Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest

White, Blaine C.; Gadzinski, Daniel S.; Hoehner, Paul J.; Krome, Charles; Hoehner, Thomas; White, James R.; Trombley, John H.

doi:10.1016/s0196-0644(82)80235-7

Cited by 136 publications

(26 citation statements)

References 25 publications

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“…Flunarizine prevented the increase in the resistance, and it preserved the normal cerebral cortical blood flow and 02 consump tion (34). In the present study, reoxygenation persistently contracted cerebral arteries pre viously exposed to severe hypoxia and stimu lated by PGF:a.…”

Section: Resultssupporting

confidence: 58%

“…White et al (34) reported that cerebral cortical blood flow and 02 con sumption reached zero following 90 min re suscitation in dogs subjected to prolonged ischemia, in association with a progressive increase in cerebral vascular resistance. Flunarizine prevented the increase in the resistance, and it preserved the normal cerebral cortical blood flow and 02 consump tion (34).…”

Section: Resultsmentioning

confidence: 99%

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Vasodilator actions of flunarizine in isolated dog cerebral and extracerebral arteries.

Bian

Toda

1989

Jpn.J.Pharmacol

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Abstract-Flunarizine relaxed isolated canine arteries precontracted with pro staglandin (PG) F2a, epithio-methano-thromboxane A2 and K+; the relaxation was in the order of cerebral >renal>mesenteric= coronary arteries, when contracted with PGF2a or the thromboxane A2 analogue. Flunarizine-induced relaxation was unaffected by treatment with atropine, propranolol, cimetidine, chlorpheniramine, aminophylline and indomethacin, and by removal of endothelium.Under normoxia, flunarizine attenuated contractions elicited by Ca2+ in the K+-stimulated cerebral and mesenteric arteries that had been previously exposed to Ca2+-free media to a greater extent than that in PGF2a-stimulated preparations.The Ca2+-induced contraction in cerebral arteries was more sensitive to flunarizine than that in mesen teric arteries.Contractions caused by PGF2a in Ca2+-free media were not influenced by flunarizine.

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Section: Resultssupporting

confidence: 58%

Section: Resultsmentioning

confidence: 99%

Vasodilator actions of flunarizine in isolated dog cerebral and extracerebral arteries.

Bian

Toda

1989

Jpn.J.Pharmacol

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“…The first one is an im provement of postischemic hypoperfusion. It has been suggested that the neurologic damage that occurs subsequent to ischemia is due at least in part to a delayed hypoper fusion state following reperfusion (29,30). Steen et al has reported previously that in fusion of the nimodipine, administered before or after ischemia (7, 8), improved both the postischemic cerebral blood flow and the neurologic outcome.…”

Section: Discussionmentioning

confidence: 99%

Effect of Nimodipine on Ischemia-Induced Brain Edema and Mortality in a Novel Transient Middle Cerebral Artery Occlusion Model

Hara

Oda

Nagasawa

et al. 1990

Japanese Journal of Pharmacology

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“…Lidoflazine, a calcium entry blocker, may inhibit the vasospasm and the intracellular calcium overload that occur following ischemia and reperfusion (Daenen and Flameng, 1981). This drug and other calcium antagonists have been reported to decrease neurologic deficits and cardiac pathologic alterations in animals following resuscitation from cardiac arrest (Daenen and Flameng, 1981;Hoffmeister et al, 1979;White et al, 1982;Winegar et al, 1983).…”

Section: Discussionmentioning

confidence: 99%

The effect of carbon dioxide, lidoflazine and deferoxamine upon long term survival following cardiorespiratory arrest in rats

Badylak

Babbs

1986

Resuscitation

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SUMMARYThis study examined the effect of carbon dioxide, lidoflazine, and deferoxamine therapy upon the 10-day survival incidence and subsequent neurologic function of rats subjected to 7 min of cardiorespiratory arrest with resuscitation. Cardiac arrest (asystole) was induced at time zero by injection of cold, 1% KCl into the left ventricle of ketamine-anesthetized rats pretreated with succinylcholine. Positive pressure ventilation was discontinued at time zero. Cardiopulmonary resuscitation (CPR) was begun at 7 min, and animals with return of spontaneous circulation were entered into the study. Twenty treated rats were ventilated for 1 h with 7% carbon dioxide-93% oxygen and given lidoflazine (2.0 mg/kg, i.v.) and deferoxamine (50 mg/kg, i.v.) 5 min after CPR. Twenty control rats were ventilated for 1 h with 100% oxygen and given lidoflazine vehicle and deferoxamine vehicle. Lidoflazine treatment (1.0 mg/ kg) for the treated group, or lidoflazine vehicle for the control group, was repeated at 8 h postresuscitation. At 2 days postresuscitation, 75% of treated rats vs. 25% of control rats were alive (Chi-square = 10.0, d.f. = 1, P < 0.01), and at 10 days, 60% of treated rats vs. 25% of control rats were alive (Chi-square = 5.01, d.f. = 1, P < 0.05). There was no detectable neurologic deficit among survivors in either group at 15 days. The combination of carbon dioxide, lidoflazine, and deferoxamine, administered after return of spontaneous circulation, is a simple and easily administered treatment regimen that improves the survival incidence without neurologic deficits in this animal model of cardiorespiratory arrest and CPR.

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Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest

Cited by 136 publications

References 25 publications

Vasodilator actions of flunarizine in isolated dog cerebral and extracerebral arteries.

Vasodilator actions of flunarizine in isolated dog cerebral and extracerebral arteries.

Effect of Nimodipine on Ischemia-Induced Brain Edema and Mortality in a Novel Transient Middle Cerebral Artery Occlusion Model

The effect of carbon dioxide, lidoflazine and deferoxamine upon long term survival following cardiorespiratory arrest in rats

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