Stroke; a journal of cerebral circulation
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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 subarachnoid hemorrhage. Norepinephrine content in human cerebral arteries in cases of subarachnoid hemorrhage was about 5% of the control group. ⋯ In cerebral arteries obtained from the subarachnoid hemorrhage group, [3H]yohimbine binding sites were of a single class with KD of 53 nM and Bmax of 456 fmol/mg protein. These results suggest that sympathetic denervation and subsequent alterations in alpha 2-adrenergic receptors occurred after subarachnoid hemorrhage in human cerebral arteries. These changes in sympathetic innervation to cerebral arteries were considered to be one of the antecedents of delayed vasospasm after subarachnoid hemorrhage.
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Analysis of 17 patients with infective endocarditis and intracranial hemorrhage yielded several different mechanisms of bleeding. Nine of 15 (60%) symptomatic intracranial hemorrhages occurred within 48 hours of admission and 3 more (20%) after hospital discharge. In 7 patients with Staphylococcus aureus endocarditis, symptomatic intracranial hemorrhage occurred within 48 hours of admission and resulted from septic arteritis in all 3 examined pathologically. ⋯ Anticoagulation potentially contributed to intracranial hemorrhage in 4 of the 17 patients (24%). Proven mycotic aneurysms were present in only 2 patients (12%), 1 of whom presented with massive, fatal intracranial hemorrhage. Mycotic aneurysms amenable to surgery are uncommon and underlie only a fraction of intracranial hemorrhages in infective endocarditis.
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Oxygen free radicals generated during reoxygenation after cardiac arrest may impair recovery of cerebral blood flow and function. In a randomized study in vivo, we tested the following anti-free radical combination therapy administered at the beginning of cardiopulmonary resuscitation after apnea-induced cardiac arrest of 7 minutes: 1) ventilation with 100% nitrogen for 30 seconds to allow the delivery of therapy before oxygen, 2) 10 mg/kg i.a. superoxide dismutase followed by 10 mg/kg i.v. over 1 hour to scavenge the superoxide anion radical, and 3) 20 mg/kg i.v. deferoxamine over 1 hour to prevent membrane lipid peroxidation. ⋯ Compared with standard treatment (n = 10), the combined treatment (n = 10) did not affect cardiovascular variables, significantly mitigated cerebral blood flow changes after cardiac arrest, and enhanced recovery of somatosensory evoked potentials. We conclude that oxygen free radicals play a role in the pathogenesis of the arrest-related derangements of cerebral blood flow and function that are effectively reduced by this combined treatment; we recommend evaluation of its components in outcome studies.
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The frequency and severity of cardiac arrhythmias were studied in 70 patients with spontaneous subarachnoid hemorrhage investigated prospectively with 24-hour Holter monitoring. Patients were less than 70 years old and without clinical and/or ECG signs of previous heart disease; Holter monitoring was initiated within 48 hours of subarachnoid hemorrhage. Arrhythmias were detected in 64 of the 70 patients (91%). ⋯ Serious ventricular arrhythmias were associated with QTc prolongation and hypokalemia. No correlation was found between the frequency and severity of cardiac arrhythmias and the neurologic condition, the site and extent of intracranial blood on computed tomography scan, or the location of ruptured malformation. The extremely high incidence of cardiac arrhythmias, sometimes serious, in the acute period after subarachnoid hemorrhage and the absence of clinical and radiologic predictors make systematic continuous ECG monitoring compulsory to improve the overall results of subarachnoid hemorrhage, irrespective of early or delayed surgical treatment.
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Delayed neurologic deterioration from vasospasm remains the greatest cause of morbidity and mortality following subarachnoid hemorrhage. The authors assess the incidence and clinical course of symptomatic vasospasm following subarachnoid hemorrhage using a uniform management protocol over a 24-month period. One hundred eighteen consecutive patients were admitted to the neurovascular surgery service within 2 weeks of subarachnoid hemorrhage not attributed to trauma, tumor, or vascular malformation (113 patients had aneurysms). ⋯ At the end of hypervolemic hemodilution therapy, 47.6% had become neurologically normal, 33.3% had a minor neurologic deficit, and 19% had a major neurologic deficit or were dead. There were 3 instances of cardiopulmonary deterioration (7%), all of which were in patients without Swan-Ganz catheters, and all resolved with appropriate diuresis. One patient rebled and died while on hypervolemic hemodilution therapy.(ABSTRACT TRUNCATED AT 250 WORDS)