physostigmine/hemorrhage

1. The effects of physostigmine (70 micrograms kg-1, intravenously) on mean arterial blood pressure, blood volume and survival were studied in anaesthetized rabbits subjected to haemorrhagic hypovolemia. 2. It was found that physostigmine increased the mean arterial blood pressure, increased the

The intravenous injection of physostigmine (70 micrograms kg-1) produces a life-saving effect in acute haemorrhagic shock in non-anaesthetized rabbits. This effect is most probably due to a transfer of tissue fluids into circulation. The crucial beneficial effect of physostigmine might be a decrease

In rats bled to hypovolemic shock, the intracerebroventricular injection of hemicholinium-3 (20 micrograms/rat) completely prevented the shock reversal induced by the intravenous injection of ACTH (1-24) (160 micrograms/kg), but had no influence on the shock reversal induced by the intravenous

Pharmacological doses (40-160 micrograms/kg) of adrenocorticotropic hormone (ACTH) intravenously injected to urethane-anesthetized rats subjected to otherwise lethal hemorrhagic shock (mean arterial pressure stabilized at 20-25 mmHg) promptly restore blood pressure to about the pre-bleeding values,

We have previously reported that centrally-acting cholinomimetic drugs have a prompt and sustained resuscitating effect in pre-terminal conditions of hemorrhagic shock in rats. Here we have studied the effect of physostigmine in another experimental condition of hypoxia in anesthetized rats, which

BACKGROUND It has been suggested that anesthetics may protect the brain during incomplete cerebral ischemia by inhibition of sympathetic activity. This study evaluated whether physostigmine may increase plasma epinephrine and norepinephrine during carotid occlusion with hypotension and worsen

In haemorrhage-shocked rats, the recovery of mean arterial pressure (MAP), pulse pressure (PP) and respiratory rate (RR), as well as the improvement of survival rate, induced by the i.v. administration of centrally acting cholinergic drugs (physostigmine, oxotremorine) are not affected by morphine

Central administration of choline increases blood pressure in normotensive and hypotensive states by increasing plasma concentrations of vasopressin and catecholamines. We hypothesized that choline could also modulate the renin-angiotensin pathway, the third main pressor system in the body. Plasma

BACKGROUND Recently, protection in shock (hemorrhagic or septic) by physostigmine has been demonstrated. Here, we studied the protective effect of intravenous infusion of physostigmine in a rat model of severe intestinal ischemia-reperfusion (I/R) injury and shock. METHODS Mesenteric I/R was induced

1. The effects of physostigmine (70 micrograms kg-1, intravenously) on acid-base status in arterial and venous blood were studied in anaesthetized rabbits subjected to hemorrhagic hypovolemia. 2. Hemorrhagic shock was produced using intermittent bleeding of 50% of the estimated blood volume, during

Cerebral cortical ischemia was induced in anesthetized rats by occlusion of the middle cerebral artery (MCA). Cerebral blood flow (CBF) was measured with the H2 clearance technique in the center and periphery of the ischemic territory. A decrease of CBF to about 50% of pre-occlusion values was

1. In an experimental model of haemorrhagic shock resulting in the death of all rats within 20-30 min, the intravenous (i.v.) injection of the tertiary amine cholinesterase inhibitor physostigmine (17-70 micrograms kg-1) induced a prompt, sustained and dose-dependent improvement of cardiovascular

Previous studies from our laboratory have identified a role for blunted central sympathetic activation in the acute alcohol intoxication (AAI)-induced impairment of the counterregulatory response to hemorrhagic shock (HS). Immediate fluid resuscitation (FR) with acetylcholinesterase inhibitors

Previously, we have demonstrated that acute alcohol intoxication impairs hemodynamic counter-regulation to hemorrhage in unanesthetized rats, and that this phenomenon is associated with an impaired neuroendocrine response to blood loss. Moreover, we demonstrated that central acetylcholinesterase