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yohimbine/hémorragie
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The reflex control of heart rate and cardiac output in the rainbow trout: interactive influences of hypoxia, haemorrhage, and systemic vasomotor tone.
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In cannulated trout there was no cholinergic vagal tone as revealed by atropine blockade during normal heart rates. Reductions in heart rate occasionally occurred under normoxia without apparent external stimuli ('spontaneous' bradycardia) and always occurred under environmental hypoxia (hypoxic
Involvement of the sympathetic nervous system in the reversal of critical haemorrhagic hypotension by endogenous central histamine in rats.
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An increase in endogenous central histamine concentration after inhibition of histamine N-methyltransferase (HNMT) activity reverses critical hypotension and improves the survival of rats in haemorrhagic shock. The purpose of the study was to examine the involvement of the sympathetic nervous system
Cardiovascular effects of H3 histamine receptor inverse agonist/ H4 histamine receptor agonist, clobenpropit, in hemorrhage-shocked rats.
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Hemorrhagic shock has a potential to be life-threatening when it is not treated. The main causes of hemorrhagic shock involve: (1) forces causing injury; and (2) diseases that can cause hemorrhage., Therefore, due to the causes of hemorrhagic shock and the life-threatening potential, the search for
Presynaptic and postsynaptic alpha 2-adrenergic receptors in human cerebral arteries and their alteration after subarachnoid hemorrhage.
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The nature of alpha-adrenergic receptors in human cerebral arteries was characterized, and alteration of these receptors after subarachnoid hemorrhage was examined using a radioligand binding assay. Norepinephrine content of control arteries was also analyzed and compared with that of arteries after
The adrenocorticotropic hormone (ACTH)-induced reversal of hemorrhagic shock.
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Adrenocorticotropic hormone (ACTH), while having negligible effects on cardiovascular function in the intact animal, induces a potent and sustained reversal of an otherwise invariably, rapidly fatal condition of hemorrhage-induced hypovolemic shock, in rats and dogs. The main site(s) of action are
The role of the sympathetic nervous system in the resuscitative effect of stimulating the central serotonin 1A receptors in haemorrhagic shock in rats.
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Haemorrhagic shock is a life threatening condition, and, as such, it is important to understand the mechanisms taking part in its reversal. In the 1990s, it was shown that activation of serotonin 1A receptors is responsible for the circulatory decompensation and development of the sympathoinhibitory
Unilateral adrenalectomy attenuates hemorrhagic shock-induced analgesia in rats.
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OBJECTIVE
To assess the importance of the pituitary adrenal axis in producing stress-induced analgesia (SIA) after hemorrhagic shock, we performed formalin tests after hemorrhage and reinfusion in unilaterally adrenalectomized or sham-operated rats.
METHODS
Fifty-two adult Sprague-Dawley rats were
Central adrenergic mechanisms in hemorrhage-induced vasopressin secretion.
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The effect of central administration of specific adrenergic agonists and antagonists on hemorrhage-induced vasopressin secretion was studied in conscious rats. The intracerebroventricular (icv) injection of the alpha 2-antagonist yohimbine, the alpha 1-antagonist corynanthine, or the beta-agonist
Bleeding-induced decrease in duodenal HCO3- secretion in the rat is mediated via alpha 2-adrenoceptors.
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This study was performed on chloralosed rats in order to examine the influence of a minor blood loss on duodenal HCO3- secretion. The HCO3- output was measured by in situ titration in a duodenal segment. Blood loss of 0.6 ml per 100 g body wt (approximately 10% of total blood volume) reduced
Cardiovascular effects of centrally acting orexin A in haemorrhage-shocked rats.
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Orexin A influences the central cardiovascular regulation, since after intracerebroventricular (icv) administration it evokes short-lasting increases in mean arterial pressure (MAP) and heart rate (HR) in normotensive animals. The aim of the present study was to examine haemodynamic effects of
Cardiovascular adrenoreceptor function during compensatory and decompensatory hemorrhagic shock.
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Prior reports by Dr. Bond [1] have described the occurrence of an initial compensatory vasoconstriction followed by a decompensatory vasodilation response in animals that progress to irreversible shock induced by blood loss. Further analysis suggests that the secondary vascular decompensation is the
Pressor effects of the alpha 2-adrenoceptor agonist B-HT 933 in anaesthetized and haemorrhagic rats: comparison with the haemodynamic effects of amidephrine.
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1. Blood pressure responses to single and multiple bolus doses of the alpha 2-adrenoceptor agonist B-HT 933 were analysed in intact anaesthetized rats which were either normotensive or hypotensive as a result of haemorrhage. Single bolus doses of B-HT 933 in normotensive rats induced a fall in blood
Cerebrovascular responses to haemorrhagic hypotension in anaesthetized cats. Effects of alpha-adrenoceptor antagonists.
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Haemorrhagic hypotension induces the phenomenon of cerebrovascular autoregulation and, concomitantly, involves an activation of the sympathetic nervous system. As brain vessels in cats have an atypical adrenoceptor distribution we studied the effects of an alpha-adrenoceptor antagonist on the
Influence of the intravenous administration of ACTH-(1-24) on the characteristics of brain, heart and spleen adrenoceptors of haemorrhage-shocked rats.
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Urethane-anesthetized rats were bled to otherwise irreversible haemorrhagic shock (mean arterial pressure = 18-25 mmHg) and then i.v. treated with ACTH-(1-24) (160 micrograms/kg) or saline. In comparison with sham-operated, non-shocked controls, bled rats showed a significant reduction in Bmax for
Preserving cardiac output with beta-adrenergic receptor blockade and inhibiting the Bezold-Jarisch reflex during resuscitation from hemorrhage.
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BACKGROUND
Successful fluid resuscitation after severe hemorrhage may be limited by activation of the Bezold-Jarisch reflex. We postulated that pharmacologic inhibition of this reflex would restore cardiovascular hemodynamics more effectively than would volume repletion alone during resuscitation
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