Electrolyte changes in patients with subarachnoid haemorrhage.
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Biomedical subjects
Publications and source records attributed to I M James.
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The administration of ammonium salts to free ventilated dogs causes an increase in the anaerobic consumption of glucose. Prior and simultaneous administration of the drug ornithine alpha ketoglutarate not only attenuates the rise in blood ammonia but also favourably affects these changes in brain metabolism.
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Cerebral blood flow and cerebral metabolism were studied in six patients with moderately severe portosystemic encephalopathy before and after a 10-day course of lactulose. As a result of therapy there was a mean increase in cerebral oxygen utilization but no changes in either mean glucose consumption or in mean cerebral blood flow. It appears therefore that the abnormalities in cerebral metabolism that have been previously described in patients with hepatic encephalopathy can be improved by the oral administration of lactulose.
Studies of cerebral blood flow and distal intravascular pressure changes were studied in 11 patients at the time of common carotid artery ligation for the treatment of intracranial aneurysm. No neurological deterioration was observed while these patients were under observation. Cerebral blood flow in the ipsilateral hemisphere recovered rapidly while reduction in pressure, and in particular diminution of pulse pressure, persisted affording protection to the aneurysm.
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The pharmacokinetics of acebutolol have been studied in eight healthy male volunteers following the oral administration of acebutolol hydrochloride ('Sectral', May & Baker) as a single dose (400 mg), and during and after repeated oral dosing (400 mg, b.d. for 56 days). Following single dose administration, considerable inter-subject variation in plasma levels of parent drug and the major metabolite, diacetolol, was evident. Acebutolol appeared to be eliminated from plasma in a bi-phasic manner, and this was confirmed from urinary excretion rate data. Mean initial and terminal half-lives of about 2 and 11 h, respectively, were determined. Plasma levels of diacetolol were greater than those of parent drug from 3 to 4 h following dose administration. Total urinary excretion of diacetolol was generally greater than that of acebutolol. During repeated dosing, steady-state plasma levels of acebutolol and diacetolol were achieved in 6 volunteers. Acebutolol did not appear to stimulate or inhibit its metabolism.