Effects of Fentanyl Pretreatment on Regional Cerebral Blood Flow in Focal Cerebral Ischemia in Rats

Pharmacology ◽  
2010 ◽  
Vol 85 (3) ◽  
pp. 153-157 ◽  
Author(s):  
Oak Z. Chi ◽  
Christine Hunter ◽  
Xia Liu ◽  
Sagar K. Chokshi ◽  
Harvey R. Weiss
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Regional Cerebral Blood Flow ◽  
Focal Cerebral Ischemia ◽  
Regional Cerebral Blood

scholarly journals Effects of Dextromethorphan on Regional Cerebral Blood Flow in Focal Cerebral Ischemia

1991 ◽  
Vol 11 (5) ◽  
pp. 803-809 ◽  
Author(s):  
Eng H. Lo ◽  
Gary K. Steinberg
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Frequency Distribution ◽  
Regional Cerebral Blood Flow ◽  
Neuronal Damage ◽  
Focal Cerebral Ischemia ◽  
Distribution Analysis ◽  
Regional Cerebral Blood ◽  
Left And Right

Dextromethorphan (DM), a noncompetitive NMDA antagonist, has been demonstrated to reduce ischemic neuronal damage and edema, but DM's influence on cerebral blood flow has not been extensively studied. In this investigation, it is shown that DM has significant effects on regional cerebral blood flow (rCBF) patterns in a rabbit model of focal cerebral ischemia. rCBF was measured using radioactive microspheres following a 1 h permanent occlusion of the left internal carotid, anterior cerebral, and middle cerebral arteries in rabbits. Somatosensory evoked potentials (SEPs) were used to assess the degree of ischemia; only animals where SEPs were completely abolished were used for a frequency distribution analysis of rCBF. It was found that there were significantly more regions with lower flows in animals treated with normal saline (NS) ( n = 7) compared to animals treated with DM ( n = 7) ( p < 0.05, ipsilateral left side; p < 0.001, contralateral right side). The frequency distribution medians were 27.5 ml 100 g−1 min −1 (left) and 70.0 ml 100 g−1 min−1 (right) in the NS group vs. 34.5 ml 100 g−1 min−1 (left) and 80.5 ml 100 g−1 min−1 (right) in the DM group. The left and right hemispheric regional means were 29.4 ± 20 and 74.3 ± 23 ml 100 g−1 min−1, respectively, in the NS group vs. 34.4 ± 16 and 91.0 ± 28 ml 100 g−1 min−1, respectively, in the DM group. However, there were no significant differences in global CBF between the NS group (33.1 ± 18 and 79.2 ± 20 ml 100 g−1 min−1) and the DM group (35.0 ± 10 and 92.0 ± 21 ml 100 g−1 min−1) in both left and right hemispheres, respectively. These results demonstrate that DM has effects on rCBF in focal cerebral ischemia, although it is unclear if these changes represent primary effects of DM on cerebrovascular function, or secondary effects of neuronal protection.

scholarly journals l-Arginine-Induced Regional Cerebral Blood Flow Increase is Abolished after Transient Focal Cerebral Ischemia in the Rat

1997 ◽  
Vol 17 (10) ◽  
pp. 1074-1080 ◽  
Author(s):  
Bernd Sporer ◽  
K. Helge Martens ◽  
Uwe Koedel ◽  
Roman L. Haberl
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Regional Cerebral Blood Flow ◽  
Focal Cerebral Ischemia ◽  
Regional Cerebral Blood ◽  
Doppler Flowmetry ◽  
Transient Focal Cerebral Ischemia ◽  
Reperfusion Period ◽  
Synthase Inhibitor

We investigated the l-arginine-induced, regional cerebral blood flow (rCBF) enhancement after different durations of transient focal cerebral ischemia in the rat to determine if l-arginine increases rCBF after transient focal cerebral ischemia. Focal ischemia (5 minutes and 20 minutes) followed by 90 minutes of reperfusion was induced in a normotensive rat suture-model. Regional cerebral blood flow in both hemispheres was measured by laser-Doppler-flowmetry. Reactivity of rCBF to l-arginine (300 mg/kg) was measured 45 minutes after reperfusion, and hypercapnia 90 minutes after reperfusion. The effect of d-arginine and pretreatment with the nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine (l-NA) (10 mg/kg) was examined in additional groups. Hypercapnia and l-arginine increased rCBF in sham operated controls and on the nonischemic hemispheres. d-arginine did not. Twenty-minute long ischemia significantly reduced the response to l-arginine (control side: 115 ± 5.9%; ischemic side: 107 ± 6.1%, n = 7) and hypercapnia, 5 minutes of ischemia did not. Nω-nitro-l-arginine pretreatment partly restored the l-arginine-induced rCBF increase. Thus, rCBF increase caused by l-arginine in the reperfusion period was unaffected by 5 minutes of ischemia, but reduced by 20 minutes of ischemia. The restoration after pretreatment with l-NA may be caused by attenuated production of cytotoxic substances, e.g., NO and related compounds.

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