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

In pediatric cardiology tcPO2 is useful in monitoring cyanotic children given high-risk therapy such as balloon septostomy or drugs with controversial effects such as tolazoline in persistent fetal circulation. tcPO2 during administration of 100% oxygen enables a rapid, noninvasive differentiation between cyanosis due to intracardiac right-to-left shunt and that due to low cardiac output or pulmonary ventilation or diffusion difficulty. The size of the right-to-left shunt can be roughly estimated from the highest value of tcPO2, this estimation being influenced by anemia, hypothermia, and acidosis, among other factors. A trend of the tcPO2 rise is evident 90 seconds after the beginning of oxygen breathing. If tcPO2 does not rise at least 40 mm Hg over the initial value, a significant right-to-left shunt must be suspected. Interpretation of tcPO2 rise is difficult in dynamic right-to-left shunt, changing with oxygen breathing.
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PMID:tcPO2 in pediatric cardiology: application during balloon septostomy, tolazoline administration, and in children with right-to-left shunt. 53 16

The concentrations of adrenaline and noradrenaline, and dopamine-beta-hydroxylase in the plasma, and certain haemodynamic parameters, were determined in 14 children undergoing surgical correction of congenital cardiac defects under hypothermia at 30 degrees C and methoxyflurane anaesthesia. During the pre-operative phase of hypothermia at 30 degrees C, the adrenaline levels rose to about 300% of the inital levels, and the noradrenaline levels to about 200%. During the postoperative phase of re-warming at 34 degrees C, a further dysregulative release of catecholamines led to an increase in adrenaline levels to a critical concentration of about 800% of the norm, and in noradrenaline levels of about 400% of the norm. No change was seen in dopamine-beta-hydroxylase activity. Hypothermia thus results in a massive activation of the sympatho-neuronal and sympatho-adrenal systems, which is not prevented by methoxyflurane anaesthesia, and which may endanger the recently operated heart, particularly during the early post-operative period, because of the increased oxygen requirements imposed on the myocardium. In normothermia, on the other hand, methoxyflurane anaesthesia results in only a slight degree of activation of the sympathetic nervous system, which increased only slightly during the post-operative period. Under these conditions, the plasma dopamine-beta-hydroxylase activity remains unchanged. Unlike the changes in plasma catecholamine levels, dopamine-beta-hydroxylase activity cannot be regarded as an index of changes in sympatho-neuronal activity.
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PMID:[The effect of hypothermia and methoxyflurane-anaesthesia on sympatho-neuronal and sympatho-adrenal activity in the course of cardiac surgery (author's transl)]. 53 49

1. The capacity ofr thermoregulation and thermogenesis in lean and genetically obese (ob/ob) mice has been investigated. 2. At 4 degrees C ob/ob mice rapidly die of hypothermia, because of a reduced capacity for cold-induced thermogenesis, but the animals are able to survive if previously adapted to 12 degrees C. 3. At all environmental temperatures between 30 degrees C and 10 degrees C the body temperature of ob/ob mice is 2.0-2.5 degrees C below that of lean animals. This may be due to a lower "setting" for body temperature. 4. At 34 degrees C the oxygen consumption of obese mice is greater than that of the lean animals while at 30 degrees C it is similar. When the environmental temperature is below 30 degrees C the oxygen consumption of the lean mice is greater. The obese animals therefore expend less energy on thermoregulatory thermogenesis. 5. The capacity for non-shivering thermogenesis was measured in lean and obese mice by investigating the effect of an injection of L-nor-adrenaline (1000 microgram/kg body weight) on the metabolic rate at 31 degrees C. Non-shivering thermogenesis was reduced by one-half in the obese animals. 6. One cause of the obesity of the ob/ob mouse is its high metabolic efficiency. We suggest that this high metabolic efficiency is due, at least in part, to less energy being expended on thermoregulatory thermogenesis.
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PMID:Thermoregulation and non-shivering thermogenesis in the genetically obese (ob/ob) mouse. 56 45

Deep hypothermia (20 C) without cardiopulmonary bypass is a valuable technique during cardiac surgery in infants but rewarming of the heart following circulatory arrest and cardiac repair has traditionally been a lengthy and difficult process. In experimental animals rewarming the heart with microwave energy, as reported in this work, warms the heart before warming the periphery. In 18 mongrel dogs that were surface cooled to 20 C, we found that during microwave rewarming the core temperature rose 4.7 C per hour. Whole body oxygen consumption, heart rate, and cardiac output returned to normal at rates equal to the rates at which they decreased during surface cooling. Blood pressure and arterial gases remained adequate. Microwave rewarming appears to be a useful method for reestablishment of cardiac function and normothermia following deep hypothermia.
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PMID:Physiologic effects of deep hypothermia and microwave rewarming: possible application for neonatal cardiac surgery. 57 74

In six patients undergoing coronary vein graft operations under cardiopulmonary bypass and hypothermia, the temperatures of arterial and mixed-venous blood, nosopharynx, oesophagus, liver, rectum, deltoid and vastus lateralis muscles and 10 skin sites were recorded. Whole-body oxygen consumption was measured before cooling and twice during hypothermia. On average, a patient lost 1000 kJ of heat by the end of hypothermia, of which 84% was lost to the heat-exchanger and pump circuit. Evaporative and convective loss amounted to 380 kJ, while the patient's metabolism supplied 220 kJ. During rewarming, the pump returned 670 kJ to the patient. Nasopharyngeal temperature reflected accurately venous, oesophageal and hepatic temperatures in the steady state; however, it was slow to reflect changes. Compared with other sites, muscle remains warmer during hypothermia and cooler after rewarming.
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PMID:Thermal balance during cardiopulmonary bypass with moderate hypothermia in man. 58 94

Total cerebral ischaemia in rats caused a marked increase in the cisternal CSF potassium concentration but little change in CSF sodium or chloride concentration. The anaesthetic techniques studied (pentobarbitone, halothane/oxygen and nitrous oxide/oxygen/relaxant) did not effect the potassium increase following cerebral ischaemia. We conclude that the mechanism of barbiturate protection following cerebral ischaemia is different from that of hypothermia.
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PMID:Effect of anaesthetic agents on the ionic composition of cerebrospinal fluid following total cerebral ischaemia. 62 2

The influence of phenobarbitone anaesthesia on cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) during hypothermia (23 degrees C & 27 degrees C) was studied in the rat, using a modification of the Kety & Schmidt (1948) technique and arterio-venous differences for oxygen. Phenobarbitone (150 mg/kg) was found to decrease CMRo2 by 40-60% during hypothermia, when compared to N2O anaesthesia. At a body temperature of 23 degrees C, and during phenobarbitone anaesthesia, CMRo2 was reduced to about 15% of normal control value (about 10.3 ml.100g-1). CBF was reduced to about 50% of the phenobarbitone control value but was similar to the value obtained with N2O anaesthesia at 22 degrees C. It is concluded that the combination of phenobarbitone anaesthesia and hypothermia results in a more pronounced reduction in cerebral metablic rate for oxygen than can be achieved by administration of barbiturates to normothermic animals, or by reducing body temperature by 15 degrees C during superficial anaesthesia.
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PMID:Reduction of cerebral blood flow and oxygen consumption with a combination of barbiturate anaesthesia and induced hypothermia in the rat. 63 8

We evaluated the effects of methylprednisolone sodium succinate (MPSS) on 60 minutes of myocardial ischemia during profound (5 degrees C) topical cardiac hypothermia (ice chips) in a canine right heart bypass preparation. The ventricular function curve shifted to the right and downward, but not significantly, after ischemia, and stroke work declined significantly for both control and treated dogs. Contractility (rate of rise of left ventricular pressure and maximum velocity of the contractile element) declined for both groups but not significantly. Total coronary flow, oxygen consumption, and metabolism of lactate and pyruvate were not different for control and treated dogs. Ultrastructure of the outer and inner myocardium did not demonstrate benefit from MPSS. Intracellular and extracellular edema of moderate severity was slightly worse in the subendocardium, and reversible mitochondrial injury of a mild to moderate degreee was symmetrically present. Ice-related injury was not noted. We were unable to deomonstrate that pretreatment with MPSS favorably alters cardiodynamics or ultrastructure after 60 minutes of profound topical cardiac hypothermia.
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PMID:Topical cardiac hypothermia: the effect of methylprednisolone sodium succinate. 65 47

Experiments were conducted on dogs; cranio-cerebral hypothermia (a reduction of body temperature from 38 to 28 degrees C) led to increase of oxygen and to reduction of carbon dioxide tension in the blood. In case of marked hypothermia (24 degrees C) the blood gaseous concentration became less than at 28 degrees C, but remained above the initial level. This indicates prolonged preservation of adequate lung ventilation in the hypothermic organism.
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PMID:[Blood gases in craniocerebral hypothermia]. 67 45

Cerebral metabolic and vascular effects of hypothermia (30 C) and deep pentobarbital anesthesia, separately and combined, were evaluated in 15 mongrel dogs. External cardiovascular support was not used, and mean arterial blood pressures remained greater than 60 torr. Normothermic deep pentobarbital anesthesia, characterized by an electroencephalographic (EEG) frequency of less than 1 Hz, was associated with 30% decreases in cerebral metabolic rates for oxygen (CMRO2) and glucose (CMRG) from lightly anesthetized control values. Hypothermia (30 C) alone caused similar decreases in CMRO2 and CMRG in the presence of an active EEG. The use of pentobarbital anesthesia and hypothermia combined achieved significantly greater (P less than 0.05) decreases in CMRO2 (70%) and CMRG (72%) from the control state. Cerebral vascular resistance (CVR) increased by 70% (P less than 0.05) during hypothermia and about 20% when pentobarbital was administered to normothermic dogs. In hypothermic animals the addition of pentobarbital had a minimal effect on CVR. No alteration in the oxygen-glucose or lactate-glucose index indicative of cerebral hypoxia occurred in any experimental group. This study indicates that barbiturates combined with hypothermia decrease cerebral metabolism to a greater extent than hypothermia or barbiturate alone. When cerebral hypometabolism is therapeutically necessary, barbiturates may be indicated as an adjunct to moderate hypothermia.
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PMID:Cerebral hypometabolism obtained with deep pentobarbital anesthesia and hypothermia (30 C). 68 36


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