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

The suitability of plasma catecholamines (CAs) and neuropeptide-Y (NPY) as biochemical indices of sympathetic nerve activity (SNA) has been investigated, and these parameters have been compared between adult normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Plasma norepinephrine (NE), epinephrine (E) and NPY were measured in venous and arterial blood samples taken from conscious, unrestrained rats. Under resting conditions, both CAs were significantly higher in SHRSP than in WKY; plasma E in particular was raised threefold. SHRSP had higher plasma levels of NPY in arterial blood but not in venous blood. Acute hydralazine-induced hypotension caused a slight rise in NPY and striking increases of CAs, which were accentuated in SHRSP. Ganglion blockade with pentolinium reversed these increases but the differences in basal plasma CA levels between strains still persisted. Barbiturate anaesthesia had little effect on plasma levels of NPY or NE, but plasma E levels were depressed, particularly in SHRSP, so that the strain difference in plasma E taken from venous blood was no longer apparent. The results indicate that plasma levels of CAs but not NPY are useful indices of SNA in conscious rats. Comparisons between WKY and SHRSP after drug treatment demonstrate a major contribution by the adrenal medulla to plasma CA levels in SHRSP which, under resting conditions, may not be sympathetically evoked.
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PMID:Plasma catecholamines and neuropeptide-Y as indices of sympathetic nerve activity in normotensive and stroke-prone spontaneously hypertensive rats. 243 35

Fifty-six patients with elevated intracranial pressure caused by cerebrovascular accident, head injury, etc., were the subjects of this study. They were divided into three groups: low dose barbiturate therapy (15 patients), high dose barbiturate therapy (24 patients), and control group (17 patients). Barbiturate therapy was instituted using thiamylal, and the complications caused by barbiturate therapy were recorded. In the control group, complications occurred in the liver of two patients, but there were no renal or pulmonary complications. Pulmonary, renal, and hepatic complications were common in the barbiturate groups. Complications in the high dose therapy group were significantly more common than in the control group. Opportunistic infections occurred in ten patients, with seven patients having pneumonia. Only one patient, with pneumonia, was seen in the control group. The deaths of three patients were influenced by complications associated with barbiturate therapy, while the single death in the control group was not associated with the complication of barbiturate therapy.
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PMID:Complications associated with barbiturate therapy. 254 69

Barbiturate therapy has been employed for reduction of increased intracranial pressure (ICP) after acute brain injury and also for cerebral resuscitation. However, this treatment may be complicated by hypotension with an adverse impact on survival. We, therefore, investigated the acute hemodynamic effects of pentobarbital (PB) when administered in loading doses of 4-7 mg/kg and maintenance doses of 1-4 mg/kg. After pentobarbital therapy, HR, mean arterial pressure (MAP), and rectal temperature were significantly reduced. Four episodes of hypotension and 6 episodes of oliguria were observed during the initial 12 h of therapy in close relationship to reduced cardiac output, stroke volume, and MAP. These abnormalities were corrected by infusion of colloid-containing fluids. We postulate that increases in venous capacitance, hypovolemia, and decreased barostatic reflexes, rather than depression of myocardial function, accounted for the hemodynamic abnormalities.
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PMID:Hemodynamic effects of pentobarbital therapy for intracranial hypertension. 688 49

The use of barbiturates to induce coma as a means of extending the period of reversible cerebral ischemia is reviewed. Barbiturate use in patients who had had strokes or were undergoing aneurysm surgery was initially encouraging. In uncontrolled feasibility trials in patients with cardiopulmonary arrest or in deep coma, 40 patients received 10 mg/kg thiopental sodium by i.v. push followed by 20 mg/kg thiopental sodium i.v. over the next 30 minutes; 60% of these patients regained consciousness. In a subgroup of 22 patients who had ischemia normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 patients with severe head injury and elevated intracranial pressure received 3--5 mg/kg pentobarbital over 10--20 minutes. A serum barbiturate level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these patients recovered but with neurologic deficits. Other results in stroke and drowning victims were not as encouraging. It is concluded that barbiturate therapy is beneficial in the lowering of intracranial pressure. Focal and global cerebral ischemia have been shown amenable to barbiturate therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal cerebral anoxia appears to be beneficial. Controlled trials of the use of barbiturate-induced coma are clearly indicated.
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PMID:Barbiturate-induced coma to protect against cerebral ischemia and increased intracranial pressure. 702 14

Barbiturates are administered in a variety of clinical conditions to control elevated intracranial pressure (ICP). However, their routine use to treat elevated ICP has been questioned because it may cause severe side effects. We therefore investigated the effect of high-dose barbiturate therapy on ICP and outcome in patients with severe brain edema after severe middle cerebral artery (MCA) or hemispheric infarction. Barbiturate coma was induced with thiopental infusion in 60 patients with critically increased ICP due to large hemispheric or MCA territory infarction, defined by CT. ICP was monitored in all patients during barbiturate therapy. Barbiturate coma was induced after a standardized treatment protocol for increased ICP after failure of osmotherapy and mild hyperventilation. During barbiturate administration, cerebral perfusion pressure (CPP) and mean arterial pressure were recorded. Clinical outcome of these patients and the individual effect on ICP were analyzed. Only five of 60 patients who were treated with barbiturate coma survived (8%). All other patients died after transtentorial herniation with subsequent brain death. Barbiturate infusion was followed by a drop in ICP in 50 patients and showed no effect on ICP values in 10 patients. CPP decreased with a mean of 9 mm Hg (range, 5 to 20 mm Hg). Although barbiturates were initially effective, only in some patients was ICP control sustained. Severe side effects of barbiturate therapy, besides arterial hypotension, were seen in 15 patients (25%). Barbiturate coma in the therapy of increased ICP after severe ischemic hemispheric stroke can lower critically elevated ICP levels. However, it seems to have no positive effect on neurologic outcome.
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PMID:Barbiturate coma in severe hemispheric stroke: useful or obsolete? 919 75

Malignant cerebral edema following ischemic stroke is life threatening, as it can cause inadequate blood flow and perfusion leading to irreversible tissue hypoxia and metabolic crisis. Increased intracranial pressure and brain shift can cause herniation syndrome and finally brain death. Multiple randomized clinical trials have shown that preemptive decompressive hemicraniectomy effectively reduces mortality and morbidity in patients with malignant middle cerebral artery infarction. Another life-saving decompressive surgery is suboccipital craniectomy for patients with brainstem compression by edematous cerebellar infarction. In addition to decompressive surgery, cerebrospinal fluid drainage by ventriculostomy should be considered for patients with acute hydrocephalus following stroke. Medical treatment begins with sedation, analgesia, and general measures including ventilatory support, head elevation, maintaining a neutral neck position, and avoiding conditions associated with intracranial hypertension. Optimization of cerebral perfusion pressure and reduction of intracranial pressure should always be pursued simultaneously. Osmotherapy with mannitol is the standard treatment for intracranial hypertension, but hypertonic saline is also an effective alternative. Therapeutic hypothermia may also be considered for treatment of brain edema and intracranial hypertension, but its neuroprotective effects have not been demonstrated in stroke. Barbiturate coma therapy has been used to reduce metabolic demand, but has become less popular because of its systemic adverse effects. Furthermore, general medical care is critical because of the complex interactions between the brain and other organ systems. Some challenging aspects of critical care, including ventilator support, sedation and analgesia, and performing neurological examinations in the setting of a minimal stimulation protocol, are addressed in this review.
J Stroke 2014 Sep
PMID:Critical care for patients with massive ischemic stroke. 2532 73