scholarly journals Effect of calcium antagonist NC-1100 on cerebral blood flow and tissue metabolism after acute cerebral ischemia in spontaneously hypertensive rats.

Nosotchu ◽  
1991 ◽  
Vol 13 (5) ◽  
pp. 346-351
Author(s):  
Seizo Sadoshima ◽  
Setsuro Ibayashi ◽  
Mitsuko Ooshima ◽  
Sakan Mori ◽  
Masatoshi Fujishima
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Calcium Antagonist ◽  
Cerebral Ischemia ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Tissue Metabolism ◽  
Acute Cerebral Ischemia

scholarly journals Chronic Parasympathetic Sectioning Decreases Regional Cerebral Blood Flow during Hemorrhagic Hypotension and Increases Infarct Size after Middle Cerebral Artery Occlusion in Spontaneously Hypertensive Rats

1992 ◽  
Vol 12 (4) ◽  
pp. 613-620 ◽  
Author(s):  
Naoki Koketsu ◽  
Michael A. Moskowitz ◽  
Hermes A. Kontos ◽  
Masayuki Yokota ◽  
Takeo Shimizu
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Regional Cerebral Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Regional Cerebral Blood ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Hemorrhagic Hypotension

Regional cerebral blood flow (rCBF) during controlled hemorrhagic hypotension (140–20 mm Hg) was assessed 10–14 days after chronic unilateral sectioning of parasympathetic and/or sensory fibers innervating pial vessels in spontaneously hypertensive rats (SHR). rCBF was measured in the cortical barrel fields bilaterally by laser Doppler blood flowmetry. Immunohistochemistry of middle cerebral artery (MCA) whole mount preparations was used to verify the surgical lesion. During hemorrhagic hypotension, rCBF was equivalent on the two sides in shams, after selective sensory denervation, or in parasympathetically sectioned animals exhibiting small decreases (≤30%) in immunoreactive vasoactive intestinal peptide (VIP)-containing fibers. After chronic parasympathetic denervation, decreases in perfusion pressure were accompanied by greater reductions in rCBF on the lesioned side; changes in vascular resistance were also attenuated on that side. The rCBF response to hypercapnia (Paco2 50 mm Hg), however, was symmetrical and robust. To examine the effects of impaired neurogenic vasodilation on the pathophysiology of cerebral ischemia, infarct size was measured 24 h following tandem MCA occlusion in denervated animals. Infarction volume was larger after selective parasympathetic sectioning (sham, 156 ± 27 vs. 196 ± 32 mm3, respectively) but only in those denervated animals demonstrating ≥40% decrease in immunoreactive VIP-containing fibers within the ipsilateral MCA. Lower than expected blood flow/perfusion pressure in the cortex distal to an occluded blood vessel may relate the observed blood flow responses to the occurrence of larger cortical infarcts in parasympathetically denervated animals. If true, the findings suggest a novel role for neurogenic vasodilation in the pathophysiology of cerebral ischemia and in rCBF regulation within the peri-infarction zone.

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