An experimental circulatory arrest model in the rat to evaluate calcium antagonists in cerebral resuscitation

Garavilla, Lawrence de; Babbs, Charles F.; Tacker, Willis A.

doi:10.1016/0735-6757(84)90127-x

Cited by 33 publications

(10 citation statements)

References 15 publications

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“…The absence of convulsions in the latter group raises a question of the extent to which seizures might have contributed to the deteriorated morphology and much higher mortality among control and acute IB-MECA animals. Seizures are a frequent complication of recovery from complete global ischemia in gerbils and in other species, including man (De Garavilla et al, 1984;Todd et al, 1982;Wauquier et al, 1987). We have shown, however, that 10, 20, and even 30 min ischemia causes predominant damage in the dorsolateral aspect of gerbil striaturn (Von Lubitz et al, 1989Lubitz et al, , 1993a, while the seizuresensitive ventrolateral quadrant remains virtually intact.…”

Section: Discussionmentioning

confidence: 82%

Adenosine A3 receptor stimulation and cerebral ischemia

Lubitz

Lin

Popik

et al. 1994

European Journal of Pharmacology

271

257

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Chronic treatment with the selective adenosine A 3 receptor agonist N 6 -(3-iodobenzyl)adenosine-5'-N-methylcarboxamide (IB-MECA) administered prior to either 10 or 20 min forebrain ischemia in gerbils resulted in improved postischemic cerebral blood circulation, survival, and neuronal preservation. Opposite effects, i.e., impaired postischemic blood flow, enhanced mortality, and extensive neuronal destruction in the hippocampus were seen when IB-MECA was given acutely. Neither adenosine A 1 nor A 2 receptors are involved in these actions. The data indicate that stimulation of adenosine A 3 receptors may play an important role in the development of ischemic damage, and that adenosine A 3 receptors may offer a new target for therapeutic interventions.

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Section: Discussionmentioning

confidence: 82%

Adenosine A3 receptor stimulation and cerebral ischemia

Lubitz

Lin

Popik

et al. 1994

European Journal of Pharmacology

271

257

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“…Following anesthesia with an intraperitoneal injection of ketamine (60 mg/kg) and neuromuscular blockade with succinylcholine (1.5 mg/ kg), cardiorespiratory arrest (asystole) was induced in each rat by a percutaneous intracardiac injection of 0.4-0.8 ml of a cold 1% KCI cardioplegic solution and digital compression of the thorax (DeGaravilla et al, 1984). Electrocardiograms were monitored throughout the arrest and immediate postresuscitation period.…”

Section: Methodsmentioning

confidence: 99%

“…In the present study, we evaluated the effectiveness of a simple and easily administered multi-modal therapy, including a cerebral vasodilator (carbon dioxide), a calcium entry blocker (lidoflazine), and an iron chelator (deferoxamine), intended to minimize reperfusion injury following total circulatory arrest and CPR in rats. All therapy was administered after return of spontaneous circulation in a clinically realistic time frame (DeGaravilla et al, 1984).…”

Section: Introductionmentioning

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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“…Cardiorespiratory arrest was induced in each rat by discontinuation of jet ventilation, percutaneous intracardiac injection of 0.8 mL cold 1% KCl cardioplegic solution, and steady digital compression of the thorax [10]. The ECG was monitored throughout the arrest and immediate post-resuscitation periods.…”

Section: Methodsmentioning

confidence: 99%

“…The rat circulatory arrest model used has been described previously [10]. Fifty male Wistar rats, each weighing between 350 and 450 g, were sorted randomly into experimental and control groups of 25 animals each.…”

Section: Methodsmentioning

confidence: 99%

Effect of deferoxamine on late deaths following CPR in rats

Kompala¹,

Cf²

1985

Annals of Emergency Medicine

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The iron chelating agent deferoxamine was studied in an animal model as post-resuscitation therapy to prevent late deaths and brain damage following total circulatory arrest and resuscitation. Cardio-respiratory arrest was induced by injection of cold, 1% KC1 into the left ventricles of ketamine anesthetized rats pretreated with succinylcholine chloride, and by discontinuation of positive pressure ventilation. CPR was begun after six minutes, and animals with return of spontaneous circulation were entered into the study. Within five minutes after return of spontaneous circulation, treated animals received deferoxamine (50 mg/kg, IV). At ten days, 16 of 25 (64%) of treated animals had survived without neurologic deficit, compared to nine of 25 (36%) of controls (chi square = 3.92, P < .05). Chelation of intracellular iron by deferoxamine may have prevented free-radical-mediated reactions that led to late deaths in control animals.

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An experimental circulatory arrest model in the rat to evaluate calcium antagonists in cerebral resuscitation

Cited by 33 publications

References 15 publications

Adenosine A3 receptor stimulation and cerebral ischemia

Adenosine A3 receptor stimulation and cerebral ischemia

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

Effect of deferoxamine on late deaths following CPR in rats

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