Neurological research
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Neurological research · Apr 1999
Role of inducible nitric oxide synthase in the cerebral vasospasm after subarachnoid hemorrhage in rats.
The involvement of de novo nitric oxide synthase (NOS) induction in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH) was examined using a rat model of SAH. SAH was induced by endovascular perforation with Nylon thread. The rats were killed at different time intervals, from one day to seven days after endovascular perforation. ⋯ To determine the role of iNOS in the development of cerebral vasospasm, we measured the diameter of the middle cerebral artery in animals either treated or not treated with aminoguanidine (AG), a selective inhibitor of iNOS. AG ameliorated the vasoconstrictive change after SAH. These results are thus considered to provide molecular and immunohistochemical evidence showing that iNOS expression following SAH and NO produced by iNOS can develop cerebral vasospasm after SAH.
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Neurological research · Apr 1999
A nonNMDA antagonist, GYKI 52466 improves microscopic O2 balance in the cortex during focal cerebral ischemia.
This study was performed to test whether GYKI 52466, a nonNMDA receptor antagonist, would improve microregional oxygen supply and consumption balance in the focal cerebral ischemic area. Rats were anesthetized with 1.4% isoflurane. For the GYKI Group (n = 8), 10 min before middle cerebral artery (MCA) occlusion, a bolus of 5 mg kg-1 of GYKI 52466 i.v. was administered and was followed by an infusion of 5 mg kg-1 h-1. ⋯ In the cortex contralateral to MCA occlusion, the average rCBF and the average O2 consumption were lower in the GYKI Group than in the Control Group (rCBF: GYKI 65.5 +/- 24.1 ml 100 g-1 min-1, Control 97.7 +/- 33.4 ml 100 g-1 min-1; O2 consumption: GYKI 3.9 +/- 1.2 ml O2 100 g-1 min-1, Control 6.2 +/- 2.5 ml O2 100 g-1 min-1) without a significant difference in the number of veins with SvO2 < 50%. In the ischemic cortex, the number of veins with SvO2 < 50% was significantly smaller in the GYKI Group (21 veins out of 63) than in the Control Group (45 out of 59) without a significant difference in the average rCBF (GYKI 44.9 +/- 17.7, Control 29.7 +/- 10.4) or regional O2 consumption between these two groups (GYKI 3.3 +/- 1.4, Control 2.7 +/- 1.2). Our data demonstrated that GYKI 52466 was effective in improving microscopic O2 balance in the focal ischemic cortical area of the brain and it decreased O2 consumption in the non-ischemic cortex.