Biomedical subjects
Publications and source records attributed to M T Lin.
I.p. administration of p-chlorophenylalanine produced a fall in rectal temperature in rats. The hypothermia was attenuated after pretreatment of the animals with 5,6-dihydroxytryptamine, but was unaffected after pretreatment of the animals with 6-hydroxydopamine.
The effect of the 5-hydroxytryptamine (5-HT) precursor 5-hydroxytryptophan (5-HTP) on the thermoregulatory responses of unanesthetized rats were assessed at three different ambient temperatures (Ta) of 8, 22 and 31 degrees C. Intraperitoneal administration of either 5-HTP alone or 5-HTP plus R04-4602 (the peripheral decarboxylase inhibitor) produced dose-dependent hypothermia at both Ta's of 8 and 22 degrees C. The hypothermia was brought about solely by a decrease in metabolic heat production at 8 degrees C Ta. At 22 degrees C Ta, the hypothermia was due to both a decrease in metabolic heat production and an increase in tail and footsole skin temperature. However, at 31 degrees C Ta, there were no changes in rectal temperature in response to either 5-HTP or 5-HTP plus R04-4602 application. The data suggest that an increase in 5-HT levels in brain decreases heat production and/or increase heat loss and leads to hypothermia in rats.
Intraventricular administration of 6-OHDA or 5,6-DHT suppressed food intake, whereas their effect on active avoidance produced a suppression with the former and an enhancement with the latter. The increased water intake was specifically associated with 5,6-DHT treatment in rats.
The prostaglandin E1-induced fever was neither potentiated nor attenuated at all levels of the ambient temperatures (2, 22 and 32 degrees C) studied after pretreatment of the conscious rabbits with p-chlorophenylalanine, when compared to the untreated control.
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Muscle and adipose tissue were obtained from steers and dairy cows following subcutaneous administration of [14C] progesterone. Following extraction, purification and separation by column, thin layer and gas-liquid chromatography, various radioactive residues from these tissues were identified by their chromatographic mobility, crystallization to constant specific activity and mass spectra. Progesterone constituted 54% of free radioactivity extracted from muscle and 69 and 73% of radioactivity in the free and conjugated portions of extracts, respectively, from fat. Metabolites identified were: 5alpha-pregnane-3,20-dione, 9%, 0%, 0%, 20beta-hydroxy-4-pregnen-3-one, 8%, 11%, 3%; 3alpha-hydroxy-5beta-pregnan-20-one, 13%, 2%, 2%, 3alpha-hydroxy-5alpha-pregnan-20one, 3%, 3%, 6%; 20 alpha-hydroxy-5alpha-pregnan-3-one, 0%, 2%, 3%; of radioactivity in muscle (free) and fat (free and conjugated fractions), respectively. Tentatively identified in fat extracts by chromatographic mobility were: 20alpha-hydroxy-4-pregnen-3-one, 1%, 1% and 3beta-hydroxy-5beta-pregnan-20-one, 0%, 2% of radioactivity in free and conjugated fractions, respectively. The average concentration of steroid in these animals due solely to treatment, calculated from the specific activity of the [14C] progesterone administered, was 3.4 and 18.1 ng/g in muscle and subcutaneous fat, respectively.
Selected properties of [3H]prostaglandin (PG) E1 binding to collagenase dispersed bovine luteal cells were studied and compared with those observed in luteal plasma membranes. [3H]-PGE1 specific binding to a relatively homogeneous population of luteal cells was a rapid (K1 = 4.2 X 10(5) M-1 .sec-1), reversible (K-1 = 3.9 X 10(-3) sec-1), saturable and specific process at 38 degrees C. The binding was homogeneous with an apparent dissociation constant of 2.4 nM and 1.8 X 10(5) receptors per cell. The presence of increasing amounts of unlabeled PGs inhibited [3H]PGE1 binding in a dose-dependent manner. The potency order for this inhibition of binding was: PGE 2 greater than PGE1, (15S)-15-methyl-PGE2 methyl ester greater than PGF2alpha greater than PGF1alpha greater than other PGs, PGE, PGF metabolites and PGF analogs. Other than the homogeneous nature of [3H]PGE1 binding and the greater effectiveness of PGE2 compared to PGE1 in cells, the rest of the properties of [3H]PGE1 binding to cells were in excellent agreement with those observed in plasma membranes.
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Intraperitoneal administration of a peripheral decarboxylase inhibitor benserazide (Ro4-4602) to unanesthetized rats produced alterations in body temperature which depended on ambient temperature. In the cold, hypothermia was brought about by a decrease in metabolic heat production. At room temperature, a dose-dependent hypothermia was preceded by a slight hyperthermia. The hypothermia was due to an increase in skin temperature (tail) and a decrease in metabolic heat production, while the hyperthermia was due to a decrease in skin temperatures (both tail and footsole) and an increase in metabolic heat production. In the heat, hyperthermia responses to benserazide were associated with decrease in skin temperature (both tail and footsole). Benserazide treatment produced no significant change in brain 5-HT content. Chlorpromazine-induced hypothermia was greatly enhanced after pretreatment of the animals with benserazide at room temperature (22 degrees).
1. The effects of two inhibitors of uptake pump in serotonergic neurons, Lilly 110140 and chlorimipramine, on the thermoregulatory responses of unanaesthetized rats to different ambient temperatures (Ta) of 8, 22 and 30 degrees C were assessed. 2. Intraperitoneal administration of either Lilly 110140 or chlorimipramine produced dose-dependent hypothermia at 8 and 22 degrees C Ta. At 8 degrees C Ta the hypothermia was due to a decrease in metabolic heat production. At 22 degrees C Ta, the hypothermia was brought about by both a decrease in metabolic heat production and an increase in cutaneous temperature of the tail and the footsole. 3. However, at 30 degrees C Ta, there were no changes in rectal temperature in response to either Lilly 110140 or chlorimipramine application. 4. The data suggest that an increase in serotonergic receptor activity or in functional serotonin in brain decreases heat production and/or increases heat loss and leads to hypothermia in rats.
Intraperitoneal administration of ketamine produced dose-dependent hypothermia at the ambient temperatures (Ta) of both 8 and 23 degrees C in unanesthetized rats. At a Ta of 8 degrees C, the hypothermia was brought about solely by a decrease in metabolic heat production. There were no changes in either the tail skin temperature (Ttail) or the sole skin temperature (Tsole). At a Ta of 23 degrees C, the hypothermia was due to an increase in Ttail, and increase in Tsole, and a decrease in metabolic heat production. However, at a Ta of 31 degrees C, there were no changes in rectal temperature in response to ketamine application, since neither heat production nor skin temperatures (e.g., Ttail and Tsole) was affected by ketamine at this Ta. The data indicate that the effect of the drug treatment may be to decrease heat production and (or) increase heat loss.
Elevating serotonin (5-HT) contents in brain with 5-hydroxytryptophan (5-HTP) reduced rectal temperature (Tre) in rabbits after peripheral decarboxylase inhibition with the aromatic-L-amino-acid decarboxylase inhibitor R04-4602 at two ambient temperatures (Ta), 2 and 22 degrees C. The hypothermia was brought about by both an increase in respiratory evaporative heat loss (Eres) and a decrease in metabolic rate (MR) in the cold. At a Ta of 22 degrees C, the hypothermia was achieved solely due to an increase in heat loss. Depleting brain contents of 5-HT with intraventricular, 5,7-dihydroxytryptamine (5,7-DHT) produced an increased Eres and ear blood flow even at Ta of 2 degrees C. Also, MR increased at all but the Ta of 32 degrees C. However, depleting the central and peripheral contents of 5-HT with p-chlorophenylalanine (pCPA) produced lower MR accompanied by lower Eres in the cold compared to the untreated control. Both groups of pCPA-treated and 5,7-DHT-treated animals maintained their Tre within normal limits. The data suggest that changes in 5-HT content in brain affects the MR of rabbits in the cold. Elevating brain content of 5-HT tends to depress the MR response to cold, while depleting brain content of 5-HT tends to enhance the MR response to cold.
In a double-blind study in 23 asthmatic patients Sch 1000 was found to be an effective bronchodilator with an onset of effect within 15 minutes and a duration of four hours. It was effective on both small and large airways.
The thermal responses produced by both systemic and central administration of prostaglandin E1 (PGE1) at the three different ambient temperatures (Ta) of 2, 22 and 32 degrees C were measured to assess the possible involvement of PGE1 in temperature regulation. The body temperatures, metabolic rate, respiratory evaporative heat loss and vasomotor activity in response to PGE1 were measured. Intravenous administration of PGE1 produced dose-dependent hypothermia at Ta's of both 2 and 22 degrees C. The PGE1 hypothermia was due to cutaneous vasodilation. However, at a Ta of 32 degrees C, intravenous PGE1 produced no changes in rectal temperature and ear blood flow. On the other hand, the direct injection of PGE1 into the third ventricle produced dose-dependent hyperthermia. At a Ta of 22 degrees C, PGE1 fever was due to decreased heat loss along with a small increase in heat production. In the cold, PGE1 fever was due to increased heat production while in the heat heat losses were decreased. The data suggest that elevating PGE1 levels in the periphery causes a hypothermia, while elevating PGE1 levels in the central nervous system causes a hyperthermia at Ta's of both 2 and 22 degrees C.
Three groups of Sprague-Dawley rats were kept at the ambient temperatures of 8, 24 and 32 degrees C respectively for 3 to 7 days. These animals maintained their rectal temperatures within normal limits. However, the animals of either the heat-stressed or the cold-stressed group yielded not only the functional but also the organic effects to their hearts when compared to those of the control group (24 degrees C exposure). Heat exposure produced a lower heart rate and higher cutaneous temperature, while cold exposure produced a higher heart rate and a lower cutaneous temperature. In addition, the ECG recordings showed a predominant S wave and probably a depressed S-T segment in response to either heat or cold exposure. At the end of either 3-day or the 7-day thermal exposure, the animals were subjected to decapitation. Their hearts were sampled for both light and electron microscopic examinations. It was found that the heat-stressed animals shared with the cold-stressed animals a common picture of the myocardial changes. The subcellular changes in the myocardium in response to external heat or cold were characterized by the mitochondrial hypertrophy, the intracellular edema, the destruction of myofibrils, the dilatation of the intercalated discs, and some abnormalities in their capillaries. The data demonstrate that a short term (3 to 7 days) of moderate heat (32 degrees C) or cold (8 degrees C) exposure produces myocardial lesions in rats, although they maintain their body temperatures within normal limits.
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1 Administration of chlorpromazine (Cpz), either systemically or centrally, to unanaesthetized rats at an environmental temperature of 23 degrees C caused dose-dependent hypothermia. 2 In order to achieve equivalent hypothermia, intraventricular administration required a total dose of 20 microgram Cpz and and intraperitoneal administration a dose of 9.7 mg/kg body weight. Accordingly, the dose-ratio between intraventricular and intraperitoneal administration was 1 to 110. Cpz apparently exerts its hypothermic effect by acting directly on central nervous structures rather than through peripheral sites. 3 Cpz-induced hypothermia was potentiated by preoptic anterior hypothalamic (POAH) lesions but not by lesions of the ventromedial nucleus (VMN) of the hypothalamus. It was found that Cpz induced hypothermia most readily in rats with large POAH lesions (-10.4 degrees C), less so in rats with spinal lesions (-5.5 degrees C) at least with control rats (-2.9 degrees C).