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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between early hypertension following carotid endarterectomy, and intraoperative cerebral ischemia was investigated. Two measures of the adequacy of collateral cerebral circulation during carotid clamping were used: collateral cerebral perfusion pressure (delta P), and the ratio of collateral to ipsilateral cerebral vascular resistance (R/R). Change in blood pressure was measured by the ratio of mean early post to preendarterectomy pressure (P/P). Nitroprusside or nitroglycerin (NN) was used after endarterectomy to maintain systolic blood pressure less than 160 mmHg. The mean values for NN (n = 26) and no NN (n = 81) groups were: delta P = 30.0 and 40.2 mmHg (p less than 0.001); R/R = 1.93 and 1.24 (p less than 0.005); and P/P = 1.03 and 0.857 (p less than 0.001 p by unpaired t test). Linear regression analysis of the two measures of cerebral perfusion with the ratio of post-to preoperative blood pressure gave correlation coefficients between 0.629 and 0.841 with a probability that the slope of the regression line greater than 0 of less than 0.01. Low delta P and high R/R correlate with early postcarotid endarterectomy hypertension. These results support the hypothesis that one determinant of early post endarterectomy hypertension is inadequate collateral cerebral circulation during carotid clamping.
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PMID:The relationship of early hypertension following carotid endarterectomy to intraoperative cerebral ischemia. 314 94

Nitric Oxide (NO) has been implicated as a mediator of neuronal injury in vascular stroke. On the other hand, NO is suggested to play a neuroprotective role by increasing blood flow during cerebral ischemia. In order to evaluate the role of NO in the spinal cord ischemia, effects of nitric oxide synthase (NOS) inhibition on the recovery of reflex potentials after a transient spinal cord ischemia were examined in urethane-chloralose anesthetized spinal cats. Spinal cord ischemia was produced by occlusion of the thoracic aorta and the both internal mammary arteries for 10 min. Regional blood flow (RBF) in the spinal cord was continuously measured with a laser-Doppler flow meter. The monosynaptic (MSR) and polysynaptic reflex (PSR) potentials elicited by electrical stimulation of the tibial nerve, were recorded from the L7 or S1 ventral root. The recovery process of spinal reflex potentials was reproducible when the oclusion was repeated twice at an interval of 120 min. Pretreatment with N(G)-monomethyl-L-arginine (L-NMMA, 10 mg/kg), a NOS inhibitor significantly accelerated the recovery of PSR potentials after spinal cord ischemia. The accelerating effect of L-NMMA on the recovery of PSR potentials was abolished by co-administration of L-arginine (1 mg/kg/min) but not by that of D-arginine (1 mg/kg/min). L-NMMA failed to improve RBF in the spinal cord during ischemia and reperfusion. Nitroprusside (10 microg/kg/min), a NO donor, retarded the recovery of PSR potentials after spinal cord ischemia. These results suggest that NO production has a significant influence on the functional recovery after transient spinal cord ischemia.
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PMID:Inhibition of nitric oxide synthesis accelerates the recovery of polysynaptic reflex potentials after transient spinal cord ischemia in cats. 910 59