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Biomedical subjects

S Amir

Publications and source records attributed to S Amir.

At least 109 records · Page 6Linked to original sources
PubMed1985

Central thyrotropin-releasing hormone elicits systemic hypoglycemia in mice.

Thyrotropin-releasing hormone (TRH), injected into the central nervous system (CNS) in rats, has been shown to elicit systemic hyperglycemia. In the present study, central TRH administration significantly decreased the plasma glucose in mice. The hypoglycemic response could be blocked by pretreatment with the muscarinic cholinergic antagonist, atropine methyl bromide, or the diabetogenic beta-cytotoxin, alloxan, implicating the involvement of the parasympathetic system and insulin-secreting cells in the endocrine pancreas. The role of TRH in the CNS in the autonomic regulation of glucose homeostasis is discussed.

Animals↗
PubMed1985

Systemic hypoglycemia following central injection of endotoxin in mice.

Intracerebroventricular microinjection of endotoxin in mice resulted in powerful hypoglycemia. The effect was reproduced by the biologically active moiety of endotoxin, lipid A, and prevented by coadministration of the polycationic peptide antibiotic polymyxin B (PMB) or by detoxification of endotoxin by means of mild alkaline hydrolysis. Central treatment with PMB also attenuated the hypoglycemic response to systemic administration of endotoxin or lipid A. These results suggest a direct role of the CNS in the mechanism of endotoxin hypoglycemia.

Animals↗
PubMed1985

Beneficial effect of gamma-endorphin-type peptides in anaphylactic shock.

gamma-Endorphin-type peptides (i.e. gamma-endorphin, des-tyr'-gamma-endorphin [DT gamma E]) result from the processing of the opioid peptide, beta-endorphin. Previous studies have implicated the involvement of beta-endorphin in various types of shock, including anaphylactic shock. In the present experiments the intracerebroventricular (i.c.v.) administration of gamma-endorphin (10 micrograms) or DT gamma E (3.3-10 micrograms) significantly improved survival in anaphylactic shock in mice. Moreover, DT gamma E (10 micrograms) reversed the effect of i.c.v. beta-endorphin (3.3 micrograms) to exacerbate shock. A similar dose of DT gamma E was ineffective in antagonizing beta-endorphin-induced analgesia. The anti-anaphylactic action of DT gamma E as well as its effect to block the pro-anaphylactic action of beta-endorphin were prevented by pretreatment with the sympathetic ganglionic blocker, chlorisondamine chloride. The results suggest that gamma-endorphin-type peptides may act in the central nervous system (CNS) to physiologically oppose the autonomic pathophysiologic influences of beta-endorphin.

Anaphylaxis↗
PubMed1984

Anti-anaphylactic action in the mouse of thyrotropin-releasing hormone (TRH) is mediated through beta 1-adrenoceptive effectors.

Intravenous or intracerebroventricular administration of thyrotropin-releasing hormone (TRH) significantly improved survival in immunized mice subjected to fatal anaphylaxis by intravenous challenge with an antigen. This protective action of TRH was blocked by pretreatment with the beta-adrenergic antagonist propranolol (5 mg/kg), or by prior administration of the cardioselective beta 1-antagonist, metoprolol (5 mg/kg), but not by pretreatment with the beta 2-selective antagonist, butoxamine (5 mg/kg). It is suggested, based on the present and previous findings that the anti-anaphylactic effect of TRH in the mouse is mediated through activation of beta 1-adrenoceptive effectors, secondary to central stimulation of sympathomedullary release of catecholamines.

Adrenal Medulla↗
PubMed1984

Thyrotropin-releasing hormone (TRH) improves survival in anaphylactic shock: a central effect mediated by the sympatho-adrenomedullary beta-adrenoceptive system.

Treatment with thyrotropin-releasing hormone (TRH) significantly improved survival following induction of fatal systemic anaphylaxis in mice. The protective effect was mediated centrally since survival was increased by intracerebroventricular (i.c.v.) administration of TRH at doses which had no effect when given systemically (5-25 micrograms). Acid-TRH, a deamidated metabolite of TRH which lacks hypophysiotropic influences, was as effective as TRH when administered i.c.v., but it was inactive following intravenous (i.v.) administration. The protective effect of TRH in anaphylaxis was reversed by treatments which diminished sympathetic outflow to the adrenal medulla, i.e. ganglionic blockade by chlorisondamine chloride or surgical denervation of the adrenal glands. Destruction of sympathetic nerve endings by the catecholamine neurotoxin 6-hydroxydopamine did not alter the response to TRH. Finally, selective blockade of beta-adrenoceptive sites by propranolol diminished the effect of TRH. Blockade of alpha-adrenoceptors by phentolamine or dopaminergic receptors by domperidone did not alter the protective effect of TRH in anaphylaxis. Collectively, these results indicate that the beneficial effect of TRH in anaphylactic shock involves central nervous system actions which are mediated peripherally through interaction of sympatho-adrenomedullary catecholamines with beta-adrenoceptive effectors. The possibility that TRH exerts its protective actions in shock by acting centrally to functionally antagonize the pathophysiologic effects of endogenous opiate peptides (endorphins) will be discussed.

Adrenal Medulla↗
PubMed1984

Naloxone improves, and morphine exacerbates, experimental shock induced by release of endogenous histamine by compound 48/80.

In mice, fatal shock induced by release of endogenous histamine by compound 48/80 was reversed by the intracerebroventricular (i.c.v.) administration of the opiate antagonist naloxone (10-25 micrograms) but not by the systemic administration of the selective peripherally acting antagonist, naltrexone methyl bromide (1-5 mg/kg). Moreover, systemic or i.c.v. administration of morphine (25 mg/kg and 25 micrograms, respectively) exacerbated shock induced by compound 40/80. This effect was blocked by i.c.v. naloxone (10 micrograms) or naltrexone methyl bromide (10 micrograms) but not by systemic naltrexone methyl bromide (5 mg/kg). The pathogenic effect of i.c.v. morphine was blocked by the systemic administration of the opiate antagonist Win 44,441-3 (5 mg/kg) but not by its inactive (+) isomer, Win 44,441-2. The results suggest possible involvement of central opiate (endorphin) mechanisms in the pathophysiology of fatal histamine shock in mice.

Animals↗
PubMed1984

Beneficial effect of i.c.v. naloxone in anaphylactic shock is mediated through peripheral beta-adrenoceptive mechanisms.

Intracerebroventricular (i.c.v.) administration of 10 micrograms naloxone significantly improved survival following experimental anaphylaxis in mice. The protective effect of i.c.v. naloxone was reversed by treatments which disrupted sympathetic outflow to the adrenal medulla, i.e. ganglionic blockade by chorisondamine chloride or denervation of the adrenal glands or by inhibition of beta-adrenoceptive sites by propranolol. These results indicate that naloxone's beneficial effect in anaphylactic shock involves central actions which are peripherally mediated through activation of beta-adrenoceptive mechanisms.

Adrenal Medulla↗
PubMed1984

Opiate antagonists reverse the hypoactivity associated with systemic anaphylaxis in mice.

Systemic anaphylaxis in the mouse is associated with marked hypoactivity. This effect is reversed by treatment with the opiate antagonists, naloxone (5-10 mg/kg) or naltrexone (1 mg/kg). Administration of naltrexone methyl bromide (1 mg/kg), a selective peripherally acting opiate antagonist, is ineffective in reversing the hypoactivity induced by anaphylaxis. These results suggest a role for central nervous system opiate mechanisms in the hypoactivity induced by anaphylaxis. They support the hypothesis that endogenous opiates contribute to the pathophysiologic consequences of anaphylactic shock.

Anaphylaxis↗
PubMed1984

Effects of hyperprolactinaemia on core temperature of the rat.

The effects of endogenous hyperprolactinaemia (HPRL), as induced by pituitary homografts under the kidney capsule, on core temperature (Tc) was investigated in rats before and after the application of restraint stress. HPRL was accompanied by a significant decrease in Tc of freely moving rats, as observed for four days after pituitary homografts. HPRL-induced hypothermia was totally reversed by intraperitoneal (IP) injection of naloxone. In normoprolactinaemic (NPRL) rats, IP administration of naloxone caused a small but significant decrease in Tc and attenuated rise in temperature following the application of restraint stress. After application of restraint stress, Tc of HPRL rats raised to the level of unstressed NPRL rats. However, HRPL rats injected IP with naloxone showed no increase in Tc after restraint stress application. The effects of HPRL on Tc seem to involve an opioid component, and support the concept of a role played by stress hormones of hypophyseal origin in the control of Tc.

Animals↗
PubMed1983

Proanaphylactic action of morphine is mediated through a central cholinergic mechanism.

Intracerebroventricular (i.c.v.) or intravenous (i.v.) administration of morphine (10 micrograms or 25 mg/kg, respectively) increased the mortality rate in experimental anaphylaxis in mice. This effect was blocked by the opiate antagonist naltrexone administered systemically (5 mg/kg) or i.c.v. (10 micrograms). Moreover, the effect of morphine was blocked by i.c.v. administration of the muscarine antagonist methyl atropine (10 micrograms). The systemic administration of 5 mg/kg methyl atropine was ineffective in blocking the action of morphine. The results suggest that the proanaphylactic effect of morphine involves activation of cholinergic mechanisms in the central nervous system.

Anaphylaxis↗
PubMed1983

Morphine exacerbates anaphylactic shock in mice by stimulating central opiate receptors.

Intravenous (i.v.) administration of 25 mg/kg morphine significantly increased mortality following induction of systemic anaphylaxis in mice. This effect was blocked by pretreatment with the opiate antagonist naltrexone but not by the selective peripherally acting antagonist naltrexone methyl bromide. Additionally, the effect of i.v. morphine was blocked by the opiate antagonist Win 44,441-3, but not by its inactive (+)-isomer Win 44,441-2. Furthermore, intracerebroventricular (i.c.v.) administration of 25 micrograms morphine increased anaphylactic mortality. This effect was blocked by i.v. naloxone. Finally, the effect of i.v. morphine, 25 mg/kg, on anaphylactic mortality was reversed by i.c.v. naloxone. Collectively, these findings demonstrate that morphine can exacerbate anaphylactic shock reactivity by stimulating specific CNS opiate receptors. The role of endogenous opiate mechanisms in the pathogenic sequence of circulatory shock is discussed.

Anaphylaxis↗
PubMed1983

Antianaphylactic effect of naloxone in mice is mediated by increased central sympathetic outflow to sympathetic nerve endings and adrenal medulla.

Intravenous naloxone, 1 or 10 mg/kg, protects sensitized mice from lethal anaphylaxis. The protective effect is reversed by pretreatment with the ganglionic blocker, chlorisondamine chloride, peripheral chemical sympathectomy with 6-hydroxydopamine or bilateral adrenal gland denervation. The possible involvement of the sympathetic nervous system in naloxone's antianaphylactic action, suggested by these findings, is discussed.

Adrenal Medulla↗
PubMed1983

Regulation of opiate receptors in mouse brain: arcuate nuclear lesion induces receptor up-regulation and supersensitivity to opiates.

Lesion of the hypothalamic arcuate nucleus of the mouse by neonatal application of monosodium glutamate (MSG) increased the binding of [3H]dihydromorphine to membranes prepared from the midbrain. A saturation curve of [3H]dihydromorphine binding indicated that MSG increased the number of the opiate receptors. The MSG-treated mice also exhibited an enhanced response to morphine and naltrexone regarding thermal pain sensitivity. The physiological implications of opiate receptors up-regulations upon arcuate nuclear lesion are discussed.

Animals↗
PubMed1983

Endorphins in endotoxin-induced hyperglycemia in mice.

This study assessed the role of endogenous opiate systems in the hyperglycemic response to endotoxin challenge in mice. Blockade of opiate receptors by administration of the opiate antagonists naloxone (1.0 mg/kg) or naltrexone (1.0 or 5.0 mg/kg) significantly lessened to degree of hyperglycemia cause by endotoxin challenge (80 micrograms). Methyl naltrexone, a peripherally acting opiate antagonist, had no demonstrable effect on endotoxin-induced hyperglycemia. Finally, induction of tolerance to morphine prevented the hyperglycemic response to endotoxin challenge. These results suggest a causative role for central nervous system endorphinergic mechanisms in the hyperglycemic response to endotoxin administration. They support the view that centrally acting opiate antagonist, by blocking the brain opiate receptors, can influence metabolic adaptation to endotoxin shock.

Animals↗
PubMed1983

Role of endorphins in endotoxin-induced hyperglycaemia in mice.

The present study assessed the role of endogenous opiate systems in the hyperglycaemic response to challenge with endotoxin in mice. Blockade of opiate receptors by administration of the opiate antagonists naloxone (1.0 mg/kg) or naltrexone (1.0 or 5.0 mg/kg) significantly decreased the degree of hyperglycaemia caused by challenge with endotoxin (80 micrograms). Naltrexone methyl bromide, a peripherally acting opiate antagonist, had no demonstrable effect on the endotoxin-induced hyperglycaemia. Finally, induction of tolerance to morphine prevented the hyperglycaemic response to challenge with endotoxin. These results suggest a causative role for central endorphinergic mechanisms in the hyperglycaemic response to administration of endotoxin. They support the view that the centrally acting opiate antagonist, by blocking the brain opiate receptors, can influence metabolic adaptation to endotoxin-induced shock.

Animals↗