferentially concentrated in active muscle. After MFA, tissue citrate accumulates behind the block and the highest levels are reported in the heart and diaphragm, suggesting enhanced blockade or enhanced compensation in these two continuously active muscles. To test the hypothesis that vasodilation in the heart after MFA is not unique and that similar vasodilation will be evoked in active respiratory muscles, we measured blood flow to the myocardium, kidney, diaphragm, intercostals, transverse abdominals, and triceps brachii in anesthetized dogs using radionuclide-labeled microspheres, before and after MFA, and in another set of dogs before and after IA. Before MFA or IA, inspiratory loading significantly increased blood flow to active muscles of breathing in proportion to the added load. After MFA, blood flow to active muscles of breathing as well as to the heart became abnormally elevated with respect to mechanical work, and loading evoked no further increase in blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 63 (6) ◽  
pp. 595-598 ◽  
Author(s):  
W. H. Harris ◽  
D. O. Foster ◽  
B. E. Nadeau

This study was undertaken to determine if brown adipose tissue was involved in heat production during fever produced by S. abortus equi (1 μg) in unanesthetized rabbits aged 19–26 days. The fever (0.9–1.6 °C) occurred after a delay of 20–30 min and was frequently biphasic. Radiolabelled microspheres for measuring tissue blood flow were injected intraventricularly into three groups of animals: rabbits not given pyrogen, rabbits in which the febrile response to pyrogen was developing, and rabbits in which the febrile response had peaked. Blood flow to brown fat deposits and other organs was calculated from the fractional distribution of the microspheres and the recovery of microspheres in a reference arterial blood sample. At the fever peak, blood flow to brown fat was not significantly different (p > 0.05) from the control value (0.9 ± 0.2), but during the rising phase of the fever the flow increased significantly (p < 0.01) to 2.6 ± 0.4 mL min−1 g−1. The blood flow to muscles of the forelimbs and hind limbs was also increased significantly (p < 0.05) during the rising phase of the fever. No significant change in blood flow to other organs or tissues was found during the rising phase of the fever. These results indicate that both nonshivering as well as shivering thermogenesis contribute to heat production during development of fever in the young rabbit. However, nonshivering thermogenesis was not involved in the maintenance of the elevated body temperature after the fever had peaked.


1994 ◽  
Vol 76 (4) ◽  
pp. 1481-1488 ◽  
Author(s):  
L. Clarke ◽  
C. J. Darby ◽  
M. A. Lomax ◽  
M. E. Symonds

We examined the effect of delivering near-term twin lambs by cesarean section into a warm (30 degrees C) or cool (15 degrees C) ambient temperature on the control of thermoregulation. Heat production was measured 20–30 h after birth during non-rapid-eye-movement sleep at 29 and 14 degrees C. At 29 degrees C there was no difference in heat production between groups, but at 14 degrees C cool-delivered (CD) lambs exhibited a 62% greater metabolic response. Irrespective of delivery temperature, 15 of the 18 lambs used shivering thermogenesis during cold exposure, indicating a reduction in the ability to use nonshivering thermogenesis in brown adipose tissue (BAT). Mean plasma concentrations of thyroxine and triiodothyronine were 35 and 45% greater, respectively, in CD lambs than in warm-delivered lambs. The level of guanosine 5′-diphosphate binding in BAT was lower than in normally delivered lambs and was not different between CD and warm-delivered lambs. Cesarean section delivery prevents the rise in BAT thermogenic activity, which results in an increased reliance on shivering thermogenesis to maintain colonic temperature. Under these conditions, delivery into a cool environment increases the plasma concentration of thyroid hormones, which benefits the neonate by enabling a greater thermogenic response via shivering.


1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.


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