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PubMed2000

[Treatment of accidental hypothermia].

New knowledge about accidental hypothermia acquired in recent years may simplify treatment and aid the evaluation of prognosis. Evidence of death or severe collapse due to the feared afterdrop has not been published. Afterdrop is a phenomenon of conductive heat loss. Evaluation of rewarming techniques shows that results from forced air rewarming techniques are equivalent to or better than results from invasive rewarming methods, except for rewarming with cardiopulmonary bypass. In hypothermia the most important differential diagnosis is death. Patients who are cold and could be resuscitated must be differentiated from patients, who are cold because they are dead. Experience from abroad has shown that extreme hyperkalaemia may be a useful diagnostic tool.

Accidents↗

PubMed2002

[Accidental hypothermia in the elderly].

BACKGROUND: Accidental hypothermia is unintended body core temperature of 35 degrees C or below, a known hazard to elderly people in temperate and cold climates. MATERIAL AND METHODS: We present two old patients with severe hypothermia and a review of the literature focusing on risk factors, clinical presentation, and the treatment of hypothermia in the elderly. RESULTS: Two patients, aged 90 and 102 years, with body core temperature < 28 degrees C were successfully treated at Ullevål University Hospital, Oslo, Norway with slow active external rewarming and a low stress strategy as recommended in the geriatric literature. Successful treatment with more rapid rewarming and use of internal rewarming like peritoneal lavage has also been published. The prognosis of elderly victims of hypothermia is known to be worse than for younger individuals. Epidemiological data are scanty. The most important risk factors are connected to ageing itself and to the morbidity often found in elderly hypothermia victims. Treatment is based on experience from few cases, minor prospective studies mainly on rewarming of younger patients and clinical experience from younger patients. INTERPRETATION: There is a need for more knowledge and experience of treating elderly hypothermia victims.

Accidents↗

PubMed1994

Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy.

Acute postoperative left ventricular dysfunction after hypothermic, crystalloid potassium cardioplegia occasionally occurs. This project examined myocyte contractility and inotropic responsiveness after hypothermic arrest with and without potassium cardioplegia. Isolated swine left ventricular myocytes were placed in a thermostatically controlled chamber (37 degrees C) that contained a standard cell medium, pulse stimulated at 1 Hz, and steady-state contractions were measured by computer-assisted video microscopy with and without isoproterenol (25 nmol/L). After baseline measurements were taken the myocytes were randomly assigned to the following treatments: (1) control group with infusion of 37 degrees C crystalloid solution and maintained at 37 degrees C for 3 hours (n = 23), (2) hypothermia group with infusion of 4 degrees C crystalloid without potassium and stored at 4 degrees C for 3 hours (n = 22), (3) hypothermic cardioplegia group with infusion of a crystalloid cardioplegia (oxygenated, buffered 4 degrees C Ringer's solution with 24 mEq/L K+) and then stored at 4 degrees C for 3 hours (n = 35). After treatment the myocytes were then rewarmed to 37 degrees C by infusion of medium, and contractile measurements were repeated. In the control group, the percent and velocity of shortening were identical to those in baseline measurements: 6.4% +/- 0.4% and 53 +/- 5 microns/sec, respectively, and these values remained unchanged in the hypothermia group: 6.5% +/- 0.4% and 51 +/- 3 microns/sec, respectively. However, in the hypothermic cardioplegia group, the percent and velocity of shortening were significantly lower with rewarming: 4.8% +/- 0.4% and 35 +/- 3 microns/sec, respectively, p < 0.05). Isoproterenol caused increased percent and velocity of shortening in both the control and hypothermia groups: 10.0% +/- 0.6% and 9.5% +/- 0.9% and 81.6 +/- 8 microns/sec and 71.4 +/- 8 microns/sec, respectively. This response was significantly blunted in the cardioplegia group (8.9% +/- 0.8% and 56.9 +/- 7 microns/sec, p < 0.05). With an isolated myocyte system that is independent of extracellular and perfusion effects, hyperkalemic cardioplegic solution resulted in depressed myocyte contractile performance after rewarming. Potassium cardioplegia also caused a blunted inotropic responsiveness on rewarming. A potential contributory factor for the depressed left ventricular function after the use of potassium cardioplegia is a direct depression in myocyte contractility.

Analysis of Variance↗

PubMed1996

Changes in blood flow distribution and capillary function after deep hypothermia in rat.

The present experiments were carried out in the rat to investigate the peripheral vascular function prior to the development of posthypothermic circulatory collapse. In the first study, mean arterial blood pressure, heart rate, cardiac output, regional blood flow, and plasma volume of hypothermic (4 h, 15-13 degrees C) and rewarmed rats were compared with normothermic controls. In response to hypothermia, arterial blood pressure, heart rate, and cardiac output declined markedly. After rewarming, arterial blood pressure and heart rate recovered fully, whereas cardiac output was only 33 +/- 7% of the control value (p < 0.025). Tissue blood flow was markedly depressed during hypothermia (p < 0.025), except for the abdominal skin. After rewarming, blood flow in skeletal muscle returned to within control levels, whereas blood flow in internal organs remained low (p < 0.025 vs. control). Posthypothermic plasma volume was 77 +/- 3% of control (p < 0.05). In the second study, the transcapillary colloid osmotic pressure gradient (COPp-COPi) was calculated following measurement of colloid osmotic pressure in plasma (COPp) and interstitium (COPi) in prehypothermic, hypothermic, and posthypothermic rats. The posthypothermic value of COPp-COPi was 76 +/- 4% of the prehypothermic value (p < 0.05). In conclusion this study demonstrates that the reduced cardiac output in rewarmed rats is associated with an altered regional blood flow distribution compared with that of normal rats. Capillary integrity also seemed perturbed. Thus, changes in both control and function of the peripheral vasculature are important mechanisms in the development of a posthypothermic circulatory collapse.

Animals↗

PubMed2003

Prolonged therapeutic hypothermia after traumatic brain injury in adults: a systematic review.

CONTEXT: The benefits of therapeutic hypothermia as a treatment for traumatic brain injury (TBI) remain unclear. OBJECTIVE: To explore the effects of depth, duration, and rate of rewarming after discontinuation of hypothermia on mortality and neurologic outcome in adults after TBI. DATA SOURCES: An electronic search of MEDLINE (OVID), EMBASE, Current Contents, the Cochrane library and a hand search of key journals were performed. Corresponding authors of identified studies were contacted for additional unpublished or ongoing clinical trials. STUDY SELECTION: All randomized controlled trials of therapeutic hypothermia for at least 24 hours vs normothermia in adults with TBI. DATA EXTRACTION: Demographic and clinical data, hypothermia interventions and cointerventions, mortality and neurologic outcomes, and methodological quality were abstracted by 2 independent reviewers. DATA SYNTHESIS: Twelve trials met eligibility criteria and were included in the analysis. We also performed subanalyses by different hypothermia interventions (ie, depth, duration, and rapidity of rewarming after hypothermia) and methodological quality. Therapeutic hypothermia was associated with a 19% reduction in the risk of death (95% confidence interval [CI], 0.69-0.96) and a 22% reduction in the risk of poor neurologic outcome (95% CI, 0.63-0.98) compared with normothermia. Hypothermia longer than 48 hours was associated with a reduction in the risks of death and of poor neurologic outcome (relative risk [RR], 0.70; 95% CI, 0.56-0.87 and RR, 0.65; 95% CI, 0.48-0.89, respectively) compared with normothermia. Hypothermia to a target temperature between 32 degrees C and 33 degrees C, a duration of 24 hours, and rewarming within 24 hours were all associated with reduced risks of poor neurologic outcome compared with normothermia. Assessment of methodological quality did not reveal evidence of bias. CONCLUSIONS: Therapeutic hypothermia may reduce the risks of mortality and poor neurologic outcome in adults with TBI. Outcomes were influenced, however, by depth and duration of hypothermia as well as rate of rewarming (<or=24 hours) after discontinuation of hypothermia. Nonetheless, the evidence is not yet sufficient to recommend routine use of therapeutic hypothermia for TBI outside of research settings.

Adult↗

PubMed1994

Improved rat heart function after low Ca2+ perfused preservation at 5 degrees C for 18 hours.

To evaluate the effect of Ca2+ on recovery of heart function after hypothermic preservation, isolated working rat hearts were perfused continuously in different [Ca2+] (0.35-2.0 mM) at 37 degrees C for 30 min, during cooling to 5 degrees C, and then at 5 degrees C for 1, 6 or 18 h. After rewarming to 37 degrees C, contractile functions were assessed in working hearts perfused with Krebs-Henseleit (K-H) solution containing 2.0 mM free Ca2+. In normal K-H solution (2.0 mM Ca2+), cardiac function recovered completely after perfusion at 5 degrees C for 1 h (measured by the maximal rate of pressure development, +dP/dtmax, and heart rate x left ventricular systolic pressure, HR x LVSP). After 6 h at 5 degrees C, significant (P < 0.05) loss in function began to appear. Further, 18 h at 5 degrees C resulted in significant decreases in LVSP, +dP/dtmax, and coronary flow (CF) and a significant increase in left ventricular diastolic pressure. The deterioration of heart function consequent to hypothermic preservation could be prevented by reducing the Ca2+ in perfusion medium prior to and during cooling and rewarming from hypothermia. The optimal Ca2+ concentration was 0.5 mM. At lower Ca2+ (0.35 mM), reductions in HR, LVSP. +dP/dtmax, and CF after rewarming were evident. Our results indicate that by reducing cellular Ca2+ prior to cooling through perfusion of 0.5 mM Ca2+ K-H solution, significant benefits can be obtained both in prolonging the duration of cardiac preservation and in retaining functional integrity upon rewarming.

Animals↗

PubMed1997

Stimulation of carbohydrate metabolism reduces hypothermia-induced calcium load in fatty acid-perfused rat hearts.

In the present study we examined the impact of glycolysis and glucose oxidation on myocardial calcium control and mechanical function of fatty acid-perfused rat hearts subjected to hypothermia rewarming. One group (control) was given glucose (11.1 mM) and palmitate (1.2 mM) as energy substrates. In a second group glycolysis was inhibited by iodoacetate (IAA, 100 microM) and replacement of glucose with pyruvate (5 mM), whereas in the third group glucose oxidation was stimulated by administration of dichloroacetate (DCA, 1 mM) and insulin (500 microU/ml). All groups showed a rise in myocardial calcium ([Ca]total in response to hypothermia (10 degrees C). However, [Ca]total was significantly lower both in IAA- and DCA-treated hearts, as compared to controls (2.20 +/- 0.22 and 2.94 +/- 0.20 v 3.83 +/- 0.29 nmol/mg dry wt., P < 0.025). The reduced calcium load in the treated hearts was correlated with higher levels of high energy phosphates. Following rewarming control and DCA-treated hearts still showed elevated [Ca]total, whereas IAA-treated hearts [Ca]total was not different from the pre-hypothermic value. All groups showed a reduction in cardiac output following rewarming. Furthermore, the control group, in contrast to both IAA- and DCA-treated hearts, showed a significant reduction in systolic pressure. These results show that hypothermia-induced calcium uptake in glucose and fatty acid-perfused rat hearts was reduced by two different metabolic approaches: (1) inhibition of glycolysis by IAA while simultaneously by-passing the glycolytic pathway by exogenous pyruvate: and (2) stimulation of glucose oxidation by DCA. Thus, glycolytic ATP is not an essential regulator of sarcolemmal calcium transport under the present experimental conditions. Instead, we suggest that a change in oxidative substrate utilization in favour of carbohydrates may improve myocardial calcium homeostasis during hypothermia and rewarming.

Adenosine Triphosphate↗

PubMed1999

Ultrastructural analysis of human endothelial cells after hypothermic storage in organ preservation solutions.

BACKGROUND: Protection of vascular endothelium is a critical factor in organ preservation for transplantation. This study aims at a morphological assessment of endothelial cell injury in a comparison of storage solutions, using a cell culture model of cold preservation and rewarming. MATERIALS AND METHODS: Human umbilical vein endothelial cells (HUVEC) were cultured in monolayer and exposed to hypothermic storage in University of Wisconsin (UW), histidine-tryptophane-ketoglutarate (HTK), and EuroCollins solutions for 6 h and subsequent rewarming for 30 min or 6 h. Alterations of subcellular structures and cell-cell contacts were analyzed by transmission electron microscopy (TEM) and light microscopic assessment after actin and nuclear staining. RESULTS: Structural alterations of mitochondria, endoplasmic reticulum, nuclei, and cytoskeletal fibers as well as disruption of intercellular contacts were found after cold storage in HTK and EuroCollins solutions. In contrast, storage in UW solution resulted in minimum changes of stress fibers only. A rapid rearrangement of structural alterations was achieved during rewarming in cell culture medium in all experimental groups. CONCLUSIONS: Preservation of endothelial cell structure is best achieved by UW solution. Ultrastructural cell damage is a direct consequence of hypothermic storage and is fully reversible during rewarming after short storage times.

Adenosine↗

PubMed2003

Changes in cerebrovascular response during brain hypothermia after traumatic brain injury.

OBJECTIVE: Transcranial Doppler sonography (TCD) provides a rapid and noninvasive assessment of cerebral hemodynamics after traumatic brain injury. This study evaluates the change of cerebrovascular response at the rewarming stage of brain hypothermia using TCD. MATERIAL AND METHODS: Seventeen patients who had suffered from closed brain injury were investigated with daily TCD recordings and the changes in flow velocities were evaluated to determine whether they reflected the temperature during brain hypothermia. All patients who had treated brain hypothermia underwent continuous monitoring of SjO2, mean arterial blood pressure, and intracranial pressure (ICP). RESULTS: No significant changes in ICP and cerebral perfusion pressure (CPP) were recorded in all cases. Of 17 patients, 5 had a significant increase in SjO2 > 75% or more, retrospectively, with a robust increase in flow velocities of the middle cerebral artery (P < .01) at the rewarming stage. These cases marked a decrease in pulsatility index (P < .05) concomitant with an increase in SjO2 values. The CT scan revealed acute brain swelling in these cases. CONCLUSION: These data suggest cerebral vasoactivity could be altered at the rewarming stage. Hypothermia runs a risk of hyperemia at the rewarming stage, which induced a decrease in cerebral vasoresistance.

Acute Disease↗

PubMedDate not supplied

Brief report: The declining incidence of cerebral hyperthermia during cardiac surgery: a seven-year experience in 6,334 patients.

PURPOSE: Cerebral hyperthermia during rewarming from hypothermic cardiopulmonary bypass (CPB) commonly occurs and has been associated with postoperative neurocognitive dysfunction. Increased awareness of this has likely led to changes in rewarming strategies, including the reduction of rewarming rates and lowering of target rewarming temperatures. As a result, we hypothesized that the maximum temperature reached during cardiac surgery has decreased at our institution over time. METHODS: We retrospectively reviewed the maximum intraoperative nasopharyngeal (NP) temperature in 6,334 patients having undergone cardiac surgery utilizing hypothermic CPB from January 1993 to June 2000. The incidence of cerebral hyperthermia (defined by a NP temperature > 38 degrees C) was examined over time using Chi-square testing and the relationship between maximum temperature and date of surgery was studied using linear regression. RESULTS: Maximum temperature decreased over time (P < 0.0001; r2 = 0.40) having the greatest reduction from January 1993 to December 1996 (0.34 degrees C temperature drop per year), while from January 1997 to June 2000, it continued to decrease, but at a slower rate (0.10 degrees C per yr; P < 0.0001). The incidence of cerebral hyperthermia decreased over time with 83% of the first 10% of patients and 3% of the latter 10% of patients during the study period having a maximum temperature > 38 degrees C (P < 0.0001). CONCLUSION: The incidence of cerebral hyperthermia has decreased at our institution suggesting that a change in temperature management has occurred at our institution from January 1993 to June 2000 thereby outlining a temporal evolution in temperature management during CPB.

Aged↗

PubMed1999

The aetiology and pathogenesis of cardiopulmonary bypass-associated metabolic acidosis using polygeline pump prime.

OBJECTIVE: The pathogenesis of the metabolic acidosis of cardiopulmonary bypass (CPB) is not fully understood. New quantitative methods of acid-base balance now make it possible to describe it more clearly. Accordingly, we studied acid-base changes during CPB with polygeline pump prime and defined and quantified the factors which contribute to metabolic acidosis. DESIGN: Prospective cohort study. SETTING: Tertiary institution. PARTICIPANTS: 10 cardiac bypass graft surgery patients. INTERVENTIONS: Sampling of arterial blood at four time intervals: post-induction, on CPB during cooling and rewarming, and at skin closure. Measurement of serum Na+, K+, Mg++, Ca++, Cl-, bicarbonate, and phosphate concentrations, arterial blood gases, and serum albumin, lactate, and pyruvate concentrations at each collection point. Analysis of findings according to quantitative physicochemical principles, including calculation of the strong ion difference apparent, the strong ion difference effective, and the strong ion gap (SIG). MEASUREMENTS AND MAIN RESULTS: All patients developed a mild metabolic acidosis. The median serum standard bicarbonate concentration decreased from 25.0 mEq/l post-induction to 22.3 mEq/l at cooling and 22.2 mEq/l at rewarming (p < 0.05). The standard base excess decreased from a median of 1.55 mEq/l prior to CPB, to -2.50 mEq/l at cooling, -1.65 mEq/l at rewarming and, -0.85 mEq/l at skin closure (p < 0.001). This mild metabolic acidosis occurred despite a decrease in the median serum lactate concentration from 3.20 mEq/l post-induction to 1.83, 1.80, and 1.58 mEq/l at the three other time points. The increase in the median serum chloride concentration from 104.9 mEq/l post induction to 111.0, 111.1, and 110.0 mEq/l at the subsequent time points (p < 0.0001) was the main cause of the acidosis. There was also a significant increase in the SIG of 3.8 mEq/l at cooling and rewarming (p < 0.0001), suggesting a role for other unmeasured anions (polygeline) in the genesis of this acidosis. CONCLUSIONS: Using quantitative biophysical methods, it can be demonstrated that, in patients receiving a pump prime rich in chloride and polygeline, the metabolic acidosis of CPB is mostly due to iatrogenic increases in serum chloride concentration and unmeasured strong anions (SIG). Its development is partially attenuated by iatrogenic hypoalbuminaemia. Changes in lactate concentrations did not play a role in the development of metabolic acidosis in our patients.

Acid-Base Equilibrium↗

PubMed1991

Fatty acids suppress recovery of heart function after hypothermic perfusion.

Working rat hearts were perfused for 15 minutes at 37 degrees C before switching to a Langendorff perfusion (60 mm Hg aortic pressure) at 10 degrees C for 40 minutes of hypothermic arrest. Ventricular function was allowed to recover for 15 minutes at 37 degrees C by reestablishing the prehypothermic conditions. The perfusate was Krebs-Henseleit bicarbonate buffer containing 3% bovine serum albumin and either glucose (11 mmol/L) or glucose (11 mmol/L) plus palmitate (1.2 mmol/L) and gassed with 95% O2 and 5% CO2. In hearts receiving glucose alone as substrate, coronary flow was maintained constant during the 40 minutes of hypothermic arrest and returned to prehypothermic rates with rewarming. Ventricular function, as estimated by peak systolic pressure and heart rate, recovered to the prehypothermic level. When palmitate was added, coronary flow decreased continuously throughout the hypothermic perfusion (22% decrease by 40 minutes), and ventricular pressure development was lower throughout the rewarming perfusion. Tissue levels of adenosine triphosphate and creatine phosphate were well maintained and long-chain acyl coenzyme A and acyl carnitine decreased during hypothermia regardless of the substrate provided. With rewarming, tissue levels of adenosine triphosphate and creatine phosphate decreased in those hearts receiving palmitate. Omission of fatty acid either during hypothermia or during the first 5 minutes of rewarming improved recovery of function. Addition of oxfenicine to inhibit fatty acid oxidation, or inhibition of Ca2+ overload by verapamil and low perfusate Ca2+, prevented the effects of palmitate on ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Acyl Coenzyme A↗

PubMed1988

Glucose, glycogen, and insulin responses in the hypothermic rat.

The rat appears to be unable to utilize glucose during hypothermia. The objective of this study was to examine carbohydrate homeostasis during induction, hypothermia, and rewarming phases. Groups of normothermic animals were euthanized to serve as time controls for comparison. Hypothermia (15 degrees C) was produced by exposure to helox (80% helium:20% oxygen) at 0 +/- 1 degree C. Hyperglycemia was noted during the induction process (169 +/- 8 in control vs 326 +/- 49 mg/dl). Serum glucose increased further during 4 hr of hypothermia, but following rewarming (Tre of 33 +/- 1 degrees C) was reduced (153 +/- 16 mg/dl) significantly (P less than 0.05). Serum insulin was depressed during hypothermic induction (from 48 +/- 4 in controls to 19 +/- 3 microU/ml in hypothermic rats) and increased only slightly during the arousal process, remaining significantly lower than in normothermic subjects. Initial hepatic, skeletal muscle, and cardiac glycogen concentrations were reduced 34, 68, and 75%, respectively, during hypothermic induction. While liver glycogen decreased further during 4 hr of hypothermia, skeletal and cardiac stores increased markedly. During rewarming, hepatic glycogen was markedly decreased, while skeletal and cardiac stores were maintained. These data suggest that hyperglycemia in the hypothermic rat can be accounted for by glycogenolysis and hypoinsulinemia. In addition, this study indicates repletion of skeletal and cardiac muscle glycogen during maintained hypothermia and sparing of muscle glycogen during rewarming.

Animals↗

PubMed1986

Ventilatory recovery from hypothermia in anesthetized cats.

Ventilation and breathing pattern were recorded in a group of seven anesthetized cats during rewarming from 24 to 38 degrees C of esophageal temperature. It was found that at 24 degrees C, ventilation was very much depressed accounting for an alveolar hypoventilation resulting in hypoxia and hypercapnia. During rewarming, ventilation increased steadily; this was caused by sequential changes in central inspiratory activity (VT/Ti) and Ti/Tt ratio reflecting breath timing. Changes in VT/Ti have been initially attributed to an improvement in chemoresponsiveness and subsequently, to an involvement of supra-pontine thermoregulatory control areas during rewarming. Marked changes in breath timing, especially observed between 28 and 34 degrees C, have been attributed to a direct effect of rewarming upon the brain stem respiratory network. It has the result, that during hypothermia, several components of the respiratory control system are differently affected causing marked changes in breathing pattern and ventilation. They are accompanied by modifications in arterial blood pressure and heart rate.

Animals↗

PubMed1983

Accidental hypothermia.

Knowledge of the effects of hypothermia has increased greatly over the past 25 yr. Thousands of patients have been cooled intentionally in the operating room, and hundreds of thousands of living hearts have been temporarily stopped by cold cardioplegia and restarted without difficulty or apparent ill-effect. Yet in spite of the acquisition of this vast body of clinical experience an aura of mystery stills surrounds the patient who becomes hypothermic accidentally. The best treatment in any particular case is not always clear, and published accounts do not always give the impression that the hypothermic patient is treated with the same rational approach with which other sick and comatose patients are treated. In summarizing, therefore, conclusions that might be reached from reviewing past experience several important points emerge. The severely hypothermic patient should be treated in an intensive care unit where appropriate monitoring of temperature, cardiovascular function and respiratory function are available, and where full respiratory support including assisted ventilation can be given. The final outcome depends upon the etiology. The young healthy victim of exposure has a good chance of surviving. The patient poisoned by alcohol or barbiturates has a good chance of surviving provided the level of intoxication is not itself lethal. The elderly without severe underlying disease have a good chance of surviving. The patient with severe underlying disease of the endocrine, cardiovascular or neurologic system probably has, at best, a 50% chance of surviving and, at worst, a chance of only 10-20%, depending upon the associated disease. There is no statistical evidence that any one method of rewarming is significantly better than any other. But there is anecdotal evidence that in the absence of full monitoring and support systems slow rewarming is safer than over-energetic external rewarming. Internal rewarming, peritoneal dialysis, hemodialysis, inhalation of warmed oxygen and extracorporeal circulation are effective in severe cases and can be used with safety. The causes of, and triggering mechanism for, ventricular fibrillation are still largely unknown but the onset of ventricular fibrillation in a very cold patient may often be an irreversible complication. The place of modern anti-arrhythmic drugs in the prevention and management of this complication has yet to be elucidated. Cardiopulmonary resuscitation is difficult in profoundly hypothermic patients but should be maintained until a body temperature of 30 degrees C has been achieved.(ABSTRACT TRUNCATED AT 400 WORDS)

Accidents↗

PubMed1978

Dependence of the calorigenic effect of adrenaline on the secretory activity of the adrenal medulla in posthypothermic rats.

Posthypothermic rats, 13 h after spontaneous rewarming as well as between days 6 and 7, produced the same quantity of heat as euthermic control animals. At the same time both urinary adrenaline excretion and adrenaline content of the adrenals were markedly changed. In the initial phase of the posthypothermic state (13 h after spontaneous rewarming) urinary adrenaline excretion was significantly increased whereas adrenaline content in the adrenals was lower than in normothermic control rats (P less than 0.001). Between days 6 and 7 after rewarming, the rate of urinary adrenaline excretion and adrenaline content in the adrenals returned to the control values. The calorigenic effect of exogenous adrenaline (50 microgram/100 g), found in the euthermic control rats, was not observed in posthypothermic animals 13 h after spontaneous rewarming when the secretory activity of the adrenal medulla was increased. The restitution of the calorigenic action of exogenous adrenaline occurred between days 6 and 7 after hypothermia.

Adrenal Glands↗

PubMed1987

Intermittent reperfusion extends myocardial preservation for transplantation.

A protocol was developed to compare prolonged heart preservation by hypothermic storage with prolonged hypothermic storage interrupted by a period of reperfusion. Hearts from adult mongrel dogs were excised after administration of 4 degrees C crystalloid cardioplegia. Group A hearts (N = 7) underwent 7.5 hours of ischemia at 4 degrees C followed by 1.5 hours of reperfusion and rewarming (A0). Group B hearts (N = 8) underwent 3 hours of ischemia at 4 degrees C, 1.5 hours of reperfusion and rewarming (B1), 3 additional hours of ischemia at 4 degrees C following repeat cardioplegia, and finally 1.5 hours of reperfusion and rewarming (B2). During reperfusion, hearts were defibrillated and left ventricular (LV) function was assessed by measuring isovolumic peak systolic pressure and maximum positive rate of rise of LV pressure (+dP/dtmax) with an intraventricular balloon. LV biopsy samples for adenosine triphosphate (ATP) assay were obtained before ischemia and after each rewarming period. One Group A heart could not be defibrillated and studied. All Group B hearts completed the protocol. LV function, as assessed by peak pressure and +dP/dtmax, at B1 and B2 exceeded values obtained at A0, but the differences were not statistically significant. The mean ATP level was 63.4 +/- 7.7% of baseline at B1 and 79.7 +/- 4.3% of baseline at B2 (p less than .03). The mean ATP level was 57.9 +/- 5.9% of baseline at A0 (p less than .007, B2 vs. A0). It is presumed that intermittent reperfusion allows repletion of substrate stores, which results in improved myocardial protection.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1999

Cellular and molecular therapeutic targets for treatment of contractile dysfunction after cardioplegic arrest.

Transient left ventricular (LV) dysfunction can occur after hypothermic hyperkalemic cardioplegic arrest. This laboratory has developed an isolated LV myocyte system of simulated cardioplegic arrest and rewarming in order to examine cellular and molecular events that may contribute to the LV dysfunction after cardioplegic arrest. Contractile function was examined using high-speed video microscopy after reperfusion and rewarming. After cardioplegic arrest and reperfusion, indices of myocyte contractility were reduced by over 40% from normothermic control values. The capacity of the myocyte to respond to an inotropic stimulus was examined through beta-adrenergic receptor stimulation with isoproterenol. After cardioplegic arrest, the contractile response to isoproterenol was reduced by over 50% from normothermic values. The next series of studies focused upon preventing these changes in myocyte contractile processes after cardioplegic arrest. First, the cardioplegic solutions were augmented with adenosine or an ATP-sensitive potassium channel opener, aprikalim. Both adenosine and aprikalim augmentation significantly improved myocyte function compared with cardioplegia alone values. A potential intracellular mechanism for the protective effects of either adenosine or the ATP-sensitive potassium channel is the activation of protein kinase C (PKC). A brief period of PKC activation before cardioplegic arrest provided protective effects on myocyte contractility with subsequent reperfusion and rewarming. In another set of studies, the potential protective effects of the active form of thyroid hormone (T3) were examined. In myocytes pretreated with T3, myocyte contractile function and beta-adrenergic responsiveness were significantly improved after hypothermic cardioplegic arrest and rewarming. Thus, endogenous means of providing improved myocardial protection during prolonged cardioplegic arrest can be achieved through a brief period of PKC activation or pretreatment with T3. Future studies, which more carefully deduce the basis for these pretreatment effects, will likely yield novel methods by which to protect myocyte contractile processes during cardioplegic arrest.

Adenosine↗