Search PubMed⌕ Search

Biomedical subjects

T Mizobe

Publications and source records attributed to T Mizobe.

44 records · Page 3Linked to original sources
PubMed1990

Changes in brain monoamines and their metabolites during and after hemorrhagic shock in the rat.

The alteration of monoamines and their metabolites in the brain during and after hemorrhagic shock in the conscious state was measured in rats. Blood pressure was maintained at 40-70 mmHg (5.3-9.3 kPa) for 60 min by withdrawing 8 ml of blood intermittently. The content of monoamines, as well as their metabolites, increased in various brain regions during hemorrhage, compared with the content in the control rats. Sixty min after the end of the bleeding period, almost no significant change in the contents of brain monoamines nor of their metabolites was observed. These results may indicate not only an increased release of monoamines from nerve terminals, but also an increased synthesis of them during hemorrhagic shock. Soon after the bleeding was stopped, the increased monoamine turnover rate returned to almost normal levels.

Journal Article↗
PubMed1989

Pathophysiology of circulatory shock: an overview.

Recent developments in three categories of shock research are discussed. Organ perfusion and humoral pathophysiological responses were investigated first, since the cause of fatal shock is always ischemia, tissue hypoxia and resulting cell damage with abolishment of mitochrondrial function. Both centrally and peripherally administered thyrotropin-releasing hormone (TRH) had vasopressor effects that are mediated by a central cholinergic mechanism. A derivative of TRH, DN-1417, had a longer-acting vasopressor action. TRH content increased in the brain in reversible shock, while amino acids increased in irreversible shock.

Adrenal Cortex Hormones↗
PubMed1988

Involvement of endogenous thyrotropin-releasing hormone in central regulation of the cardiovascular system after bleeding in conscious rats.

The 4th ventricle of a conscious rat was perfused using a push-pull cannula. The concentration of thyrotropin-releasing hormone (TRH) in the perfusate was significantly increased after withdrawal of 30% of the total blood. Administration of antiserum of TRH into the ventricle potentiated and prolonged the hypotension induced by the bleeding. These results suggest that endogenous brain TRH is involved in the central regulation of the cardiovascular system after bleeding in conscious rats.

Animals↗
PubMed1988

Effects of hypothermia on thyrotropin-releasing hormone content in the rat brain.

The thyrotropin-releasing hormone (TRH) content in the brain was determined in normothermic and hypothermic rats subjected to immobilization stress. TRH contents in the hypothalamus, midbrain and cerebral cortex significantly decreased during mild hypothermia (body temperature about 34 degrees C), but not during profound hypothermia (about 24 degrees C). The decreases in the TRH content during mild hypothermia were readily reversed by rewarming the animal. These results indicate that cerebral TRH is involved in the response to a mild body temperature drop when the animal is exposed to a cold environment.

Animals↗
PubMed1988

Suppression of the pressor effect of centrally administered thyrotropin-releasing hormone under halothane, pentobarbital and flunitrazepam anaesthesia.

Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) caused an increase in blood pressure (BP) and heart rate (HR) in conscious rats. The pressor effect was greatly diminished by adrenalectomy as well as after pretreatment with phentolamine, an alpha-receptor antagonist or with mecamylamine, a ganglion blocker, suggesting that centrally administered TRH increases BP mainly by stimulating sympathetic activity. Under halothane (0.8%), pentobarbital (33 mg/kg, i.p.) and flunitrazepam (0.8 mg/kg, i.v.) anaesthesia, the pressor effect of TRH was almost completely blocked. The increase in BP induced by peripheral alpha-receptor stimulation with phenylephrine was not affected by the anaesthetics at these doses. Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH. Intracerebroventricularly administered haloperidol and bicuculline also partially diminished the increase in BP produced by TRH, while other neurotransmitter blockers such as phentolamine, propranolol and naloxone did not. These results indicate that the anaesthetics at the doses employed interfere with the central neuronal pathway(s), probably cholinergic pathways, through which TRH exerts its pressor effect.

Animals↗
PubMed1988

Changes in brain thyrotropin-releasing hormone in reversible and irreversible hemorrhagic shock in the rat.

Alterations in thyrotropin-releasing hormone (TRH) content in the brain during hemorrhagic shock were examined in conscious rats, and the results were interpreted in relation to the reversibility of the shock. Two sets of experiments were run. The first one was to establish reversible and irreversible shock models. Hemorrhagic shock was induced by the initial withdrawal of 4 ml of blood followed by 1 ml bleeds at 5, 15, 30, and 60 min to maintain the blood pressure at 40-70 mmHg for 60 min. Blood withdrawn during and 60 min after the end of the shock was used to measure plasma lactate levels and blood gases. Shock was considered to be reversible if the animal survived for 24 hr after the hemorrhage. The plasma lactate levels as well as Base Excess and PaCO2 during and 60 min after the end of the hemorrhage of the surviving rats were significantly different from those of the animals which died within 24 hr. In particular, the plasma lactate levels at 60 min after the end of the hemorrhagic period were good indicators of the mortality of animals; it was predicted that rats whose plasma lactate levels are higher than 3.8 mEq/L would die within 24 hr (0.69% probability of misdiscrimination). The second experiment was to measure brain TRH content during and after hemorrhage produced using the same bleeding procedure as the first. During hemorrhage, brain TRH contents in the medulla oblongata and midbrain were found to be significantly increased compared with the control values. At 60 min after the end of hemorrhage, significantly higher TRH content values were obtained in the medulla oblongata, midbrain, cerebral cortex, striatum, and cerebellum in the rats whose plasma lactate levels were lower than 3.8 mEq/L compared with those of animals having plasma lactate values higher than 3.8 mEq/L. From the results of the two sets of experiments, it is concluded that the surviving animals have more TRH in the brain regions mentioned above than the non-surviving animals after hemorrhagic shock, and it is suggested that brain TRH plays a beneficial role in the course of recovery from hemorrhagic shock.

Animals↗
PubMed1987

The involvement of central cholinergic mechanisms in cardiovascular responses to intracerebroventricular and intravenous administration of thyrotropin-releasing hormone.

Intracerebroventricular (i.c.v.) administration of thyrotropin-releasing hormone (TRH) in a range from 0.1 to 100 micrograms induced a dose-related increase in blood pressure in conscious rats, whereas TRH-free acid (TRH-OH) and histidyl-proline diketopiperazine (His-Pro-DKP), metabolites of TRH, did not. The blood pressure responses to intravenous (i.v.) injection of 5 mg/Kg TRH were similar to those induced by TRH (i.c.v.). Pretreatment with atropine (50 micrograms, i.c.v.) significantly reduced the pressor effect of TRH administered through either route. Hemicholinium-3 (50 micrograms, i.c.v.), an inhibitor of choline uptake, also prevented the increase in blood pressure induced by TRH (10 micrograms, i.c.v.). These results indicate that both centrally and peripherally administered TRH have pressor effects that are mediated by central cholinergic mechanisms, probably by activating cholinergic neurons.

Animals↗