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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydroxyl is one of the most cytotoxic of all oxygen-derived free radicals produced during the myocardial ischaemia-reperfusion sequence. The purpose of the present study was to determine the effects of various interventions aimed at diminishing the production of hydroxyl radicals by reducing either one of their precursors (hydrogen peroxide) or the metal (ferric iron) which catalyzes the reaction generating these radicals. Sixty isolated and perfused rat hearts with isovolaemic contraction were studied. Except for non-ischaemic controls, these hearts were subjected to a 3-hour cardioplegic arrest in hypothermia (15-18 degrees C) followed by a 45-min reperfusion. The following interventions were performed: pretreatment with peroxidase, a hydrogen peroxide scavenger; pretreatment with peroxidase combined with deferoxamine, an ironchelating agent; pretreatment with peroxidase followed by addition of deferoxamine to the cardioplegic solution; addition of deferoxamine to the cardioplegic solution without pretreatment with the enzyme. Judging from the post-ischaemic values of developed pressure (maximum systolic pressure--diastolic pressure), left ventricular dP/dt and diastolic pressure and coronary flow rate, it appeared that the best myocardial protection was provided by deferoxamine-enriched cardioplegia. This study confirms that hydroxyl radicals most probably play a role in the genesis of the myocardial lesions associated with global ischaemia followed by reperfusion. Moreover, our results highlight the potential value of deferoxamine added to cardioplegic protection in heart surgery performed under extracorporeal circulation.
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PMID:[A new concept of cardioplegic protection in cardiac surgery: iron chelation]. 314 54

Regional hypothermia is known to protect many tissues from ischemic injury. We investigated the relationship between regional hypothermia and skeletal muscle ischemia-reperfusion injury in a bilateral in vivo isolated canine gracilis muscle model. In five anesthetized dogs, one gracilis muscle was subjected to 6 hours of ischemia followed by 1 hour of reperfusion while the contralateral muscle served as a nonischemic control. Localization and quantitation of skeletal muscle injury was determined by histochemical staining with triphenyl tetrazolium chloride (TTC) followed by computerized planimetry of the infarct size. Muscle pH and temperature were monitored continuously in the proximal, middle, and distal segments by using pH electrodes and needle thermistors. Muscle pH was calculated by use of the Nernst equation with temperature correction, and hydrogen ion washout rates (H+) were derived from the observed change in muscle pH during reperfusion. A significant (p less than 0.05) regional hypothermia was observed in the distal third of the muscle. The preischemic temperature in the distal muscle was 27 +/- 2 degrees (SEM) C, compared to 34 +/- 1 degree and 32 +/- 2 degrees C in the proximal and middle segments of muscle, respectively. This temperature gradient was sustained throughout the experiment. The distal third of the ischemic muscle demonstrated significantly less (p less than 0.05) injury than the proximal and middle thirds as measured by TTC infarct size (31 +/- 10%, compared to 71 +/- 3% and 78 +/- 6%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional hypothermia protects against ischemia-reperfusion injury in isolated canine gracilis muscle. 339 82

An interstitial microwave antenna system was devised for differential hypothermia treatment. It was evaluated for its ability to induce localized brain hyperthermia in hypothermic monkey. Ten brain hyperthermia trials have been performed in 6 monkeys. Under general anesthesia, the animals were put into ice water bath to keep the total body temperature at 30 degrees C. Following parieto-occipital craniectomy, a microwave antenna of 1.5 mm in diameter was inserted into the brain at depth of 2 cm, and the brain tissue was heated by 2450 MHz microwave irradiation. Thermal distribution was measured by thermistor probes and local cerebral blood flow (1-CBF) before and after heating was simultaneously measured by hydrogen clearance method. After the experiment, the animals were sacrificed and histopathological changes of the heated brain tissue were studied. Under total body hypothermia of 30 degrees C, the maximum cross-sectional diameter of the heated brain to 37 degrees C or above was about 4 cm. The temperature profile on the vertical plane presented a bell-shaped distribution. The 1-CBF of the heated brain increased with the elevation of the brain temperature and the blood flow at 37 degrees C is nearly twice as much as that of 30 degrees C. After one hour DH treatment, necrotic tissue was noted along the antenna axis where the temperature was maintained more than 50 degrees C, and this change was not recognized at a distance of 1 cm from the antenna where the temperature was maintained at 42 degrees C. This study indicates that interstitial microwave hyperthermia system can be used effectively to heat the localized brain tissue.
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PMID:[Fundamental study of differential hypothermia treatment of brain tumor using an interstitial microwave antenna]. 344 98

The composition of the ideal cardioplegic solution is controversial. Blood cardioplegia is an attractive alternative to standard crystalloid solutions, though its superiority in preserving myocardial metabolism has not been demonstrated. Using a new pH electrode system, this study contrasts the effects of blood and crystalloid solutions upon the generation of myocardial acidosis during global ischemia. Thirty-eight mongrel dogs underwent a 120-min period of aortic cross clamping using systemic hypothermia. To maintain myocardial temperature below 15 degrees C, 19 dogs received multiple doses of a bicarbonate containing crystalloid cardioplegic solution (Group I), while 19 dogs received multiple doses of blood cardioplegia (Group II). Myocardial pH and temperature were continuously monitored in the subendocardial region of the left ventricle. There was no difference in baseline pH between Group I (7.13 +/- 0.05) and Group II (7.17 +/- 0.05, P:NS). With systemic cooling and the initial bolus of cardioplegia, myocardial pH rose to 7.42 +/- 0.04 in Group I and 7.42 +/- 0.06 in Group II (P:NS). After 120 min of global ischemia, myocardial pH decreased to 6.61 +/- 0.05 in Group I and 7.07 +/- 0.05 in Group II (P less than 0.001). Blood cardioplegia was most effective during the first hour of aortic cross clamp when myocardial pH rose by 0.13 +/- 0.04 pH units. In contrast, myocardial pH in Group I during the first hour of global ischemia fell -0.35 +/- 0.08 pH units (P less than 0.001 compared to Group II). During the second hour of cross clamp, myocardial pH declined both in Group I (0.26 +/- 0.03 pH units) and in Group II (0.24 +/- 0.05 pH units, P:NS). However, the accumulation of hydrogen ion during the second hour was significantly greater in Group I (+128.0 +/- 21.4 nm/liter) than in Group II (+36.6 +/- 9.0 nm/liter, P less than 0.001). Thus, myocardial acidosis was reduced during the administration of blood cardioplegia when compared to a bicarbonate-buffered crystalloid solution. The salutary effects of blood cardioplegia on myocardial metabolism stem from blood's significant buffering capacity and its ability to deliver oxygen.
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PMID:Reduction in myocardial acidosis using blood cardioplegia. 382 Oct 87

Pauling and Miller have independently proposed that the presence of an anesthetic gas in tissue induces a cage-like arrangement of hydrogen-bonded water molecules. The theories recognize that most gas-hydrate crystals would not form at the temperature and pressure that exist during anesthesia and propose that other components of tissue such as protein should have a stabilizing effect. Measurements of the behavior of water, rather than the anesthetic agent, would provide alternative information about the likelihood of hydrate crystal formation and this information could be such as to be applicable to body temperature and to pressures used for anesthesia. If the number of hydrogen-bonded water molecules in tissue is increased, then the movement of an average water molecule should be hindered. Movement of water through the tissue may be measured by tagging it with tritium and the anesthetic gas should then slow the movement of tritiated water through the tissue. The flux of tritiated water through rat cecum is indeed slowed when the cecum is exposed to the anesthetic gas, xenon, which can participate biochemically only by virtue of its van der Waals interaction. The decrement in water flux is in reasonable agreement with what could be expected theoretically from calculations based on the activation energy for the self-diffusion of water and the degree of hypothermia necessary to produce narcosis.
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PMID:Anesthetic gases and water structure. The effect of xenon on tritiated water flux across the gut. 572 84

In 1975 H. Rahn put forward a new concept of hydrogen ions regulation which explains acid-base regulation in relation to body temperature and applies to all animal species. At the root of this concept is the finding that maintenance of intracellular neutrality is governed by water dissociation and regulated by imidazole-rich protein buffers. The pH of the extracellular fluid, which receives acid by-products of cell activity, is kept higher than that of the intracellular fluid (relative alkalinity). The difference between extracellular pH and neutrality is constant for each species and ranges from 0.6 to 0.8 pH units. It is unaffected by changes in temperature, and the total CO2 content of extracellular fluid remains constant. The authors were able to confirm the value of this new concept in man by experimental studies of in vitro and in vivo blood of patients undergoing aorto-coronary bypass under controlled hypothermia. They draw the following practical conclusions: (1) in subjects under moderate or deep hypothermia for surgical purposes, the acid-base status can be controlled and the extracellular pH adjusted by ensuring intracellular neutrality; this is done by keeping PCO 2 at such a level that the arterial blood pH measured at 37 degrees C remains around 7.40; (2) the problem of correcting acid-base values (pH-PCO 2) according to body temperature is solved simply by using pH and PCO 2 values measured at 37 degrees C and interpreting them, as usual, in terms of metabolic or respiratory acidosis or alkalosis.
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PMID:[Relations between acid-base equilibrium and body temperature. Physiological concepts and practical applications]. 622 30

Fundamental physicochemical characteristics of the acid-base related constituents of extracellular and intracellular fluid spaces of vertebrates in relation to changes in temperature have been reviewed. Emphasis has been placed upon the dissociation constant of water, the solubility constant of CO2, the dissociation constant of histidine imidazole, the hydroxyl-hydrogen ion ratio, the protein charge state and the alpha-imidazole regulation concept. Because pN and pKIm change in parallel when temperature varies, the OH/H ratio and the alpha-imidazole value for any sample of blood or plasma held anaerobically in vitro are invariant with changing temperature, since a constant CO2 content is maintained. Thus, when blood or plasma cools, pH increases and PCO2 decreases, but relative alkalinity and the protein charge state remain constant. These responses are solely the consequence of physical constants, that is, equilibrium constants and gas solubility, changing with temperature. In vivo, the set of PCO2 is established in each poikilothermic species by its normal ventilatory pattern designed to maintain constant CO2 content. Regulation in vivo in poikilotherms consists of adjustments of ventilation per unit metabolism (VA/VCO2) appropriate to every temperature. When the ventilatory and renal mechanisms of human beings are suppressed by anesthesia and hypothermia, their extracellular and intracellular responses mimic those of poikilotherms. Clinical management of hypothermia in humans requires ventilatory control using oxygen-augmented room air without added CO2 monitored by pH measurements of arterial blood warmed anaerobically to 37 degrees C. Finally, the need for new techniques to measure intracellular pH as temperature is lowered and some areas for further investigation are suggested.
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PMID:The hydroxyl-hydrogen ion concentration ratio during hypothermia. 629 7

The effect of experimental hypothermia on changes of the electrophysiological equivalent of minute ventilation (Veq) was studied in rabbits under urethane-chloralose general anaesthesia with muscle relaxation and artificial ventilation. The animals were subjected to bilateral vagotomy prior to the experiment. During normothermia (37.5 +/- 0.7 degree C) and hypothermia (29.9 +/- 1.7 degrees C) the animals were given for breathing a hypercapnic mixture of gases (CO2 5% with O2 95%) and asphyxia was produced by switching off the respirator. The arterial blood pressure, blood flow in the common carotid artery, end-expiratory CO2 concentration, "integrated" phernic nerve activity and brain-stem temperature were recorded. The partial pressure of carbon dioxide and oxygen, hydrogen ion concentration and arterial acid-base balance were determined with correction for temperature changes. The equivalent of minute ventilation (being the product of the frequency and amplitude of "integrated" phrenic nerve activity) decreased in hypothermia by 91%, with a simultaneous fall of PaCO2 from 33,48 +/- 3.84 mmHg to 23.40 +/- 3.59 mmHg (by 30%). The hypercapnic stimulus applied during hypothermia produced a fivefold lower Veq value than in normothermia and under control conditions (despite a similar value of PaCO2 of 28.89 +/- 3.12 mmHg). The Veq value approaching that found under normal conditions in normothermia was observed during hypothermia only when asphyxia was induced when the value of PaCO2 was 37.07 +/- 8.74 mm Hg and that of PaO2 was 37.41 +/- 29.11 mmHg. During hypothermia the blood flow in the common carotid artery decreased by 16% when the animals were breathing the hypercapnic mixture. The analysis of the obtained results showed a direct effect of temperature on respiratory activity generation and regulation of arterial blood flow to the brain. It may be supposed also that hypothermia raises the response threshold to CO2 level in the breathed air.
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PMID:Minute ventilation changes in rabbits during experimental hypothermia. 642 Oct 87

Ketotifen (4-/1-methyl-4-piperidylidene/-4H-benzo[4,5]cyclohepta[1,2-b]thiophen-10(9H)-one hydrogen fumarate) inhibited spontaneous locomotor activity and amphetamine hypermotility in mice and rats, as well as L-DOPA-induced motor stimulation in mice. It produced in mice a slight hypothermia and did not prevent reserpine-induced hypothermia; thus, it does not posses properties or tricyclic antidepressants. Ketotifen showed some features of serotoninolytic: it inhibited the head twitch response to 5-hydroxytryptophan in mice, depressed tryptamine-induced clonic convulsions in rats, antagonized fenfluramine-induced hyperthermia in rats at high ambient temperature and showed weak antiserotonin action in the flexor reflex preparation. Ketotifen did not affect spiperone- or reserpine-induced catalepsy and showed no cholinolytic activity. LD50 of ketotifen (after 24 h) was 122.5 mg/kg ip in mice and 62.6 mg/kg ip in rats.
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PMID:Central action of ketotifen. 733 54

Using an intramyocardial pH needle probe (21 gauge) to monitor myocardial metabolism during ischemia, we determined the effect of potassium cardioplegia at both moderate and deep hypothermia. Five groups of 5 dogs each were placed on cardiopulmonary bypass and the pH probe was inserted approximately 10 mm into the left ventricular free wall. Cardiac ischemia was achieved by cross-clamping the ascending aorta at 37 degrees C (Group 1), 27 degrees C (Group 2), or 17 degrees C (Group 3). In the remaining two groups, aortic cross-clamping was followed by the infusion of 600 to 800 ml of potassium cardioplegic solution adjusted to cardiac temperatures of 27 degrees C (Group 4) or 17 degrees C (Group 5). In each group, myocardial temperature was maintained constant, electrical and mechanical activity observed, and pH recorded until a plateau was reached or for 3 hours. Our results show a progressive and significant decrease in the metabolic rate with reduction in temperature over the 37 degrees to 17 degrees C range. By abolishing contractile activity, potassium cardioplegia markedly reduces the rate of hydrogen ion accumulation at 27 degrees C, but at 17 degrees C the additive effect of cardioplegia is much less pronounced. These observations support the principle of reducing contractile activity to a minimum during elective arrest of the heart but indicate that potassium cardioplegia does little to further reduce the rate of anaerobic metabolism, as shown by the measurement of intramyocardial pH, under conditions of deep hypothermia.
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PMID:Intramyocardial pH during elective arrest of the heart: relative effects of hypothermia versus potassium cardioplegia on anaerobic metabolism. 2665 50


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