Brain Cooling in the Prevention of Brain Damage During Periods of Circulatory Occlusion in Dogs

Parkins, W. M.; Jensen, Jay M.; Vars, Harry M.

doi:10.1097/00000658-195409000-00004

Cited by 94 publications

(16 citation statements)

References 9 publications

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“…An early study by Parkins et al (1954) unilaterally perfused the common carotid artery in dogs in an attempt to reduce brain temperature, but their method also caused bradycardia and systemic hypotension as well as moderate systemic hypothermia of 24-30°C. That study was later replicated by Kimoto et al (1956) with less severe systemic hypothermia (29-31°C rectal) but was also complicated by ventricular fibrillation that was observed in five of 15 dogs.…”

Section: Discussionmentioning

confidence: 99%

Marked Protection by Selective Cerebral Profound Hypothermia after Complete Cerebral Ischemia in Primates

Jiang

Yang

et al. 2006

Journal of Neurotrauma

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Hypothermia has been demonstrated to protect the brain from ischemia or traumatic brain injury. Achieving profound hypothermia has relied on techniques requiring total body cooling, which may result in serious cardiovascular and pulmonary complications. A technique to selectively cool the brain could conceivably exert a marked protection on cerebral structures and provide a relatively bloodless operative surgical field without systemic complications. Accordingly, this approach was tried in 7 rhesus monkeys after induction of general anesthesia. The right internal carotid artery and both internal jugular veins were each occlusively cannulated and connected to a circulation pump. The left internal carotid artery, both external carotid arteries, and both external jugular veins were temporarily clamped to establish severe cerebral ischemia. Using a closed-circuit system, cooled Ringer's lactate liquid (4 degrees C) was infused through right internal carotid artery with outflow draining though both internal jugular veins. Cooled perfusate decreased cerebral temperature to the target temperature of 15 degrees C. Thereafter, pump flow was discontinued, and brains were rewarmed spontaneously, while the temporarily clamped carotid arteries and jugular veins were opened to resume normal cerebral blood circulation. Neurological functions were recorded daily and cerebral histology was examined at the conclusion of the experiment. Magnetic resonance (MR) scans were routinely taken before and 3 weeks after ischemia. In the normothermia control group of five rhesus monkeys, Ringer's solution at 37 degrees C was infused in the same manner as the cold solution with cerebral temperature maintained at 36.7 +/- 0.32 degrees C. Right cerebral temperature decreased from 36.5 +/- 0.49 to 15.5 +/- 2.29 degrees C, and simultaneously the left cerebral temperature decreased from 36.4 +/- 0.38 to 16.3 +/- 2.4 degrees C for 62.8 +/- 9.76 min during selective cerebral cooled Ringer's liquid perfusion. In contrast, rectal temperature was only reduced to 32.4 +/- 0.96 degrees C from a baseline of 37.2 +/- 0.76 degrees C. Internal jugular vein hematocrit was 38.2 +/- 0.31% before perfusion and 2.82 +/- 0.46% at the end of perfusion in profound hypothermia group; hematocrit was 39.7 +/- 0.62% before perfusion and 3.42 +/- 0.38% at the end of perfusion in the normothermia group. In the hypothermic group, neurological functions were normal during 6 months of follow-up, and microscopic examination of brain tissue did not show evidence of pathological changes in hippocampus or medulla. MR scans did not show any cerebral infarction. In contrast, none of the monkeys in normothermia group survived for more than several hours, and microscopic examination of the brain revealed extensive neuronal necrosis within the medulla. Selective cerebral profound hypothermia provides significant histologic and neurologic protection after severe cerebral ischemia. In addition, there were no major complications, and the operative field remained relatively bloodless in ...

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Section: Discussionmentioning

confidence: 99%

Marked Protection by Selective Cerebral Profound Hypothermia after Complete Cerebral Ischemia in Primates

Jiang

Yang

et al. 2006

Journal of Neurotrauma

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“…11,17,42 A number of investigators have reported significant complications arising from systemic methods, including coagulopathy, hemodynamic instability, and even fatal arrhythmias. 13,43 Although selective brain hypothermic techniques offer the greatest promise in reducing systemic complications, true brain hypothermia is difficult to achieve. Application of ice to the head and neck or ice caps can be initiated quickly and offer some brain cooling, 8,9,11 although they fail to provide significant temperature reduction of deep brain structures.…”

Section: Discussionmentioning

confidence: 99%

Untitled

2001

Academic Emergency Medicine

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Abstract. Objectives: Increasing human and laboratory evidence suggests that post-resuscitative brain hypothermia reduces the pathologic consequences of brain ischemia. Using a swine model of prolonged cardiac arrest, this investigation sought to determine whether unilateral hypothermic carotid bypass was capable of inducing selective brain hypothermia and reducing neurohistologic damage. Methods: Ventricular fibrillation was induced in common swine (n = 12). After 20 minutes of cardiopulmonary arrest (without ventilatory support or cardiopulmonary resuscitation), systemic extracorporeal bypass was instituted to restore coronary and cerebral perfusion, followed by restoration of normal sinus rhythm. Animals randomized to the normal brain temperature (NBT) cohort received mechanical ventilation and intravenous fluids for 24 hours. The selective brain hypothermia (SBH) cohort received 12 hours of femoral/ carotid bypass at 32ЊC. The bypass temperature was then increased one degree per hour until reaching 37ЊC and continued at this temperature until completion of the protocol (24 hours). Histopathologic damage was evaluated in two areas of the hippocampus. Results: Normal sinus rhythm was restored in all animals after the systemic (femoral/femoral) bypass was initiated. Nasal temperature (surrogate measure of brain temperature) remained higher than 37.0ЊC throughout the 24-hour recovery period in the NBT animals. In the SBH cohort, right nasal temperature dropped to the mild hypothermic range (<34ЊC) two hours after institution of femoral/carotid bypass. This was maintained throughout the 12-hour cooling period without hemodynamic compromise. There was a significant improvement in the neurohistology scores in the CA1 region of the hippocampus of the SBH treated animals as compared with those of the NBT cohort. Conclusions: Post-resuscitative selective brain hypothermia reduced regional ischemic brain damage in swine with prolonged ventricular fibrillation.

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“…Even a minor amount of coagulation can cause a blockage of the microcirculation of the brain and heart, which ironically creates the exact problem that hypothermia atempts to treat [21]. Furthermore, whole-body cooling increases the likelihood of ventricular ibrillations, bradycardia, reduced cardiac output, hemostatic or hemorrhagic changes, decreased urine output, and metabolic dysfunction [14,23,24]. With this extensive list of severe complications, a more graceful therapeutic modality is urgently needed.…”

Section: Systemic Hypothermiamentioning

confidence: 99%

Hypothermia in Stroke Therapy: Systemic versus Local Application

Huber¹,

Duan²,

Chandra³

et al. 2017

Hypoxia and Human Diseases

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Presently, there are no efective, widely applicable therapies for ischemic stroke. There is strong clinical evidence for the neuroprotective beneits of hypothermia, and surfacecooling methods have been utilized for decades in the treatment of cerebral ischemia during cardiac arrest, but complications with hypothermia induction have hindered its clinical acceptance in ischemic stroke therapy. Recently, the microcatheter-based local endovascular infusion (LEVI) of cold saline directly to the infarct site has been proposed as a solution to the drawbacks of surface cooling. The safety and eicacy of LEVI in rat models have been established, and implementation in larger animals has been similarly encouraging. A recent pilot study even established the safety of LEVI in humans. This review seeks to outline the major research on LEVI, discusses the mechanisms that mediate its superior neuroprotection over surface and systemic cooling, and identiies areas that warrant further investigation. While LEVI features improvements on surface cooling, its core mechanisms of neuroprotection are still largely shared with therapeutic hypothermia in general. As such, the mechanisms of hypothermia-based neuroprotection are discussed as well.

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Brain Cooling in the Prevention of Brain Damage During Periods of Circulatory Occlusion in Dogs

Cited by 94 publications

References 9 publications

Marked Protection by Selective Cerebral Profound Hypothermia after Complete Cerebral Ischemia in Primates

Marked Protection by Selective Cerebral Profound Hypothermia after Complete Cerebral Ischemia in Primates

Untitled

Hypothermia in Stroke Therapy: Systemic versus Local Application

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