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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of clonidine, naloxone, and their combination on arterial blood pressure (BP), heart rate (HR), and hemodynamic and biochemical parameters were examined in 29 patients with essential hypertension. Treatment for 3 days with 0.3 mg/day clonidine reduced BP and HR, and these effects were quickly reversed by a single injection of 0.4 mg iv naloxone in 17 of the patients (responders), but not in the remaining 12 (nonresponders). Responders had higher control values for cardiac output, stroke index, plasma renin activity (PRA), and plasma epinephrine levels than did nonresponders. Basal BP was similar in the two groups, but clonidine decreased BP, PRA, and plasma epinephrine more in responders than in nonresponders. Naloxone given during placebo treatment had no significant effects. During clonidine treatment naloxone increased BP, HR, total peripheral resistance, PRA, and plasma epinephrine and norepinephrine, and decreased stroke volume in responders, whereas in nonresponders its only effect was a small increase in HR. It is concluded that in a subset of hyperadrenergic, hypertensive patients the antihypertensive effect of clonidine involves a naloxone-reversible inhibition of central sympathetic outflow, probably mediated by the release of an endogenous opioid.
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PMID:Reversal by naloxone of the antihypertensive action of clonidine: involvement of the sympathetic nervous system. 636 5

Naloxone, an opiate antagonist, has recently been reported to temporarily reverse neurologic deficits associated with subarachnoid hemorrhage. To determine if this unexpected effect of naloxone might also occur in other forms of cerebrovascular diseases, 13 patients who presented with acute neurologic deficits were administered intravenous naloxone. In 3 of these patients, coincidental improvement in neurologic status was seen. In one patient the improvement was permanent. Ten of the 11 patients with non fatal neurologic damage improved later in their hospital course--7 of them to their pre-admission state. The only side effect noted was the temporally related onset of a single focal seizure in an ethanol intoxicated patient with an intracerebral hemorrhage.
Stroke
PMID:Naloxone administration to patients with acute stroke. 636 63

Daily doses of 0.3 mg clonidine and 3 mg guanfacine were equiactive in decreasing blood pressure and heart rate in 17 subjects with essential hypertension. Clonidine decreased cardiac output and guanfacine decreased total peripheral resistance, while clonidine had no effect on stroke volume but guanfacine increased it. Both clonidine and guanfacine decreased plasma renin activity. Naloxone, 0.4 mg iv, reversed the antihypertensive effect of clonidine but was ineffective even at higher doses (1.6 mg iv) when subjects were treated with placebo or guanfacine. It is suggested that the hemodynamic differences between the two centrally acting alpha 2-adrenoceptor agonist antihypertensive drugs may at least in part result from the involvement of opioid mechanisms only in the action of clonidine.
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PMID:Effects of clonidine and guanfacine in essential hypertension. 638 75

Naloxone and methylprednisolone sodium succinate (MPSS) may act in synergy to improve hemodynamics in patients with septic shock by enhancement of sympathomedullary discharge. This randomized double-blind study describes the effect of various dosing regimens of naloxone and MPSS upon hemodynamics and plasma catecholamines in patients with septic shock (n = 57). Consecutive bolus doses of naloxone were given 30 minutes apart (10 micrograms/kg;-100 micrograms/kg) and a single dose of MPSS (30 mg/kg); bolus doses of 5% dextrose in water solution plus single dose of MPSS as above; bolus dose of naloxone (30 micrograms/kg) followed by continuous infusion (30 micrograms/kg/hr for 1 hour) with single dose of MPSS as above; a bolus and continuous infusion of naloxone as above without MPSS; MPSS alone and standard therapy alone. In patients treated with bolus doses of naloxone in combination with MPSS, plasma levels of epinephrine and norepinephrine were increased approximately five-to tenfold. In patients treated with bolus plus continuous infusion of naloxone given with or without MPSS, only plasma epinephrine levels were increased. Systolic blood pressure and left ventricular stroke work index were improved within 15 minutes in groups which received naloxone and corticosteroids regardless of dose. In those groups, there were no changes in heart rate or filling pressure. Systemic vascular resistance improved significantly only in the group which received low dose bolus and continuous infusion of naloxone and MPSS. Naloxone and MPSS quickly improved cardiac function in patients with septic shock by enhanced sympathomedullary discharge and may be useful as an adjunct in the therapy of this disorder.
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PMID:Naloxone and methylprednisolone sodium succinate enhance sympathomedullary discharge in patients with septic shock. 639 57

Conflicting reports have appeared in the literature regarding the effect of the opiate antagonist naloxone on ischemic neurologic deficits. We report the results of a study using naloxone in our model of focal cerebral ischemia in the awake primate. A total of 14 adult baboons were subjected to six-hour occlusion of the left middle cerebral artery (MCA). Seven animals served as controls and seven received treatment with naloxone (5 mg/kg) beginning 30 min after MCA occlusion and continuing until two hours after reperfusion. All animals developed profound hemiparesis and homonymous hemianopsia within seconds of inflating the MCA occluder. Acutely, therapy with naloxone partially reversed ischemic neurologic deficits in five of the seven treatment animals. Within minutes of receiving the loading dose of naloxone, responding animals were more alert and demonstrated improvements in motor function. Naloxone did not affect mortality: Three animals in the treatment group and two in the naloxone group died secondary to malignant intracranial pressure within 48 hours of the ischemic episode. In animals surviving the ischemic insult however, treatment with naloxone significantly improved neurologic outcome at 10 days (p less than 0.05). Neuropathologic examinations in these animals revealed amelioration of ischemic tissue damage, with three of the five suffering only small focal areas of infarction. (All control animals suffered large infarcts of the MCA territory.) Our results verify that naloxone can reverse ischemic deficits, and more importantly may improve the outcome from focal ischemic insults.
Stroke
PMID:Naloxone therapy during focal cerebral ischemia evaluation in a primate model. 646 54

Stroke-prone, spontaneously hypertensive rats (SP/SHR) were fed a low protein (8%) fish diet + 1% saline at the time of weaning; some were treated with Naloxone (0.4 mg/100 gms bw/sc/2 X daily/5 days per week). Naloxone-treated animals did not develop high blood pressure or strokes. Sixty-two days after feeding the low protein fish diet, blood pressure levels reached 260-300 mmHg and all of the non-treated animals exhibited acute and severe strokes; Naloxone treatment was again initiated for half of the SP/SHR. By Day 4 (post stroke), all of the non-treated SP/SHR were dead; Naloxone-treated SP/SHR survived until Day 12 (post stroke). Naloxone-treatment during the post-stroke period caused significant reduction of blood pressure, ACTH, and beta-endorphin levels concomitant with reduced cerebral edema and clearance of hepatic lipid infiltration. It is suggested that anti-opiate treatment may ameliorate the severe hypertension-inducing effects of a low protein fish diet and thereby prevent the appearance of strokes in SP/SHR as well as palliate the cerebral edema and fatty liver which characteristically appear in the immediate post-stroke period in fish-fed SP/SHR. The central mechanism of this palliative effect may be through reduced hypothalamic-pituitary-adrenal activity.
Stroke
PMID:Naloxone ameliorates the pathophysiologic changes which lead to and attend an acute stroke in stroke-prone/SHR. 646 55

Temporary aortic occlusion produces a consistent degree of spinal cord injury in the unanesthetized rabbit. This 'spinal stroke' model was utilized to examine the potential therapeutic effects of the opiate antagonist naloxone in central nervous system ischemia. Naloxone treatment resulted in dose-related enhancement of motor recovery; greatest functional recovery was observed in rabbits treated with a dose of 2 mg/kg per h. This dose compares well with the high doses of naloxone shown to have a beneficial effect in other experimental models of stroke and spinal injury. In contrast, clinical stroke studies, which have been largely unsuccessful, have utilized naloxone doses which are several orders of magnitude lower than those successfully employed in experimental models.
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PMID:Naloxone in experimental spinal cord ischemia: dose-response studies. 647 24

This study was conducted in order to investigate naloxone's in vitro action on both epinephrine-induced constriction of mesenteric artery and norephinephrine-induced constriction of cerebral arteries in different species (cat and monkey). Naloxone (3 X 10(-5)M) augmented the epinephrine-induced constriction of both feline and monkey mesenteric artery at epinephrine concentrations of 10(-7) to 10(-5) M. Naloxone (3 X 10(-5)M) suppressed the constriction of feline basilar artery induced by high concentrations (10(-4), 10(-3) and 3 X 10(-3)M) of norepinephrine, while it failed to alter the constriction induced by lower concentrations (10(-7) to 10(-5)M) of norepinephrine. The constrictor response of monkey basilar artery to norepinephrine (10(-8) to 10(-5) M) was not altered by treatment with naloxone (3 X 10(-6) and 3 X 10(-5)M). Such varying effects of naloxone in different tissues and species may have to be taken into account when evaluating the cerebral blood flow changes following naloxone administration.
Stroke
PMID:Comparison of the effect of naloxone on cerebral versus mesenteric arterial smooth muscle in feline and primate species. 650 14

Naloxone failed to improve motor strength in any of 19 patients with acute stroke, even though 4 patients eventually demonstrated complete recovery. Two patients worsened, and sensory abnormalities increased in two others. Motor tone increased in eight patients. Naloxone amelioration of stroke deficits is therefore not common, and this treatment may not be entirely benign.
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PMID:Failure of naloxone to reverse vascular neurologic deficits. 668 46

In this study, 10 mongrel dogs were anesthetized with sodium pentobarbital and nitrous oxide. Blood flow was determined using the radioactive microsphere technique before and after the bolus intravenous injection of naloxone (10 mg/kg). Naloxone significantly increased cerebral blood flow to cerebral cortex and the total cerebral hemisphere without an associated change in the cerebral metabolic rate of oxygen. The increase in cerebral blood flow was proportional to the elevation in mean arterial pressure. There were no consistent changes in electrical activity as measured by electroencephalography (EEG) and Fourier analysis of EEG. Systemically, naloxone induced a proportional rise in mean arterial pressure and peripheral vascular resistance and also stimulated the myocardium, as evidenced by an improved cardiac index and stroke volume. These data suggest that naloxone may interfere with cerebral autoregulation or have direct vasodilatory effects on cerebral blood vessels that are not associated with opiate receptor blockade or changes in cerebral metabolism. In addition, naloxone did not appear to reverse the cerebral depressive effects of pentobarbital. Systemically, naloxone seemed to potentiate pentobarbital-induced vasoconstriction and reverse myocardial depression.
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PMID:Cerebral and systemic vascular effects of naloxone in pentobarbital-anesthetized normal dogs. 670 51


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