Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Rewarming”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,117 records · Page 62Linked to original sources
PubMed1994

Effects of cardiopulmonary bypass on gut blood flow, oxygen utilization, and intramucosal pH.

Studies documenting rises in endotoxin after cardiopulmonary bypass (CPB) have postulated gut mucosal hypoperfusion. We have investigated alterations in jejunal blood flow by laser Doppler flow measurement, intramucosal pH (pHi) by tonometry, and oxygen utilization in a canine model of hypothermic CPB (n = 11 dogs). After 10 minutes of hypothermic CPB, despite no major reduction in superior mesenteric artery flow, mucosal laser Doppler flow decreased to -38.2% +/- 9.3% of levels obtained before bypass (p = 0.008) and serosal laser Doppler flow, to -47.3% +/- 11.4% (p = 0.006). During the hypothermic phase, mesenteric oxygen consumption fell from 0.18 +/- 0.01 to 0.098 +/- 0.01 mL.min-1.kg-1 (p = 0.005), and mesenteric oxygen delivery fell from 1.97 +/- 0.39 to 1.14 +/- 0.12 mL.min-1.kg-1 (p = 0.05). There was no change in jejunal pHi. During the rewarming phase, there was a substantial increase in mucosal laser Doppler flow, peaking at +69.8% +/- 15.2% (p = 0.03), whereas serosal laser Doppler flow returned to values seen prior to CPB (-16.4% +/- 21.5%; p = 0.25). These changes coincided with a surge in oxygen consumption (0.33 +/- 0.042 mL.min-1.kg-1; p = 0.009), while mesenteric oxygen delivery remained depressed at 1.09 +/- 0.12 mL.min-1.kg-1 (p = 0.04). Jejunal pHi fell from a value of 7.36 +/- 0.04 before CPB to 7.12 +/- 0.07 (p = 0.02), thus indicating mucosal hypoxia. During the rewarming phase of hypothermic CPB, there is a disparity between mesenteric oxygen consumption and oxygen delivery with villus tip ischemia; these findings may explain the pathophysiology of endotoxemia during CPB.

Animals↗
PubMed1995

Retrograde cerebral perfusion during profound hypothermia and circulatory arrest in pigs.

The purpose of this study was to evaluate the use of retrograde cerebral perfusion via the superior vena cava during profound hypothermia and circulatory arrest (CA) in pigs. In three groups of 5 pigs each, group A (control) underwent cardiopulmonary bypass and normothermic CA for 1 hour, group B underwent cardiopulmonary bypass, profound hypothermia, and CA (15 degrees C nasopharyngeal) for 1 hour, and group C underwent the same procedure as group B plus retrograde cerebral perfusion. In group A none awoke. In group B, 2 of 5 did not awake and 3 of 5 awoke unable to stand, 2 with perceptive hind limb movement and 1 moving all extremities. In group C all awoke, 4 of 5 able to stand and 1 of 5 unable to stand but moving all limbs. In neurologic evaluation group B had significantly lower Tarlov scores than group C (p = 0.0090). Group B mean wake-up time, plus or minus standard error of the mean, was 124.6 +/- 4.6 minutes versus 29.2 +/- 5.1 in group C (p = 0.0090). In group B late phase CA cerebral blood flow dropped 30.9% +/- 4.8%, but in group C it rose 24.7% +/- 9.3% (p = 0.0007, pooled variance t test, two-tailed). In group B late phase CA brain oxygenation decreased 46.0% +/- 13.9% but it increased 26.1% +/- 5.4% in group C (p = 0.0013). This difference was reduced somewhat during rewarming (B, -21.2% +/- 14.9%; C, 16.4% +/- 4.7%; p = 0.043). Group B rewarming jugular venous O2 saturation was 30.8% +/- 2.5% versus 56.0% +/- 4.4% in group C (p = 0.0011). We conclude that in pigs retrograde cerebral perfusion combined with profound hypothermia during CA significantly reduces neurologic dysfunction, providing superior brain protection.

Animals↗
PubMed1996

Beneficial effects of myocyte preconditioning on contractile processes after cardioplegic arrest.

BACKGROUND: Myocardial precondition, which can be achieved through short intervals of ischemia or hypoxia followed by reperfusion, protects the myocardium with subsequent prolonged periods of ischemia. Accordingly, the present study tested the hypothesis that hypoxic preconditioning before cardioplegic arrest would have direct and beneficial effects on myocyte contractile processes with reperfusion. METHODS: Left ventricular porcine myocytes (n = 335) were randomly assigned to one of three treatments: normothermia, maintained in cell media (37 degrees C, 2 hours); cardioplegia, hyperkalemic arrest (24 mEq K+, 4 degrees C, 2 hours) followed by normothermic reperfusion; preconditioning, hypoxia (20 minutes) and reperfusion (20 minutes), and then followed by cardioplegic arrest and rewarming. Myocyte velocity of shortening was measured using computer-assisted videomicroscopy at baseline and with beta-adrenergic receptor stimulation with isoproterenol (25 nmol/L). RESULTS: In the cardioplegia group, myocyte function was reduced at baseline (22 +/- 1 versus 57 +/- 2 microns/s) and with beta-adrenergic receptor stimulation (81 +/- 5 versus 156 +/- 7 microns/s) compared to normothermic controls (p < 0.05). Preconditioning improved myocyte function at baseline (38 +/- 2 microns/s) and with beta-adrenergic receptor stimulation (130 +/- 6 microns/s) compared to the cardioplegic alone group (p < 0.05). CONCLUSIONS: The important findings from this study are twofold. First, preconditioning can be induced directly at the level of the myocyte, independent of nonmyocyte populations and extracellular influences. Second, myocyte preconditioning provides protective effects on myocyte function and beta-adrenergic responsiveness after cardioplegic arrest and rewarming. These findings suggest that preconditioning may provide a novel approach in protecting myocyte contractile processes during cardioplegic arrest.

Adaptation, Physiological↗
PubMed1975

Effects of low temperatures on microtubules in the non-myelinated axons of post-ganglionic sympathetic nerves.

The effect of temperature changes on the number of microtubules in non-myelinated axons has been studied in cat inferior mesenteric ganglion/hypogastric nerve preparations incubated at various temperatures in Eagles minimal essential tissue culture medium in vitro. At 37 degrees C the non-myelinated axons contained 28.4 plus or minus 0.8 S.E.M. (54) microtubules per axon. After incubation at 0 degrees C for 4 h this number fell to 2.3 plus or minus 0.1 S.E.M. (41) but returned to normal levels when the nerves were rewarmed. This loss of microtubules on cooling the nerves and their reappearance on rewarming was a rapid process; it was independent of the influence of the nueronal cell body and of protein synthesis within the axon. The preservation of the microtubules was improved when D2O was present in the incubation medium. Reformed microtubules appeared to function normally with respect to their possible role in the transport of noradrenaline storage vesicles along the axons.

Animals↗
PubMed1993

Regional cerebral blood flow following hypothermic circulatory arrest in newborn dogs.

A model of hypothermic circulatory arrest has been developed in newborn dogs which simulates the procedure used for the operative repair of congenital cardiac defects in human infants. Hypothermic circulatory arrest for 1.0 h causes no brain damage, whereas cardiac arrest for 1.75 h results in damage of the cerebral cortex, basal ganglia and to a lesser extent the claustrum and amygdaloid nucleus. In the present study, we determined regional cerebral blood flow (rCBF) during 24 h of recovery from hypothermic circulatory arrest. Newborn nitrous oxide anesthetized and artificially ventilated dogs were cooled to 20 degrees C and subjected to cardiac arrest by the i.v. injection of KCl for either 1.0 or 1.75 h. Thereafter, animals were resuscitated, rewarmed to 37 degrees C, and rCBF measured with [14C]iodoantipyrine at either 2 or 18 h of recovery. Control animals were rendered hypothermic to 20 degrees C without cardiac arrest for 1.0 or 1.75 h prior to rewarming. No alterations in CBF at either 2 or 18 h of recovery were present in any of 16 analyzed structures in animals previously subjected to hypothermic circulatory arrest compared to controls rendered hypothermic alone. A direct linear correlation existed between mean arterial blood pressure and blood flow within frontal, parietal and occipital cortex, occipital white matter, hypothalamus and cerebellar vermis in puppies arrested for 1.75 h and recovered for 2 h, suggesting a loss of CBF autoregulation at this interval. No such association between blood pressure and CBF was apparent at 18 h of recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The influence of temperature on the function of renal cortical slices frozen in various cryoprotectants.

Renal cortical slices were frozen to various subzero temperatures after treatment with 2.1 M of one of three cryoprotectants, dimethyl sulfoxide (Me2SO), ethylene glycol, or glycerol. The effects on tissue [K+]/[Na+] of cooling to these temperatures were tested (using identical procedure times, cooling rates, and warming rates) by holding the slices at each experimental temperature for appropriate periods of time prior to rewarming. The effects of the holding time were assessed by comparison with slices which were cooled and rewarmed with no intermediate holding time. Slices treated with ethylene glycol or glycerol were found to exhibit a continuous decrease in [K+]/[Na+] with lowered temperatures, in contrast to those treated with Me2SO. Slices treated with Me2SO actually experienced a continuous increase in [K+]/[Na+] with lowered temperature (-12 to -33 degrees C). Me2SO does exhibit toxic effects at subzero temperatures. Adverse effects of holding time on viability are seen for Me2SO-treated slices at higher subzero temperatures. These effects were alleviated as the temperature is reduced, suggesting that temperature has a greater effect on survival of renal cortical tissue than Me2SO concentration. However, the toxicity observed at higher subzero temperatures is expected to be of importance, particularly for slowly cooled tissues which are exposed to these temperatures for relatively long periods of time.

Animals↗
PubMed1986

Glass-forming tendency and stability of the amorphous state in the aqueous solutions of linear polyalcohols with four carbons. I. Binary systems water-polyalcohol.

All the aqueous solutions of linear saturated polyalcohols with four carbons have been investigated at low temperature. Only ice has been observed in the solutions of 1,3-butanediol and 1,2,3- and 1,2,4-butanetriol. For same solute concentration, the glass-forming tendency on cooling is highest with 2,3-butanediol, where it is comparable to that with 1,2-propanediol, the best solute reported to date. However, the quantity of ice and hydrate crystallized is particularly high on slow cooling or on subsequent rewarming. The highest stability of the amorphous state is observed on rewarming the 1,2-butanediol and 1,3-butanediol solutions. With respect to this property, these compounds come just after 1,2-propanediol and before all the other compounds studied so far. They are followed by dimethylsulfoxide and 1,2,3-butanetriol. The glass-forming tendency of the 1,3-butanediol solutions is also very high; it is third only to that of 1,2-propanediol and 2,3-butanediol. The glass-forming tendency is a little smaller with 1,2-butanediol, but it is cubic instead of ordinary hexagonal ice which crystallizes on cooling rapidly with 35% 1,2-butanediol. Cubic ice is thought to be innocuous. A gigantic glass transition is observed with 45% of this strange solute. 1,4-Butanediol, 45% also favors cubic ice greatly. Therefore, 1,2- and 1,3-butanediol with comparable physical properties are perhaps as interesting as 1,2-propanediol for cryopreservation of cells or organs by complete vitrification. Together with 1,2-propanediol, 1,2- and 1,3-butanetriol, 1,2,3-butanetriol, and perhaps 2,3-butanediol provide an interesting battery of solutions for cryopreservation by vitrification.

Alcohols↗
PubMed1988

Cryoprotection of red blood cells by 1,3-butanediol and 2,3-butanediol.

1,3-Butanediol and 2,3-butanediol have been used in buffered solutions with 20, 30, or 35% (w/w) alcohol to cool erythrocytes to -196 degrees C at different cooling rates between 1 to 3500 degrees C/min, followed by slow or rapid rewarming. 1,3-butanediol shows the same shapes of red blood cell survival curves as 1,2-propanediol. Having nearly the same physical properties, they have comparable effects on cell survival. The classical maximum of survival for intermediate cooling rates and an increase for the highest cooling rates are observed. This increase seems to be correlated with the glass-forming tendency of the solution. After the fastest cooling rates, a warming rate of 5000 degrees C/min is sufficient to avoid cell damage, but a warming rate of 100-200 degrees C/min is not. Yet both of these rates would be insufficient to avoid the intracellular ice crystallization on warming. The damage on warming after fast cooling seems once again to be correlated with the transition from cubic to hexagonal ice. For all our results, 1,3-butanediol is like a "second" 1,2-propanediol and could be useful as a cryoprotectant for preservation by total vitrification. 2,3-Butanediol always gives extremely low survival rates, though it presents good physical properties. The crystallization of its hydrate seems to be lethal on cooling or on rewarming.

Blood Preservation↗
PubMed1989

An evaluation of the ability of the peripheral vasodilator buflomedil to improve vascular patency after acute frostbite.

The extent of microvascular damage from frostbite can be accurately demonstrated by vascular microcorrosion casting techniques (P. S. Daum, W. D. Bowers, Jr., J. Tejada, and M. P. Hamlet, Cryobiology 24, 65-73, 1987). In the present investigation, the peripheral vasodilator buflomedil was evaluated for its ability to ameliorate microcirculatory damage from acute experimentally induced freeze injury. This drug has been reported to decrease tissue loss in human frostbite patients when given intravenously during thawing (J. Foray, P. E. Baisse, J. P. Mont, and Cl. Cahen, Sem. Hop. Paris 56, 490-497, 1980). In seven groups of anesthetized rats, left hindpaws were cooled to heat of fusion; cooling continued until the temperature in the footpads fell to -15 degrees C. Prior to cooling, group 1 received a tail vein injection of 1 ml saline/kg, while group 2 received 10 mg buflomedil/kg. Immediately following cooling, group 3 received an injection of 10 mg buflomedil/kg. Hindpaws were rapidly rewarmed in a 40 degree C bath. During rewarming, left hindpaws from group 4 were immersed in deionized water, from group 5 in 24 mg buflomedil in deionized water, from group 6 in 30% dimethyl sulfoxide (Me2SO), and from group 7 in 24 mg buflomedil in 30% Me2SO. Right hindpaws served as controls. Vascular microcorrosion casts were made from left and right hindpaws of all groups. There was no significant difference in mean cast weights when frozen hindpaws of the seven groups were compared, although treatment with buflomedil increased the mean cast weight of control hindpaws from groups 3 and 7. It therefore appears that, in this acute model for frostbite, buflomedil does not improve vascular patency.

Animals↗
PubMed1991

Effect of polyethylene glycol on lipid peroxidation in cold-stored rat hepatocytes.

A mechanism suggested to cause injury to preserved organs is the generation of oxygen free radicals either during the cold-storage period or after transplantation (reperfusion). Oxygen free radicals can cause peroxidation of lipids and alter the structural and functional properties of the cell membranes. Methods to suppress generation of oxygen free radicals of suppression of lipid peroxidation may lead to improved methods of organ preservation. In this study we determined how cold storage of rat hepatocytes affected lipid peroxidation by measuring thiobarbituric acid reactive products (malondialdehyde, MDA). Hepatocytes were stored in the UW solution +/- glutathione (GSH) or +/- polyethylene glycol (PEG) for up to 96 h and rewarmed (resuspended in a physiologically balanced saline solution and incubated at 37 degrees C under an atmosphere of oxygen) after each day of storage. Hepatocytes rewarmed after storage in the UW solution not containing PEG or GSH showed a nearly linear increase in MDA production with time of storage and contained 1.618 +/- 0.731 nmol MDA/mg protein after 96 h. When the storage solution contained PEG and GSH there was no significant increase in MDA production after up to 72 h of storage and at 96 h MDA was 0.827 +/- 0.564 nmol/mg protein. When freshly isolated hepatocytes were incubated (37 degrees C) in the presence of iron (160 microM) MDA formation was maximally stimulated (3.314 +/- 0.941 nmol/mg protein). When hepatocytes were stored in the presence of PEG there was a decrease in the capability of iron to maximally stimulate lipid peroxidation. The decrease in iron-stimulated MDA production was dependent upon the time of storage in PEG (1.773 nmol/mg protein at 24 h and 0.752 nmol/mg protein at 48 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effects of hypothermia on the cat brain-stem auditory evoked response.

Effects of systemic hypothermia on the brain-stem auditory evoked responses (BAERs) in 4 pentobarbital anesthetized adult cats placed on total cardiopulmonary bypass were investigated. Hypothermia was achieved by slowly cooling the bypass blood through a heat exchanger. Serial BAERs were recorded at 2 min intervals as brain temperature was lowered from 37 to 22 degrees C and then rewarmed over a 1-2 h period. Temperatures were recorded from the brain, esophagus and rectum. Three effects were produced by controlled systemic hypothermia. First, latencies of each component wave (I-V) of the BAER increased exponentially as brain temperature was lowered to 19 degrees C. Latencies of earlier waves (I-III) increased less than those of the later waves (IV-V). Arrhenius plots of inverse latency (rate) versus reciprocal of the absolute temperature generated a family of straight lines of similar slope for each of the 5 component waves of the BAER. The activation energy for each of the 5 BAER waves was derived from the slope of the Arrhenius plot. The mean and standard deviation of the activation energy of all 5 waves was 9.7 +/- 0.5 kcal/mole degree C. The fact that the activation energy was similar for each BAER component wave (I-V) indicated that the increase in latencies for all 5 waves was governed by the same rate-limiting, temperature-dependent process(es). Second, the rise time and duration of each of the component waves of the BAER increased with decreasing temperature. Third, wave amplitudes increased from 37 to 32 degrees C in a quasiparabolic relation and then, decreased at approximately a linear rate. The BAER wave form completely disappeared below 20.3 degrees C. Slow rewarming of the brain to its initial temperature restored the BAER component waves to their original latencies and amplitudes.

Animals↗
PubMed1989

Morphological characterization of beta-VLDL and acetylated-LDL binding and internalization by cultured pigeon monocytes.

The ultrastructure of binding, internalization, and translocation of beta-migrating very low density lipoprotein (beta-VLDL) and acetylated low density lipoprotein (Ac-LDL) by cultured pigeon monocytes was examined using lipoprotein-gold conjugates. Through morphometry, differences in the binding and uptake of beta-VLDL-gold and Ac-LDL-gold were documented. Cells exposed to either beta-VLDL-gold or Ac-LDL-gold for 2 hr at 4 degrees C had the label over noncoated regions of the plasma membrane. Upon warming the cells to 37 degrees C for 2 min, 35% of the surface-bound beta-VLDL-gold was within coated pits on the cell surface. Although coated pits occupied less than 2% of the surface, binding of beta-VLDL-gold was 53 times more concentrated in coated pits as compared to noncoated membrane regions. In contrast, Ac-LDL-gold neither bound to coated pits nor relocated into coated regions of the membrane upon warming to 37 degrees C. Both the beta-VLDL-gold and the Ac-LDL-gold were internalized when the cells were rewarmed at 37 degrees C. Most of the internalized gold particles for both lipoproteins were located in electron-lucent vesicles; however, 9% of the intracellular beta-VLDL-gold was observed within coated vesicles at early times. Upon prolonged rewarming (30-90 min), both lipoprotein-gold conjugates were within acid phosphatase-positive lysosomes. Ultimately 83% of the Ac-LDL-gold and 90% of the beta-VLDL-gold were within electron-dense and electron-lucent lysosomes. These results suggested that the receptor-mediated binding and internalization of beta-VLDL and Ac-LDL by pigeon monocyte macrophages proceeded by separate, distinct routes; beta-VLDL by both coated and noncoated pathways while Ac-LDL was internalized exclusively by noncoated mechanisms. Regardless of these internalization differences, both lipoproteins were delivered to lysosomes for degradation.

Acid Phosphatase↗
PubMed1991

Prevention of myocardial intracellular edema induced by St. Thomas' Hospital cardioplegic solution.

During cardiac surgery, the heart is infused with cold crystalloid cardioplegic solutions such as St. Thomas' Hospital (StT) solution, which contains high concentrations of K+ and Mg2+. The high K+ and Mg2+ block impulse conduction and inhibit Ca2+ influx, thereby arresting the heart and reducing cardiac oxygen consumption. Nevertheless, myocardial edema and post-operative abnormalities have been noted after cardioplegia and attributed to ischemia and reflow or to hypothermia. We found, however, that cold StT (9 degrees C) was hypotonic and induced cell swelling in the absence of ischemic injury. Cell swelling in cold StT was not due to hypothermia alone, but rather was caused by KCl influx and was prevented by partially replacing Cl- with an impermeant anion. After exposure to cold StT, cells transiently shrank to less than control volume on rewarming in physiological saline (Tyrode's solution, 37 degrees C). The transient shrinkage was blocked by ouabain suggesting that Na+ loading of depolarized hypothermic cells and Na(+)-K+ pump activation on rewarming were responsible. Hypothermic ventricular cells seem to follow Donnan equilibrium, and the product of [K+] x [Cl-] in cardioplegic solutions affects cell volume in the absence of ischemic injury.

Animals↗
PubMed1994

Anesthesia blocks nonshivering thermogenesis in the neonatal rabbit.

Nonshivering thermogenesis (NST) is a normal physiological response of the neonate to cold exposure, characterized by increased blood flow to metabolically active brown fat stores. It is standard practice during neonatal surgery to warm the ambient environment in order to avoid consuming vital energy stores. While NST has been well-studied in the neonate, the response during anesthesia and paralysis has not been fully characterized. Rabbit pups (aged 1 to 7 days) were randomized into several groups. The experimental groups consisted of animals mechanically ventilated and administered either metocurine, pancuronium, curare, fentanyl, nitrous oxide (N2O), or halothane. The controls were spontaneously breathing animals. Oxygen consumption (VO2), an index of metabolic activity, was measured at thermoneutrality (39 degrees C) and after cold exposure (25 degrees C). Control and metocurine animals had a significant increase in VO2 in response to cold exposure. The increase in VO2 was not noted in animals that received curare, pancuronium, fentanyl, N2O, or halothane. To test the effect of anesthetic withdrawal during cold exposure on VO2, additional series of animals were studied. One group received continuous halothane throughout the period of cold exposure; the other had cessation of the halothane during cold exposure. Both groups were rewarmed subsequently. The animals that had withdrawal of halothane during cold exposure had a marked and significant increase in VO2 compared with the control group (continuous halothane). VO2 returned to near-baseline levels upon rewarming. The authors conclude that many commonly used anesthetic and paralyzing agents inhibit the thermogenic response to cold exposure. However, cessation of anesthesia (halothane) in a cold environment results in a marked increase in metabolic activity.

Anesthetics, Inhalation↗
PubMed1983

Effect of venting on myocardial protection by hypothermic cardioplegic arrest.

UNLABELLED: Myocardial rewarming between cardioplegic (CP) infusions is in part attributable to blood circulating through the heart from collateral channels. This experiment was performed to determine if the type of left ventricular (LV) venting affects myocardial temperature (temp) or alters myocardial protection. Twelve dogs underwent cardiopulmonary bypass (CPB) at 37 degrees C and were subjected to 100 min of cardioplegic arrest by intermittent coronary infusion of 300 ml 0-4 degrees C CP solution. Arterial, central venous, left atrial, and LV pressures; cardiac output; systemic, septal (S), right ventricular (RV), and LV temp; myocardial ATP and glycogen were measured; LV pressure/volume curves and LV dp/dt were calculated. Group A (6 dogs) had an LV vent during CPB, and Group B (6 dogs) had the aorta vented via the CP line. CP infusion lowered LV temp to 8 degrees C in Group A vs 13 degrees C in Group B (P less than 0.000002); S temp was lowered to 7 degrees C in Group A vs 11 C in Group B (P less than 0.00007); and RV temp was lowered to 16 degrees C in Groups A and B. Ten minutes after CP, LV and S temp increased to 20-21 degrees C in Groups A and B, and RV temp to 24-25 degrees C in Groups A and B. Twenty minutes after CP all temperatures were the same. Hemodynamics and myocardial metabolic studies were similar in the two groups. CONCLUSIONS: Hearts vented via the LV cooled to a lower temperature vs those vented via the aorta. Venting did not affect myocardial rewarming, myocardial metabolites, or ventricular function.

Animals↗
PubMed1988

Surface-induced hypothermia: effects on coronary blood flow autoregulation and vascular reserve.

Surface-induced hypothermia has been shown to exert a protective effect in canine models of myocardial infarction. However, its effects on coronary blood flow (CBF) autoregulation and coronary vascular reserve (CVR) have not been investigated. The effects of mild (32 degrees C) and moderate (27 degrees C) hypothermia on CBF autoregulation and CVR (at 60 mm Hg diastolic pressure) were studied using a chronically instrumented canine preparation. Coronary artery pressure-flow relations were obtained over a wide range of coronary diastolic pressures (10 to 106 mm Hg) with autoregulation intact and during adenosine-induced maximal coronary conductance (MCC) at 37, 32, 27 degrees C (n = 7 dogs), and after rewarming (n = 5 dogs). Halothane (1 MAC end-tidal concentration, temperature adjusted) was the anesthetic. Autoregulation remained intact during hypothermia. CBF remained relatively constant between diastolic pressures of 43.1 +/- 9.0 and 84.0 +/- 14.4 mm Hg (mean +/- SD). No significant differences were observed between temperatures in the autoregulated pressure range. CBF correlated well with myocardial oxygen consumption (MVO2) (r2 = 0.81, P less than 0.0001). There were no significant changes in MVO2, CBF, MCC, or CVR at 32 degrees C. At 27 degrees C, MVO2 (3.65 +/- 1.3 at 37 degrees C vs 2.35 +/- 1.4 ml O2.min-1 at 27 degrees C), autoregulated CBF (34.9 +/- 15.1 vs 19.5 +/- 10.8 ml.min-1), the slope of the line of MCC (4.31 +/- 0.7 vs 2.7 +/- 0.4 ml.mm-1.min-1), and CVR (147.1 +/- 24.6 vs 90.1 +/- 27.3 ml.min-1) were all less than control (P less than 0.05). After rewarming to 37 degrees C, no significant changes from control were noted. The authors conclude that coronary autoregulation remains intact at both 32 and 27 degrees C, although MCC and CVR are significantly decreased at 27 degrees C.

Animals↗
PubMed1990

Effect of different degrees of hypothermia on myocardium in treatment of hemorrhagic shock.

The use of hypothermia in cardiac and neurologic surgery is well established, but its use in treating hemorrhagic shock is controversial. Using a modified Wiggers hemorrhagic shock model, we examined the effects of hypothermia (group 1, 33 degrees C, N = 7; group 2, 28 degrees C, N = 12) after inducing hemorrhagic shock. In group 3, N = 6, dogs were maintained at body temperature in hemorrhagic shock and throughout resuscitation (normothermic shock). Sixty minutes after resuscitation (shed blood and lactated Ringer's solution, 50 ml/kg body wt), all hypothermic dogs were rewarmed and studied for an additional 120 min. Comparison of moderately hypothermic, severely hypothermic, and normothermic dogs showed a lower heart rate (80.6 +/- 3.3, 62.5 +/- 4.1, and 136.7 +/- 4.2 beats/min, P less than 0.05), reduced rate of left ventricular pressure fall (938 +/- 125, 700 +/- 75, and 1550 +/- 275 mm Hg/sec, P less than 0.05), a lower arterial pH (7.15 +/- 0.02, 7.10 +/- 0.03, and 7.24 +/- 0.02, P less than 0.05), a lower respiratory rate (18 +/- 1, 14 +/- 1, and 24 +/- 2 breaths/min, P less than 0.05), and a higher arterial pCO2 (36.6 +/- 1.6, 46.9 +/- 4.6, and 20.3 +/- 2.0 mm Hg, P less than 0.05). Left ventricular end-diastolic pressure was lower in the severely hypothermic dogs while stroke volume was higher in this group. Rewarming ablated all differences in cardiovascular performance and acid-base balance. Our data show that moderate hypothermia during hemorrhagic shock increased coronary perfusion, enhanced cardiac contractile performance, and significantly reduced myocardial oxygen requirements.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Hypothermia impairs performance in the Morris water maze.

Fifteen rats were trained to learn the location of a spatially fixed platform hidden in a Morris water maze (14-16 degrees C). Asymptotic performance was achieved over six training days (10 trials/day). Then retention of the task was assessed immediately after lowering core body temperature (Tc) to 28 degrees or 30 degrees C or stabilizing at 37 degrees C (the normothermic control). The hypothermia treatment order was counterbalanced according to a Latin-square design. Hypothermia significantly impaired all measures of spatial performance. Hypothermic animals were then rewarmed in a 40 degrees C water bath to 37 degrees C Tc and spatial performance tested again. Artificial rewarming resulted in complete recovery of all measures of spatial performance. These results demonstrate that hypothermia impairs performance in the Morris water maze, possibly by an amnesic mechanism, and that returning Tc to normothermic levels initiates recovery of performance.

Animals↗