Regional cerebral blood flow following hypothermic circulatory arrest in newborn dogs

Yager, Jerome Y.; Christensen, Melanie A.; Vannucci, Robert C.

doi:10.1016/0006-8993(93)90277-t

Cited by 8 publications

(5 citation statements)

References 21 publications

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“…Clinically relevant models of cardiac arrest were developed more recently, and CBF was thoroughly assessed using these models. These models include: ventricular fibrillation cardiac arrest (VF) ( 31 ), asphyxial cardiac arrest ( 10 , 31 ), and KCl-induced cardiac arrest ( 32 ). CBF has been characterized after cardiac arrest in pediatric and adult age groups in rats, pigs, cats, and rabbits.…”

Section: Alterations In Cbf After Cardiac Arrest: Animal Modelsmentioning

confidence: 99%

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Iordanova

Clark

et al. 2017

Front. Pediatr.

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Greater than 50% of patients successfully resuscitated from cardiac arrest have evidence of neurological disability. Numerous studies in children and adults, as well as in animal models have demonstrated that cerebral blood flow (CBF) is impaired after cardiac arrest. Stages of cerebral perfusion post-resuscitation include early hyperemia, followed by hypoperfusion, and finally either resolution of normal blood flow or protracted hyperemia. At the level of the microcirculation the blood flow is heterogeneous, with areas of no flow, low flow, and increased flow. CBF directed therapies in animal models of cardiac arrest improved neurological outcome, and therefore, the alterations in CBF after cardiac arrest likely contribute to the development of hypoxic ischemic encephalopathy. Current intensive care after cardiac arrest is centered upon maintaining systemic oxygenation, normal blood pressure values for age, maintaining general homeostasis, and avoiding hyperthermia. Assessment of CBF and oxygenation is not routinely performed after cardiac arrest. Currently available and underutilized techniques to assess cerebral perfusion include transcranial doppler, near-infrared spectroscopy, and arterial spin labeling magnetic resonance imaging. Limited clinical studies established the role of CBF and oxygenation monitoring in prognostication after cardiac arrest and few studies suggest that guiding critical care post-resuscitation to mean arterial pressures above the minimal autoregulatory range might improve outcome. Important knowledge gaps thus remain in cerebral monitoring and CBF and oxygen goal-directed therapies post-resuscitation from cardiac arrest.

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Section: Alterations In Cbf After Cardiac Arrest: Animal Modelsmentioning

confidence: 99%

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Iordanova

Clark

et al. 2017

Front. Pediatr.

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“…3335 The histologically apparent lesions in surviving newborn dogs appear to be the direct consequence of cerebral ischemia occurring only during the period of circulatory arrest, since postischemic complications do not occur (see present data) and cerebral blood flow is restored promptly after resuscitation. 36 In human infants, brain lesions, when they occur, might relate to cerebral ischemia beyond the safety margin promoted by hypothermic cardiac arrest or to an intraoperative or postoperative complication of the surgical procedure (eg, air emboli or postoperative hypotension). 33 -37 The present data in newborn dogs have additional relevance to the human situation.…”

Section: Discussionmentioning

confidence: 99%

Differences in intraischemic temperature influence neurological outcome after deep hypothermic circulatory arrest in newborn dogs.

Mujsce

Towfighi

Heitjan

et al. 1994

Stroke

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Background and Purpose Hypothermia to core temperatures ranging from 16°C to 24°C has become an established procedure to extend the "safe" interval of cardiac arrest during open heart surgery in human infants. The present experiment was designed to ascertain whether differences in core (rectal) temperature during hypothermic circulatory arrest influence the presence and extent of ischemic brain damage in newborn dogs.Methods Newborn dogs (postnatal age, 3 to 5 days) were anesthetized with halothane (4% induction; 0.5% maintenance), intubated, paralyzed, and artificially ventilated with 70% nitrous oxide/30% oxygen. Thereafter, the dogs were surface cooled with ice packs to either 16°C (n=6), 20°C (n=8), or 24°C (n=6). The dogs then were subjected to circulatory arrest for 1.75 hours by the intravenous injection of KC1, following which they were resuscitated with intravenous NaHCO 3 and epinephrine, artificial ventilation, and closed chest cardiac massage. Those dogs that survived for 8 hours of recovery (n=16) underwent neurobehavioral examination followed by perfusion-fixation of their brains for pathological analysis.Results All newborn dogs were successfully resuscitated after 1.75 hours of cardiac arrest, rewarmed to 37°C, and ultimately weaned from anesthesia and ventilatory support. Four dogs sustained secondary systemic complications with death at 4 to 7 hours. All surviving dogs remained stable, with systemic blood pressure, heart rate, arterial oxygen, and acid-base balance within the normal, normothermic range. Of

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“…Gross evaluation of damage based on the presence and extent of damage was conducted by an investigator blinded to the experimental design. Individual brains were grouped into one of five categories of damage score (DS), as previously described [6,8,9]. Specifically, DS 0 = normal; DS 1 = mild brain atrophy; DS 2 = moderate brain atrophy; DS 3 = moderate-severe atrophy with small cystic cavitation !…”

Section: Experimental Designmentioning

confidence: 99%

Delayed Cerebral Atrophy following Moderate Hypoxia-Ischemia in the Immature Rat

Vannucci²,

2001

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Hypoxia-ischemia (H/I) damages cells in the immature brain and interferes with subsequent brain development; the extent of the damage has been related to the severity, or duration, of the initial insult. This study examined the effects of both severe and moderate duration of H/I on the evolution of damage through 8 weeks of recovery. Seven-day-old rat pups were subjected to either 75 min or 2 h of 8% oxygen following a unilateral carotid artery ligation. Evaluation of brain damage included morphometric analysis of hemispheric diameter at 2, 4, and 8 weeks of recovery, and hematoxylin and eosin for evaluation of pathology at 8 weeks. Two hours of H/I produced severe infarction in the ipsilateral hemisphere in the majority of the survivors, apparent by 2 weeks of recovery with no change at 4 or 8 weeks. In marked contrast, 75 min of H/I produced no significant damage during the initial 2 weeks of recovery but resulted in progressive cerebral atrophy with delayed infarction such that the extent of damage at 8 weeks was not different from the 2-hour group. Thus, even a mild-moderate ischemic insult to the perinatal brain establishes a vulnerable region which ultimately dies without intervention.

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Regional cerebral blood flow following hypothermic circulatory arrest in newborn dogs

Cited by 8 publications

References 21 publications

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Alterations in Cerebral Blood Flow after Resuscitation from Cardiac Arrest

Differences in intraischemic temperature influence neurological outcome after deep hypothermic circulatory arrest in newborn dogs.

Delayed Cerebral Atrophy following Moderate Hypoxia-Ischemia in the Immature Rat

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