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PubMed2003

Effects of rewarming on nuclear factor-kappaB and interleukin 8 expression in cold-preserved alveolar epithelial cells.

BACKGROUND: Nuclear factor-kappaB (NF-kappaB) and interleukin (IL)-8 play important roles in the pathophysiology of acute lung injury after lung transplantation. Because alveolar epithelium is one of the most important sites at which IL-8 production takes place after reperfusion of donor lungs, we examined the effects of cold/rewarming on NF-kappaB and IL-8 expression in alveolar epithelial cells. METHODS: A549 cells were preserved at 4 degrees C for 5 hr and then rewarmed for up to 20 hr. NF-kappaB was analyzed by electrophoretic mobility shift assay. IL-8 mRNA expression was examined by reverse transcription-polymerase chain reaction. IL-8 concentration in the cell culture medium after rewarming was measured by enzyme-linked immunosorbent assay. RESULTS: NF-kappaB was increased in the nuclear extracts as early as 30 min after rewarming. There was a marked increase in the IL-8 mRNA expression at 1 and 3 hr after rewarming. IL-8 concentration in the cell culture medium was progressively increased during 20 hr following rewarming. The cell culture medium inhibited apoptosis of neutrophils significantly. The cold/rewarming-induced IL-8 production was reduced to approximately 50% by introducing an antisense oligonucleotide for the p65 subunit of NF-kappaB and by treatment with N-acetyl-leucinyl-leucinyl-norleucinal and pyrrolidine dithiocarbamate. The effect of dexamethasone treatment was dose dependent (reduced to approximately 30% at 10-5 M dexamethasone). CONCLUSIONS: Our results indicate that rewarming of cold-preserved alveolar epithelial cells itself may be an important initiator of the inflammatory cascades, including NF-kappaB activation and IL-8 release. Inhibition of NF-kappaB would be worth trying to control unnecessary IL-8 production and the inflammatory response in the donor lungs.

Apoptosis↗
PubMed2002

Tissue-specific extravasation of albumin-bound Evans blue in hypothermic and rewarmed rats.

The effects of hypothermia and rewarming on endothelial integrity were examined in intestines, kidney, heart, gastrocnemius muscle, liver, spleen, and brain by measuring albumin-bound Evans blue loss from the vasculature. Ten groups of twelve rats, normothermic with no pentobarbital, normothermic sampled at 2, 3, or 4 h after pentobarbital, hypothermic to 20, 25, or 30 degrees C, and rewarmed from 20, 25, or 30 degrees C, were cooled in copper coils through which water circulated. Hypothermic rats were cooled to the desired core temperature and maintained there for 1 h; rewarmed rats were cooled to the same core temperatures, maintained there for 1 h, and then rewarmed. Following Evans blue administration, animals were euthanized with methoxyflurane, tissues removed, and Evans blue extracted. Because hypothermia and rewarming significantly decrease blood flow, organ-specific flow rates for hypothermic and rewarmed tissues were used to predict extravasation. Hypothermia decreased extravasation in tissues with continuous endothelium (brain, muscle) and increased it in tissues with discontinuous endothelium (liver, lung, spleen). All tissues exhibited significant (p < 0.05) differences from normothermic controls. These differences are attributed to a combination of anesthesia, flow, and (or) change in endothelial permeability, suggesting that appropriate choice of organ and temperature would facilitate testing pharmacological means of promoting return to normal perfusion.

Albumins↗
PubMed2006

Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?

It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats (n = 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15 degrees C, kept at 15 degrees C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by > 50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15 degrees C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments.

Animals↗
PubMed2001

Effect and feasibility of controlled rewarming after moderate hypothermia in stroke patients with malignant infarction of the middle cerebral artery.

BACKGROUND AND PURPOSE: Moderate hypothermia has been found to reduce intracranial pressure (ICP) significantly in patients who have severe middle cerebral artery infarction. However, during passive rewarming, ICP continuously rises and some patients suffer transtentorial herniation. METHODS: We investigated the question of whether slower rewarming leads to slower increase in ICP and slower decrease in cerebral perfusion pressure (CPP). Furthermore, we studied feasibility of slow, controlled rewarming. ICP, CPP, and core body temperature were monitored continuously. Achievement of rewarming protocol was assessed by hit rate of temperature target intervals. Side effects of hypothermia were assessed. RESULTS: Rates of change of both ICP and CPP were correlated significantly with increase in temperature (ICP r=0.62, P=0.002; CPP r=-0.50, P=0.017). In feasibility analysis of 13 controlled rewarmed patients, hit rate of temperature target intervals was 63% (median; range 48% to 81%); hit rate within the target interval or below was 79% (median; range 62% to 94%). CONCLUSIONS: Slow, controlled rewarming is feasible and may be used for ICP and CPP control after moderate hypothermia for space-occupying infarction.

Body Temperature↗
PubMed2002

Adequate cerebral perfusion pressure during rewarming to prevent ischemic deterioration after therapeutic hypothermia.

Ischemic deterioration during rewarming is one of the most notable clinical complications after successful therapeutic cerebral hypothermia, but the mechanism is not completely understood. Hypothermia may cause vasoconstriction and relative ischemia, especially with insufficient cerebral perfusion pressure (CPP). Various parameters were evaluated to determine the critical CPP threshold to avoid ischemia during rewarming. Cat experimental head injury was induced by inflating an epidural rubber balloon, and intracranial pressure was maintained at 30 mmHg. During rewarming after cerebral hypothermia, CPP was maintained at >120 mmHg (n = 16), 90 mmHg (n = 11), 60 mmHg (n = 11), and 40 mmHg (n=4) by controlling the blood pressure. Cerebral blood flow, cerebral metabolic rate for oxygen, arteriovenous difference of oxygen (AVDO2), cerebral venous oxygen saturation (ScvO2), and extracellular glutamate concentrations were monitored by glutamate oxidase electrode. After rewarming, the cerebral metabolic parameters were almost restored to the pre-injury level in animals with CPP of more than 90mmHg. However, in the animals with CPP= 60 mmHg, all parameters significantly deteriorated and indicated misery perfusion; ScvO2 was low (29.5+/-1.1%), AVDO2 was significantly high (9.9+/-0.8 ml 100 g(-1) min(-1)) (one-way analysis of variance, p<0.05), and electron microscopic features showed subcellular ischemic change. Extracellular glutamate significantly increased during the rewarming period only in the CPP= 40 mmHg group. CPP less than 60 mmHg during rewarming causes secondary ischemic insult, which might indicate continuation of cerebral vasoconstriction in hypothermia. CPP higher than 90 mmHg is required to avoid the potential risk of relative ischemia after hypothermia.

Animals↗
PubMed1994

Experimental hypothermia: effects of core cooling and rewarming on hemodynamics, coronary blood flow, and myocardial metabolism in dogs.

Conflicting results have been reported as to the extent that cardiovascular function can be reestablished after rewarming from hypothermia. We measured hemodynamic function, myocardial metabolism and tissue water content in dogs core-cooled to 25 degrees C and later rewarmed. At 25 degrees C left ventricular (LV) systolic pressure (LVSP) was 54% +/- 4%, maximum rate of LV pressure rise (LV dP/dtmax) 44% +/- 5%, aortic pressure (AOP) 50% +/- 6%, heart rate (HR) 40% +/- 0%, cardiac output (CO) 37% +/- 5%, myocardial blood flow (MBF) 34% +/- 5%, and myocardial oxygen consumption (MVO2) 8% +/- 1%, compared to precooling. Stroke volume (SV) and LV end-diastolic pressure (LVEDP) were unchanged. As normothermia (37 degrees C) was reestablished, the depression of cardiac function and myocardial metabolism remained the same as that at 25 degrees C: LVSP 71% +/- 6%, LV dP/dtmax 73% +/- 7%, SV 60% +/- 9%, AOP 70% +/- 6%, CO 57% +/- 9%, MBF 53% +/- 8%, and MVO2 44% +/- 8% HR, in contrast, recovered to precooling values. The arterial concentrations of glucose and free fatty acids (FFA) did not change significantly during the experimental period, whereas an increase in lactate of nonmyocardial origin appeared after rewarming. Increased myocardial contents of creatine phosphate and water were found during both hypothermia and rewarming. The present study demonstrates a persistent depression of cardiac function after hypothermia and rewarming in spite of adequate energy stores. Thus, a direct influence on myocardial contractile function by the cooling and rewarming process is suggested.

Adenosine Triphosphate↗
PubMed1997

Induction of hypercontractility in human cerebral arteries by rewarming following hypothermia: a possible role for tyrosine kinase.

Induction of hypothermia is used routinely in neurosurgical and cardiovascular operations to protect the brain from ischemic insult. However, despite a plethora of experimental evidence supporting the use of hypothermia to protect the brain from ischemia, clinical experience using deliberate hypothermia in humans has not shown a convincing benefit. The authors tested the hypothesis that hypothermia and rewarming alter tone in human cerebral vessels and may interfere with cerebral perfusion in the setting of deliberate hypothermia. They examined human cerebral arteries during hypothermia (32 degrees C and 17 degrees C) and during rewarming to delineate the direct effects of cooling and rewarming on cerebrovascular tone. Artery segments obtained from autopsy material and from specimens excised at elective temporal lobectomies were tested in tissue baths using isometric tension measurements. Temperature-induced changes in vascular tone were measured and quantified with respect to contractile responses to serotonin (5-HT; 10(-6) M). Cooling induced mild relaxation in cerebral vessels (-38 +/- 12% 5-HT response in 50 vessels from autopsy specimens, -69 +/- 10% 5-HT response in 51 vessels from lobectomy specimens). On rewarming, vessels contracted significantly beyond their baseline tone (108 +/- 18% 5-HT response in 50 vessels from autopsy specimens, 42 +/- 12% 5-HT response in 51 vessels from lobectomy specimens). Rewarming-induced hypercontractility was inhibited by the tyrosine kinase inhibitor genistein (-5 +/- 7% vs. 70 +/- 23% 5-HT response, genistein vs. control, 14 segments, p < 0.05) and enhanced by the tyrosine phosphatase inhibitor sodium orthovanadate (339 +/- 54% vs. 104 +/- 20% 5-HT response, sodium orthovanadate vs. control, five segments, p < 0.05), indicating a possible role for tyrosine kinase activation in the rewarming-induced contraction.

Aged↗
PubMed1999

Modulation of liver cell membrane NHE-1, Na+-K+ ATPase, and GLUT-2 protein content after cold preservation and rewarming.

Liver cell pH and volume regulation are perturbed by prolonged cold storage in University of Wisconsin solution and subsequent rewarming, but the molecular basis of this effect remains unknown. We prepared membranes from hepatocytes subjected to variable periods of cold preservation with or without subsequent rewarming and probed them by Western blotting with specific antibodies against the Na+ -H+ exchanger isoform NHE-1 and the Na+ -K+ ATPase alpha subunit. Results were compared with the content of GLUT-2, an abundant basolateral protein. NHE-1 decreased significantly as cold preservation times exceeded 10 h. Subsequent rewarming by short-term culture at 37 degrees C did not further reduce this parameter. On the other hand, expression of Na+ -K+ ATPase remained stable during cold storage times lasting up to 48 h, whereas rewarming resulted in a dramatic reduction in cells cold preserved beyond 10 h. In contrast, the membrane content of GLUT-2 was unaffected by cold preservation with or without subsequent rewarming. The results indicate that cold storage and rewarming respectively and selectively modulate the expression of specific hepatocellular membrane transport proteins.

Animals↗
PubMed2001

Comparison of oxygenated perfluorocarbon and humidified oxygen for rewarming hypothermic miniswine.

This study examines a method to rapidly rewarm the core using total liquid ventilation with warmed, oxygenated perfluorocarbon. Yucatan miniswine were splenectomized and surgically implanted with telemetry devices to transmit electrocardiographic response, arterial pressure, and core temperature. Hypothermia (core temperature = 25.9 +/- 1.3 degrees C) was induced by placing cold-water circulating blankets over the animals. Control animals (N = 7) were rewarmed using warm (37.8 degrees C), humidified oxygen. Experimental animals (N = 6) were rewarmed with oxygenated perfluorocarbon liquid (37.3 degrees C). The time to rewarm was significantly shorter in experimental animals (1.98 +/- 0.5 vs. 8.61 +/- 1.6 hours, p < 0.0001), with almost no afterdrop in the experimental group. Lactate dehydrogenase and aspartate aminotransferase were significantly increased in the control animals compared with the experimental animals. All animals that survived being chilled to 25 degrees C survived rewarming. This method may provide a means of more rapidly rewarming profoundly hypothermic victims while reducing the risks associated with current methods.

Animals↗
PubMed1989

Postoperative ventilatory and circulatory effects of extended rewarming during cardiopulmonary bypass.

Postoperative effects of extended rewarming (ECR) after hypothermic cardiopulmonary bypass (CPB) were studied. All (n = 28) patients were rewarmed to a nasopharyngeal temperature exceeding 38 degrees C before terminating CPB. In 12 patients (control group) the rectal temperature (Tre) was 33.8 +/- 1.7 degrees C (mean +/- sd) at termination of CPB. In sixteen patients (ECR group) rewarming during CPB was continued to a Tre of 36.8 +/- 0.5 degrees C. Postoperative body temperatures, heat content, shivering, oxygen uptake, CO2 production and haemodynamic variables were measured. ECR reduced the heat gain required to complete core rewarming to 665 +/- 260 kJ, compared with 1037 +/- 374 kJ in the control group (p less than 0.01). The incidence of shivering was reduced (p less than 0.05) as well as shivering intensity and duration. In seven non-shivering ECR group patients this coincided with significantly reduced metabolic and ventilatory demands but these improvements were not valid for the group as a whole. The required ventilation temporarily during postoperative rewarming in both groups increased to 250 per cent of the basal need. Extending CPB rewarming (to at least 36 degrees C Tre) was inefficient when used as the sole measure to reduce the untoward effects of residual hypothermia during recovery after cardiac surgery with hypothermic CPB.

Adult↗
PubMed1994

Effects of cooling and rewarming on the meiotic spindle and chromosomes of in vitro-matured bovine oocytes.

The purpose of this study was to evaluate effects of cooling and rewarming on the meiotic spindle apparatus of bovine oocytes. In experiment 1, in vitro-matured bovine oocytes were either maintained at 39 degrees C or cooled abruptly to 4 degrees C or approximately 25 degrees C. Immunohistochemical and DNA staining for visualization of microtubules and chromosomes, respectively, revealed an anastral, barrel-shaped spindle in bovine oocytes. Exposure to 4 degrees C for 10-20 min caused complete disappearance of the spindle. Some chromosome dispersion occurred after 60 min at 4 degrees C. After exposure to approximately 25 degrees C for 30 min, 90% of oocytes appeared abnormal, having either an abnormal spindle or no spindle. In experiment 2, oocytes cooled to either approximately 25 degrees C or 4 degrees C for 30 min were rewarmed directly or in steps for 15 or 60 min. Spindles did not return to normal in most oocytes regardless of cooling temperature or rewarming scheme. Step-wise rewarming was no more beneficial than direct rewarming. More of the oocytes rewarmed directly contained dispersed chromosomes as time at 39 degrees C increased.

Animals↗
PubMed1994

The effect of head covering on rewarming and shivering in cardiac surgical patients.

In hypothermic postoperative cardiac surgical patients, heat loss from the head may interfere with rewarming and cause shivering. This study investigated the effect of head covering on rewarming rate and shivering during post-operative rewarming. The sample included 19 experimental and 21 control subjects. The heads of experimental subjects were wrapped with two terry cloth towels until urinary bladder temperature (UBT) reached 37 degrees C. Admission UBTs were mildly hypothermic (34.6 degrees C to 36.70 C). Four experimental and six control subjects shivered. There were no significant differences (P < .05) in the incidence of shivering (Yates' chi 2 = 0.33; P = 0.855). After controlling significant differences between groups in height and body surface area with analysis of covariance, there were no significant differences in rewarming rate (F = 3.270; P = .079). Shiverers were slightly colder (mean, 36.13 degrees C; t = 1.768; P = .085) on admission to the cardiac surgical intensive care unit and had significantly greater heat gain (t = -2.091, P = .043) than nonshiverers. Conclusions about the effect of head covering on shivering could not be made because of small sample size. Failure to demonstrate a significant difference in rewarming rate is due to the effects of mildly hypothermic admission UBTs on the mathematical calculation of rewarming rate and on the small sample size.

Aged↗
PubMed1998

Continuous venovenous rewarming: results from a juvenile animal model.

OBJECTIVE: To compare a standard and an experimental method of rewarming in 5-wk-old goats with induced moderate hypothermia. DESIGN: Hypothermia was induced in ten juvenile Nubian goats. Five goats were randomly assigned to be rewarmed using standard techniques, and five were assigned to the experimental rewarming technique of a modified continuous venovenous hemofiltration circuit. SETTING: Animal research facility, Greenville Hospital System/Clemson University Biomedical Cooperative, Clemson, S.C. SUBJECTS: Ten 5-wk-old goats. INTERVENTIONS: Hypothermia to a body temperature of 29.4 degrees C was induced in the goats. Each of the control group of five goats was rewarmed using standard methods. Each of the experimental group of five goats was rewarmed using a modified continuous venovenous hemofiltration circuit. MEASUREMENTS AND MAIN RESULTS: At 2 hrs, the median temperature increase in the experimental group was 6.5 degrees C, compared with an increase of only 1.5 degrees C in the control group (p=.02). The mean increase in core body temperature over time (from baseline to 150 mins) was also significantly greater in the experimental group (p=.006). CONCLUSIONS: The use of a modified continuous venovenous hemofiltration circuit for rewarming in a juvenile goat model after induction of moderate hypothermia is more effective than are standard methods.

Age Factors↗
PubMed1994

Protective effect of preservation of canine pancreas by the two-layer (University of Wisconsin solution/perfluorochemical) method against rewarming ischemic injury during implantation.

Rewarming ischemia during implantation severely compromises posttransplant pancreas graft survival because the graft has already been subjected to warm and cold ischemia before implantation. The purpose of this study was to examine whether preservation of the pancreas graft by the two-layer method ameliorates rewarming ischemic injury of the graft during implantation using a canine model. After flushing with cold University of Wisconsin solution (UW), the pancreas grafts were preserved by the two-layer (UW/perfluorochemical [PFC]) method (group 1) or simple cold storage in UW (group 2) for 24 hr and then autotransplanted. In control, the pancreas grafts were flushed out with cold UW and immediately autotransplanted without preservation (group 3). After completion of vascular anastomosis, vascular clamp was not released until 90, 120, or 150 min of rewarming ischemia, including anastomosis time, had elapsed. After 90 min of rewarming ischemia, graft survival rates were 5/5, 100%, 5/5, 100%, and 5/5, 100%, in groups 1, 2, and 3, respectively. After 120 min, all the grafts in groups 2 and 3 failed (0/5, 0%, and 0/5, 0%, respectively); however, all the grafts in group 1 survived (5/5, 100%). Even after 150 min, 1 of 3 grafts in group 1 survived (1/3, 33%). After 24 hr preservation, tissue ATP levels of the grafts in group 1 were about 2-fold the reference values before harvesting (8.23 +/- 0.72 vs. 4.44 +/- 0.49 mumol/g dry weight, P < 0.05) and significantly higher compared with group 2 (8.23 +/- 0.72 vs. 1.76 +/- 0.52 mumol/g dry weight, P < 0.01). After 120 min of rewarming ischemia, tissue ATP levels in group 1 were 84% of the reference values and significantly higher compared with group 2 (3.75 +/- 0.25 vs. 1.57 +/- 0.48 mumol/g dry weight, P < 0.05). Two hours after reperfusion, ATP levels in group 1 were 42% of reference values but significantly higher compared with group 2 (1.86 +/- 0.36 vs. 1.03 +/- 0.18 mumol/g dry weight, P < 0.05). We conclude that the two-layer (UW/PFC) method ameliorates rewarming ischemic injury of the pancreas graft during implantation by increasing tissue ATP contents during preservation and consequently maintaining tissue ATP levels during implantation.

Adenosine↗
PubMed2001

Apoptosis versus necrosis during cold storage and rewarming of human renal proximal tubular cells.

BACKGROUND: A recent clinical study demonstrated that in renal allografts preserved in the cold apoptosis occurred soon after reperfusion. The mode of cell death during cold storage is generally considered necrotic. Whether apoptosis occurs as a part of cold storage is uncertain. The objective was to determine in human renal tubular cells whether apoptosis is specific for rewarming or it also occurs during cold storage and whether it could be modified. METHODS AND RESULTS: Cold storage (4 degrees C) of primary human renal proximal tubular epithelial (RPTE) in University of Wisconsin (UW) solution up to 48 hr caused a time-dependent increase in cell death measured by lactic dehydrogenase (LDH) release and vital dye exclusion methods. Transmission electron microscopy (TEM) demonstrated that cell death in the cold was necrotic, involving considerable mitochondrial disruption, and was not apoptotic. The TUNEL assay that provides a specific, quantitative measure for apoptosis showed no increase in TUNEL-positivity during flow cytometry of cells stored in cold: 37 degrees C, 0.23+/-0.14%; 24 hr cold, 0.23+/-0.1%; 48 hr cold, 1.79+/-0.58%. Annexin-V staining, a sensitive method for detecting early apoptosis, similarly showed no increase in positively stained cells during cold storage. Addition of antioxidants 2-methyl aminochroman and deferoxamine to UW solution inhibited necrotic cell death and preserved mitochondrial structure. In contrast to cold storage alone, rewarming (37 degrees C for 24 hr) of cold stored cells, however, resulted in significant apoptosis (TUNEL positive: 48 hr cold: 2+/-0.6%, 48 hr cold and 24 hr rewarming: 54+/-17%), which was confirmed by the TEM based on typical apoptotic features. Addition of 2-MAC and DFO significantly inhibited rewarming-induced apoptotic cell death (plus 2-MAC: 3+/-1%, plus DFO: 3+/-2%). CONCLUSION: Our study in human tubular cells provides evidence that cold storage per se does not result in apoptosis, but is primarily necrotic. However, rewarming is associated with significant apoptosis in the presence of ongoing necrosis, speculatively due to the activation of the apoptotic enzymic process of sublethally injured cells. Inclusion of antioxidants in the storage solution confers protection against both cold storage and rewarming-induced necrosis and apoptosis.

Adenosine↗
PubMed1967

Survival of Plant Tissue at Super-Low Temperature VI. Effects of Cooling and Rewarming Rates on Survival.

The survival rates of the cortical parenchymal cells of mulberry tree were determined as a function of cooling and rewarming rates. When cooling was carried out slowly at 1 degrees to 15 degrees per minute, all of the cells still remained viable even when rewarmed either rapidly or slowly. Survival rates gradually decreased to zero as the cooling rate increased from about 15 degrees to 2000 degrees per minute. In the intermediate cooling rates, when the cells were cooled at the rates lower than 14 degrees per minute, from -2.2 degrees to about -10 degrees , these cells could survive subsequent rapid cooling and rewarming.However, at cooling rates above 1000 degrees per minute and with rapid rewarming, the effect of cooling rate reversed and survival increased, reaching a maximum at about 200,000 degrees per minute. As the cooling rate increased above 15 degrees per minute, survival rates became increasingly dependent on the rewarming rate, with rapid rewarming becoming less deleterious than slow rewarming.The temperature range at which damage occurred during rewarming following removal from liquid nitrogen and in which growth rate of ice crystallization was greatest, was -30 degrees to -40 degrees . The survival rates even in the prefrozen cells at -30 degrees decreased considerably by keeping them at -30 degrees for 10 minutes after removal from liquid nitrogen. This fact indicates that intracellular freezable water remains to some degree even in the prefrozen cells at -30 degrees . After removal from liquid nitrogen, all cells retained their viability, when they were passed rapidly through a temperature range between -50 degrees and -2.5 degrees within about 2 seconds, namely at the rates greater than 1000 degrees per minute.These observations are explained in terms of the size of the crystals formed within the cortical cells.

Journal Article↗
PubMed1999

Coronary endothelium-derived vasodilation during cooling and rewarming of the in situ heart.

The integrity of coronary vascular endothelial vasodilator function during core cooling and rewarming was investigated in a pentobarbital-anesthetized open-chest dog model. Vasodilator response was assessed as the change from baseline blood flow by injecting the endothelial-dependent vasodilator acetylcholine (ACh) (1.0 microg) or the endothelial-independent vasodilator nitroglycerin (NTG) (50 microg) into the left anterior descending (LAD) coronary artery. Change in blood flow was measured using a transit time ultrasonic volume flowmeter technique. During cooling and rewarming LAD blood flow was significantly decreased. After rewarming, aortic pressure was artificially elevated to reach control. This procedure restored heart work (LV-RPP, left ventricular rate pressure product) and coronary perfusion pressure, but LAD blood flow remained lowered. Ability to dilate the vascular bed supplied by LAD, after injections of ACh or NTG, was present both during cooling and rewarming. At 25 degrees C coronary blood flow (LAD) increased from 3 +/- 1 to 9 +/- 1 mL x min(-1) in response to both ACh and NTG. Posthypothermic blood flow increased from 7 +/- 1 to 19 +/- 2 and 20 +/- 3 mL x min(-1) in response to ACh and NTG, respectively. Measured as the percent change from baseline LAD blood flow, the response was not significantly different from the one obtained in prehypothermic hearts. In conclusion, coronary vasodilator function, both endothelium dependent and endothelium independent, is present but not maintained at the same level during cooling to 25 degrees C and rewarming. In spite of the deterioration of cardiac function, no selective defect in the endothelium-dependent response was detected, either during hypothermia or after rewarming.

Acetylcholine↗
PubMed1985

Peripheral blood flow during rewarming from mild hypothermia in humans.

During the initial stages of rewarming from hypothermia, there is a continued cooling of the core, or after-drop in temperature, that has been attributed to the return of cold blood due to peripheral vasodilatation, thus causing a further decrease of deep body temperature. To examine this possibility more carefully, subjects were immersed in cold water (17 degrees C), and then rewarmed from a mildly hypothermic state in a warm bath (40 degrees C). Measurements of hand blood flow were made by calorimetry and of forearm, calf, and foot blood flows by straingauge venous occlusion plethysmography at rest (Ta = 22 degrees C) and during rewarming. There was a small increase in skin blood flow during the falling phase of core temperature upon rewarming in the warm bath, but none in foot blood flow upon rewarming at room air, suggesting that skin blood flow seems to contribute to the after-drop, but only minimally. Limb blood flow changes during this phase suggest that a small muscle blood flow could also have contributed to the after-drop. It was concluded that the after-drop of core temperature during rewarming from mild hypothermia does not result from a large vasodilatation in the superficial parts of the periphery, as postulated. The possible contribution of mechanisms of heat conduction, heat convection, and cessation of shivering thermogenesis were discussed.

Adult↗