Hypothermic retrograde jugular perfusion reduces brain damage in rats with heatstroke

Wen, Yi-Szu; Huang, Mu-Shung; Lin, Mao‐Tsun; Lee, Chen‐Hsen

doi:10.1097/01.ccm.0000094229.39473.c1

Cited by 24 publications

(12 citation statements)

References 39 publications

(33 reference statements)

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“…As shown by our previous findings (17,19,34,35), ischemic neuron damage in different brain structures occurred 10 -15 mins after the onset of heatstroke. The heatstroke-induced neuron damage in different brain structures was reduced by intravenous infusion of albumin (19) or HUCBCs (present study) as well as brain cooling (34,35), initiated immediately after the onset of heatstroke.…”

Section: Discussionmentioning

confidence: 73%

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Resuscitation from experimental heatstroke by transplantation of human umbilical cord blood cells*

Chen

Chang²,

Tsai³

et al. 2005

Critical Care Medicine

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Section: Discussionmentioning

confidence: 73%

“…The heatstroke-induced neuron damage in different brain structures was reduced by intravenous infusion of albumin (19) or HUCBCs (present study) as well as brain cooling (34,35), initiated immediately after the onset of heatstroke. Apparently, this histopathologic profile was noted in rats killed 12-15 mins after the onset of heatstroke.…”

Section: Discussionmentioning

confidence: 98%

Resuscitation from experimental heatstroke by transplantation of human umbilical cord blood cells*

Chen

Chang²,

Tsai³

et al. 2005

Critical Care Medicine

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“…Indeed, whole body (9) or brain (53,54) cooling improves survival during heatstroke by reducing multiple organ dysfunction or failure. However, under the hyperthermic state, multiorgan dysfunction or failure that occurred during heatstroke still can be suppressed by CD34 + cell therapy.…”

Section: Figmentioning

confidence: 99%

Human Umbilical Cord Blood-Derived Cd34+ Cells Cause Attenuation of Multiorgan Dysfunction During Experimental Heatstroke

Chen¹,

Chang²,

Chang

et al. 2007

Shock

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Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord blood-derived CD34+ cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34- or CD34+ cells (1 x 10(5)-5 x 10(5)/mL/kg body weight) i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-alpha levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34- cell-treated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34+ cells significantly improved survival time (duration, 63-291 min). As compared with normothermic controls, all CD34- cell-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34+ cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34+ cell therapy during heatstroke. Our data indicate that CD34+ cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure.

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“…Further, it was successfully shown that direct retrograde hypothermic perfusion via the jugular vein without cardiopulmonary bypass protected the rat brain after heat stroke. This technique cooled the brain but did not significantly interfere with body temperature [65]. Furuse et al evaluated cerebral metabolic change during brain hypothermia with intravascular perfusion of cooled crystalloid solution using an extracorporeal cooling-filtration system and cerebroprotective effects of this hypothermia on brain injury in an animal model [66].…”

Section: Cooling Through Perfusing Cold Bloodmentioning

confidence: 98%

Cooling strategies and transport theories for brain hypothermia resuscitation

Jing

2007

Front. Energy Power Eng. China

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The brain is one of the most important organs in a biological body whose normal function depends heavily on an uninterrupted delivery of oxygen. Unlike skeletal muscles that can survive for hours without oxygen, neuron cells in the brain are easily subjected to an irreversible damage within minutes from the onset of oxygen deficiency. With the interruption of cardiopulmonary circulation in many cardiac surgical procedures or accidental events leading to cerebral circulation arrest, an imbalance between energy production and consumption will occur which causes a rapid depletion of oxygen due to the interrupted blood-flow to the brain. Meanwhile, the cooling function of the blood flow on the hot tissue will be stopped, while metabolic heat generation in the tissues still keeps running for awhile. Under such adverse situations, the potential for cerebral protection through hypothermia has been intensively investigated in clinics by lowering brain temperature to restrain the cerebral oxygen demands. The reason can be attributed to the decreased metabolic requirements of the cold brain tissues, which allows a longer duration for the brain to endure reduced oxygen delivery. It is now clear that hypothermia would serve as the principal way for neurologic protection in a wide variety of emergency medicines, especially in cerebral damage, anoxia, circulatory arrest, respiratory occlusion, etc. However, although brain cooling has been found uniquely significant in clinical practices, the serious lack of knowledge on the mechanisms involved prevents its further advancement in brain resuscitation. Compared with the expanded trials in clinics, only very limited efforts were made to probe the engineering issues involved, which turns out to be a major obstacle for the successful operation of brain hypothermia resuscitation. From the viewpoint of biothermal medical engineering, the major theories and strategies for administering brain cooling can generally be classified into three categories: heat transfer, oxygen transport and cooling strategy. Aiming to provide a complete overview of the brain hypothermia resuscitation, this article comprehensively summarizes the recent progresses made in theoretical, practical and experimental techniques in the area. Particularly, attention is paid to the mathematical models to quantify the heat and oxygen transport inside the cerebral tissues. Typical cooling strategies to effectively lower brain temperature and thus decrease oxygen consumption rate in the cerebral tissues are analyzed. Approaches to deliver oxygen directly to the target tissues are discussed. Meanwhile, some future efforts worth pursuing within the area of brain cooling are suggested.

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Hypothermic retrograde jugular perfusion reduces brain damage in rats with heatstroke

Abstract: We successfully demonstrated that direct retrograde hypothermic perfusion via the jugular vein without cardiopulmonary bypass protected the brain after heat stroke. This technique cooled the brain but did not significantly interfere with body temperature.

Cited by 24 publications

References 39 publications

Resuscitation from experimental heatstroke by transplantation of human umbilical cord blood cells*

Resuscitation from experimental heatstroke by transplantation of human umbilical cord blood cells*

Human Umbilical Cord Blood-Derived Cd34+ Cells Cause Attenuation of Multiorgan Dysfunction During Experimental Heatstroke

Cooling strategies and transport theories for brain hypothermia resuscitation

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