Some Physiologic Effects of Short- And Long-Term Hypothermia Upon the Liver

Fisher, BM; Fedor, E. J.; Lee, S. H.; Weitzel, W.; Selker, Robert G.; Russ, Clem

doi:10.1097/00132586-195704000-00033

Cited by 6 publications

(8 citation statements)

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“…To date, the mechanism for the protective effects of hepatic hypothermia has been attributed to reduced metabolism and oxygen consumption. Early studies showed that total body cooling to a rectal temperature as low as 23°C for up to 12 h does not adversely affect liver function (10). Subsequently, it was shown that extracorporeal cooling of the liver to 25°C resulted in a 36% reduction in the oxygen consumption by the liver (22).…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of hypothermic protection against ischemic liver injury in mice

Kato¹,

Singh

McLeish

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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Mechanisms of hypothermic protection against ischemic liver injury in mice. Am J Physiol Gastrointest Liver Physiol 282: G608-G616, 2002. 10.1152/ajpgi.00454.2001.-Hepatic hypothermia can safely prolong the duration of hepatic inflow occlusion during complex liver resectional surgeries. The mechanism(s) by which hypothermia protects against this form of liver ischemia-reperfusion injury are not completely understood. In this study, we sought to determine whether hypothermia protects against ischemia-reperfusion injury by altering the hepatic inflammatory response. Mice undergoing 90 min of partial hepatic ischemia followed by up to 8 h of reperfusion had their body temperatures regulated at 35-37°C (normothermic) or unregulated, in which rectal temperature dropped as low as 25°C by the end of ischemia (hypothermic). Hypothermic mice had less liver injury vs. normothermic mice, as assessed histologically, by serum transaminase levels (89% decrease), and by liver wet-to-dry weight ratios (91% decrease). Neutrophil accumulation was absent in hypothermic mice (99% reduction vs. normothermic mice). Production of the proinflammatory cytokines tumor necrosis factor-␣, interleukin-1␤, and macrophage inflammatory protein-2 were reduced by up to 92%. Activation of the transcription factor nuclear factor-B was not reduced in hypothermic mice, but activation of c-Jun NH 2-terminal kinase (JNK) and the transcription factor activator protein (AP)-1 were greatly diminished. These data suggest that hypothermia suppresses the hepatic inflammatory response through selective inhibition of JNK and AP-1.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of hypothermic protection against ischemic liver injury in mice

Kato¹,

Singh

McLeish

et al. 2002

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…7 Additionally, surface cooling procedures are complicated by the phenomenon of rewarming afterdrop 8 and may cause cerebral swelling during the rewarming period. 9 Equally limiting have been the deleterious side effects associated with total body hypothermia, including cardiac arrhythmias, 10 -12 coagulopathy, 13,14 hemolysis, 15 renal and hepatic dysfunction, 16,17 and immunosuppression. 18 -20 To avoid the systemic complications of total body cooling, investigators have attempted selective cerebral hypothermia.…”

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confidence: 99%

Ultrarapid, Convection-Enhanced Intravascular Hypothermia

Mack

Huang

Winfree

et al. 2003

Stroke

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Background and Purpose-Hypothermia has been shown to be neuroprotective in a variety of clinical settings.Unfortunately, poor delivery techniques and insufficient data in appropriate preclinical models have hampered its development in human stroke. To address these limitations, we have devised a 10F intravascular catheter capable of rapid systemic cooling of nonhuman primates. Methods-Placed in the inferior vena cava via a transfemoral approach, the catheter was used to induce mild systemic hypothermia 3 hours after the onset of hemispheric stroke in baboons. Results-Cooling was achieved at a rate of 6.3Ϯ0.8°C/h. Target brain temperatures (32.2Ϯ0.2°C) were reached at the same time (47.7Ϯ6.32 minutes) as target esophageal temperatures (32.0Ϯ0.0°C). Hypothermia was maintained for 6 hours in all animals. Animals did not experience the infections, coagulopathy, or cerebral edema commonly seen with surface cooling methods in human stroke. Conclusions-These data suggest that a brief episode of mild core hypothermia instituted at a clinically relevant time point can be achieved in primate stroke and that our intravascular cooling technique provides safe, rapid, and reproducible hypothermia. (Stroke.

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“…Hypothermia leads to restricted hepatic circulation (Brauer, Holloway, Krebs, Leong & Carrol, 1954;Fisher, Fedor, Lee, Weitzel, Selker & Rus, 1956;Halett, 1954;Petter, 1963;Wangensteen, Rahood, Luke & Healy, 1961) but its effect on the portal venous flow is not clear (Hinburger, Teramoto & Shoemaker, 1960;Wangensteen et al, 1961). The purpose of our investigation was to study the local effect of variations in temperature on hepatic arterial, portal venous and total hepatic flow in the isolated perfused dog liver.…”

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confidence: 99%

“…Methods.-The isolated liver of the dog was perfused with modified Tyrode solution (pH=7-35±0 15) gassed with 95% oxygen and 5% carbon dioxide (Geumei & Mahfouz, 1968;Geumei, Issa & Mahfouz, 1969 (Fisher et al, 1956;Halett, 1954), while others found that it is greater than the diminution of cardiac output (Brauer et al, 1954;Teramoto & Shoemaker, 1962). Grimes & Lewis (1963) found that cooling causes increased mesenteric resistance most of which is due to arterial constriction.…”

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confidence: 99%