The blood-brain barrier following experimental subarachnoid hemorrhage. Part 2: Response to mercuric chloride infusion.
Under controlled physiological conditions, fresh blood was injected into the cisterna magna of 10 adult cats to produce subarachnoid hemorrhage (SAH). Damage to the blood-brain barrier (BBB) was induced 30 minutes after SAH by the intracarotid injection of a 6 x 10(-5)M solution of mercuric chloride (HgCl2). A control series of five cats received the same injection of HgCl2. Intravenously injected Evans blue dye was used to indicate areas of BBB damage. The lesions were confirmed by fluorescence microscopy. All control animals showed BBB damage in the hemisphere injected with HgCl2. Of the animals in the test group with SAH, 90% were free from lesions. When lesions were present, the distribution differed from that in the control group. These results bear a similarity to the reported absence of HgCl2 lesions during the acute stages after total cerebral ischemia. This suggests that the cellular components of the BBB participate in a general metabolic inhibition following SAH.
D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects*; D001921:Brain / Q000473:pathology; D002199:Capillary Permeability / Q000187:drug effects; D002415:Cats; D004727:Endothelium; D005070:Evans Blue; D008627:Mercuric Chloride; D008628:Mercury / Q000494:pharmacology*; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*
D005070:Evans Blue; D008627:Mercuric Chloride; D008628:Mercury