Redistribution of Regional Blood Flow in Hypothermia

Delin, N. Anders; Kjartansson, Kjartan B.; Pollock, Lawrence; Schenk, Worthington G.

doi:10.1016/s0022-5223(19)33287-8

Cited by 24 publications

(4 citation statements)

References 6 publications

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“…In previous investigations using the same model, we measured significant reduction of renal blood both during hypothermia and immediately after rewarming (9). These findings are supported by others who report that proportionately the kidneys have the largest reduction in blood flow of all major organs during experimental hypothermia (19,20). Likewise, other reports support the idea that renal blood flow, and thus renal oxygen supply, suffer during hypothermia.…”

Section: Discussionsupporting

confidence: 88%

“…Likewise, other reports support the idea that renal blood flow, and thus renal oxygen supply, suffer during hypothermia. In a study using bloodstream cooling by arteriovenous shunts, Delin and associates (19) determined that there was a shift of blood flow away from the kidneys and towards the splanchnic bed. At 20 °C splanchnic blood flow was 40% of the normal, whereas renal blood flow had been reduced to 8 %.…”

Section: Discussionmentioning

confidence: 99%

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Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming

Tveita

Johansen

Lien

et al. 2005

APMIS

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Although renal failure may occur following rewarming from deep accidental hypothermia, this subject has received little attention in experimental hypothermia and clinical case reports. In order to explore the integrity of hypothermic and posthypothermic renal morphology we used an experimental animal model of accidental hypothermia where the heart supports the circulation throughout cooling and rewarming without accompanying cardioplegia or ischemia. Ultrastructural changes in renal tubular cells from three groups of pentobarbital anesthetized Wistar rats: 1) controls (n=6) maintained at 37 degrees C for 4 h, 2) hypothermic rats (n=6) core-cooled and maintained at 15-13 degrees C for 4 h, and 3) rewarmed rats (n=10), were studied as a sensitive indicator of renal damage. Electron micrographs (EM) from hypothermic kidneys showed rounded up mitochondria with loss of contrast. These changes were observed in several though not all of the biopsies, but they were found in all kidneys. Areas exhibiting focal tubular necrosis were seen on most EM from three of these kidneys. EM from rewarmed kidneys showed alterations of mitochondrial ultrastructure with similarities to those observed after hypothermia, but in general the changes were more prominent. Extracellular edema, intracellular edema, swelling of mitochondria, margination of chromatin, necrosis of single tubular cells, and disrupting necrotic debris into tubular lumen could be found in micrographs from 7 of the 10 kidneys examined. Rewarming from experimental hypothermia, without episodes of ischemia or hypoxia, thus induces ultrastructural changes in renal tubular cells similar to changes observed in acute tubular necrosis, associated with renal failure.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming

Tveita

Johansen

Lien

et al. 2005

APMIS

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“…As stipulated by the Arrhenius equation, the cellular metabolic rate is reduced by 50% for every 10°C decrease in temperature (23–26). The decrease in core temperature to 20°C resulted in the reduction of regional blood flow to 26% of normothermic levels (24). A recent study demonstrated that the local cooling to 2°C almost completely halted the regional blood flow to bone tissue (25).…”

Section: Discussionmentioning

confidence: 99%

“…We believe that the increase in MAP during the post-HS period may be due to the reduced blood flow to abdominal organs under the profound TRIC10 condition. As stipulated by the Arrhenius equation, the cellular metabolic rate is reduced by 50% for every 10°C decrease in temperature (23)(24)(25)(26). The decrease in core temperature to 20°C resulted in the reduction of regional blood flow to 26% of normothermic levels (24).…”

Section: The Tric Cooling Is An Improved Therapeutic Hypothermia Tech...mentioning

confidence: 99%

Intracolon Cooling Increases Survival Rate in the Rat Model of Lethal Hemorrhage

Arya,

Hu,

Chen

et al. 2023

Shock

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Background The objective of this study is to investigate whether Trans-Rectal Intra-Colon (TRIC) cooling can prolong the survival duration in a rat hemorrhagic shock (HS) model. Methods A lethal-HS was induced by bleeding 47% of the total blood volume. A TRIC device was placed into the colon to maintain the intra-colon temperature either at 37 °C (TRIC37°C) or TRIC10°C pos-HS. In the surface cooling (SC) rats, the body temperatures were maintained at the same level as the esophageal temperature of the TRIC10°C rats. A separated group of TRIC10°C rats were resuscitated (Res) at 90 minutes post-HS. A total six groups were: (i) Sham-TRIC37°C (n = 5); (ii) Sham-TRIC10°C (n = 5); (iii) HS-TRIC37°C (n = 5); (iv) HS-TRIC10°C (n = 6); (v) HS-SC (n = 6); and (vi) HS-TRIC10°C + Res (n = 6). Results An average post-HS survival time was 18.4 ± 9.4 minutes in HS TRIC37°C and 82 ± 27.82 minutes in the HS SC group. In striking contrast, the HS TRIC10°C group exhibited an average survival time of 150.2 ± 66.43 minutes. The post-HS blood potassium level rose significantly in the HS-TRIC37°C and HS-SC, whereas remained unchanged in the TRIC10°C groups. Post-HS intestinal damage occurred in HS-TRIC37°C and HS-SC groups but virtually absent in HS TRIC10°C groups. Following resuscitation at 90 min post-HS, all HS-TRIC10°C rats were fully recovered from the lethal HS. Conclusions TRIC10°C reversed the high blood potassium level, prevented the intestinal damage, and prolonged the survival duration by 6-fold relative to normothermia and by 2-fold compared to SC post-HS. All TRIC10°C rats were successfully resuscitated at 90 min post-HS.

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