Prolonged cardiac arrest and resuscitation in dogs: Brain mitochondrial function with different artificial perfusion methods

White, Blaine C.; Hildebrandt, J F; Evans, AT; Aronson, Lawrence D.; Indrieri, R. J.; Hoehner, Thomas; Fox, Leslie E.; Huang, Ran; Johns, David G.

doi:10.1016/s0196-0644(85)80278-x

Cited by 35 publications

(11 citation statements)

References 33 publications

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“…No significant decline in the mitochondrial respi ratory control ratio was observed for any of the fi brillated or resuscitated groups of animals. This finding is in contrast to that of White et al (1985), who observed a 50% reduction in the respiratory control ratio of isolated canine brain mitochondria after 15 min of cardiac arrest. This difference can be at least partially attributed to the fact that a slight decrease in resting (State 4) respiration after ischemia alone was observed (Table 1), whereas an apparent increase in State 4 respiration was re ported in the previous study.…”

Section: Discussioncontrasting

confidence: 99%

“…The procedure used in the present study disrupts synaptosomal vesicles thereby liberating many of the neuronal mitochondria and providing a population of isolated mitochondria that is repre sentative of both glial and neuronal tissue. The dif ference in isolation procedures may also explain why the rates of oxygen consumption for isolated canine brain mitochondria shown in Ta ble 1 are considerably higher than those reported by White et al (1985). No significant decline in the mitochondrial respi ratory control ratio was observed for any of the fi brillated or resuscitated groups of animals.…”

Section: Discussionmentioning

confidence: 73%

“…Various rat models have demonstrated that 30 min of complete cerebral ischemia results in at least a 50% decrease in phos phorylating respiration and a substantial decline in the respiratory control ratio obtained with isolated brain mitochondria (Mela, 1979;Rehncrona et aI., 1979;Siesjo, 1981;Hamud and Fiskum, 1985). U sing a cardiac arrest model to induce complete ce rebral ischemia in dogs, White et aL (1985) have also demonstrated a 50% decrease in the respira tory control ratio of dog brain mitochondria fol lowing 15 or 45 min of complete cerebral ischemia.…”

mentioning

confidence: 92%

“…Similar re covery was not observed following 30 min of isch emia. White et aL (1985) studied the effect of various forms of cardiopulmonary resuscitation fol lowing 15 min of fibriIIatory arrest in dogs. They found no statistical difference in brain mitochon drial respiration between control animals and an imals receiving 30 min of open-chest cardiopulmo nary resuscitation, while animals treated with inter posed abdominal compression cardiopulmonary resuscitation actual1y demonstrated worsening of injury.…”

mentioning

confidence: 99%

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Cerebral Ischemia and Reperfusion: Prevention of Brain Mitochondrial Injury by Lidoflazine

Rosenthal

Hamud

Fiskum

et al. 1987

J Cereb Blood Flow Metab

253

148

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Mitochondrial degradation is implicated in the irreversible cell damage that can occur during cerebral ischemia and reperfusion. In this study, the effects of 10 min of ventricular fibrillation and 100 min of spontaneous circulation on brain mitochondrial function was studied in dogs in the absence and presence of pretreatment with the Ca2+ antagonist lidoflazine. Twenty-three beagles were separated into four experimental groups: (i) nonischemic controls (ii) those undergoing 10-min ventricular fibrillation, (iii) those undergoing 10-min ventricular fibrillation pretreated with 1 mg/kg lidoflazine i.v., and (iv) those undergoing 10-min ventricular fibrillation followed by spontaneous circulation for 100 min. Brain mitochondria were isolated and tested for their ability to respire and accumulate calcium in a physiological test medium. There was a 35% decrease in the rate of phosphorylating respiration (ATP production) following 10 min of complete cerebral ischemia. Those animals pretreated with lidoflazine showed significantly less decline in phosphorylating respiration (16%) when compared with nontreated dogs. Resting and uncoupled respiration also declined following 10 min of fibrillatory arrest. One hundred minutes of spontaneous circulation following 10 min of ventricular fibrillation and 3 min of open-chest cardiac massage provided complete recovery of normal mitochondrial respiration. Energy-dependent Ca2+ accumulation by isolated brain mitochondria was unimpaired by 10 min of complete cerebral ischemia. However, by 100 min after resuscitation, there was a small, but significant rise in the capacity for mitochondrial Ca2+ sequestration when compared to either control or fibrillated groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 73%

mentioning

confidence: 92%

mentioning

confidence: 99%

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Cerebral Ischemia and Reperfusion: Prevention of Brain Mitochondrial Injury by Lidoflazine

Rosenthal

Hamud

Fiskum

et al. 1987

J Cereb Blood Flow Metab

253

148

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“…In experimental models, which are aimed to study mechanisms of reperfusion, CPB resuscitation is advantageous because it provides a relatively consistent blood flow compared to conventional CPR [19, 20]. This should significantly reduce variability caused by the inconsistent/insufficient blood flow, which itself is suggested to be responsible for additional damage particularly to the brain [21]. We previously reported that rats following 30 min asphyxial CA and 60 min CPB resuscitation showed complete absence of brain function and moderately compromised heart function, typical physiological outcomes of patient with severe CA [22].…”

Section: Introductionmentioning

confidence: 99%

Phospholipid alterations in the brain and heart in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary bypass resuscitation

et al. 2015

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Cardiac arrest (CA) induces whole-body ischemia, causing damage to multiple organs. Ischemic damage to the brain is mainly responsible for patient mortality. However, the molecular mechanism responsible for brain damage is not understood. Prior studies have provided evidence that degradation of membrane phospholipids plays key roles in ischemia/reperfusion injury. The aim of this study is to correlate organ damage to phospholipid alterations following 30 min asphyxia-induced CA or CA followed by cardiopulmonary bypass (CPB) resuscitation using a rat model. Following 30 min CA and CPB resuscitation, rats showed no brain function, moderately compromised heart function, and died within a few hours; typical outcomes of severe CA. However, we did not find any significant change in the content or composition of phospholipids in either tissue following 30 min CA or CA followed by CPB resuscitation. We found a moderate increase in lysophosphatidylinositol in both tissues, and a small increase in lysophosphatidylethanolamine and lysophosphatidylcholine only in brain tissue following CA. CPB resuscitation significantly decreased lysophosphatidylinositol but did not alter the other lyso species. These results indicate that a decrease in phospholipids is not a cause of brain damage in CA or a characteristic of brain ischemia. However, a significant increase in lysophosphatidylcholine and lysophosphatidylethanolamine found only in the brain with more damage suggests that impaired phospholipid metabolism may be correlated with the severity of ischemia in CA. In addition, the unique response of lysophosphatidylinositol suggests that phosphatidylinositol metabolism is highly sensitive to cellular conditions altered by ischemia and resuscitation.

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Prehospital Cardiopulmonary Resuscitation

White¹,

Thompson²

1985

JAMA

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Prolonged cardiac arrest and resuscitation in dogs: Brain mitochondrial function with different artificial perfusion methods

Cited by 35 publications

References 33 publications

Cerebral Ischemia and Reperfusion: Prevention of Brain Mitochondrial Injury by Lidoflazine

Cerebral Ischemia and Reperfusion: Prevention of Brain Mitochondrial Injury by Lidoflazine

Phospholipid alterations in the brain and heart in a rat model of asphyxia-induced cardiac arrest and cardiopulmonary bypass resuscitation

Prehospital Cardiopulmonary Resuscitation

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