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

The ability of nifedipine to enhance myocardial protection was assessed using an isolated rat heart model of cardiopulmonary bypass and ischaemic cardiac arrest. With normothermic ischaemic arrest (35 min, 37 degrees C), nifedipine addition improved the protective properties of the St Thomas' cardioplegic solution. Optimal protection was observed with 0.075 mumol nifedipine X litre-1, where post-ischaemic recovery of aortic flow was improved from 47.9 +/- 5.2% to 76.7 +/- 2.9% (P less than 0.001) and creatine kinase leakage was reduced by approximately 50%. Despite the marked additional protection under normothermic conditions the drug was unable to improve contractile recovery after a period of hypothermic ischaemic arrest (150 min, 20 degrees C) although it did allow a significant reduction (22%) in creatine kinase leakage. In other studies, the ability of nifedipine to replace the cardioplegic solution was examined. Under normothermic conditions, it showed a good ability to protect against ischaemia, but this protection did not match that afforded by the St Thomas' cardioplegic solution. Under hypothermic conditions the drug failed to substitute for the cardioplegic solution, suggesting that a common modality between hypothermia and nifedipine-induced protection.
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PMID:Nifedipine and cardioplegia: rat heart studies with the St Thomas' cardioplegic solution. 666 43

The ability of dl-verapamil to enhance myocardial protection when given before, during, or after myocardial ischemia was assessed with the use of an isolated working rat heart model of cardiopulmonary bypass and ischemic cardiac arrest. Under conditions of normothermic ischemic arrest (30 minutes at 37 degrees C), the addition of verapamil enhanced the protective properties of the St. Thomas' Hospital cardioplegic solution. Optimal protection was observed with verapamil concentrations of 0.5 mg/L (1.09 mumol/L) of cardioplegic solution. Under these conditions, postischemic enzyme leakage was reduced by 32.2% and the postischemic recovery of aortic flow was improved by 18.7%. Despite the additional protection at normothermia, the drug at several concentrations appeared unable to improve functional recovery after an extended period of hypothermic arrest (150 minutes at 20 degrees C), although under these conditions its inclusion in the cardioplegic solution could substantially reduce enzyme leakage. In other studies, the ability of various doses of verapamil alone as a substitute for the cardioplegic solution was examined. At the optimal dose (again 0.5 mg/L), and under normothermic conditions, verapamil alone was a good protection against ischemic injury, although this protection did not match that afforded by the St. Thomas' Hospital cardioplegic solution. In similar studies under hypothermic conditions, the drug failed to afford tissue protection, perhaps indicating some common modality between hypothermia and verapamil-induced protection. Pretreatment with verapamil (0.1 mg/L) prior to ischemia offered moderate additional protection, but its use during reperfusion failed to enhance overall recovery.
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PMID:Cardioplegia and slow calcium-channel blockers. Studies with verapamil. 687 61

Significant morbidity and mortality associated with traumatic brain injury (TBI) are allied with secondary posttrauma inflammatory complications. Hypothermia has been suggested as a possible treatment to lessen or suppress these inflammatory reactions. We report here that interleukin 1 beta, a cytokine responsible for initiating inflammatory cascades, is elevated in rat cortex within 6 h of TBI in the rat. Nerve growth factor (NGF) RNA and protein also increased subsequently, and NGF protein remained elevated for up to 7 days. Four hours of whole body hypothermia (32 degrees C), applied immediately after the TBI, attenuated the posttrauma increase in IL-1 beta RNA and eliminated the increase in NGF RNA and protein observed in cerebral cortex following TBI. Thus, hypothermia may be an effective therapy to diminish the posttrauma inflammatory cascade in the brain (as suggested by the decrease in IL-1 beta). However, the same treatment may hinder the brain's intrinsic repair mechanisms. Optimal treatment may, therefore, require supplemental administration of neurotrophic factors or other agents along with hypothermia.
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PMID:Hypothermia attenuates the normal increase in interleukin 1 beta RNA and nerve growth factor following traumatic brain injury in the rat. 762 62

Because many infants who require cardiac operation have cyanotic heart disease, we determined whether the existing calcium content of St. Thomas' II solution (1.2 mmol/L) is optimal to protect the immature rabbit heart hypoxemic from birth during subsequent ischemia. Modified hypothermic St. Thomas' II solutions (calcium content, 0 to 2.4 mmol/L) were compared with hypothermic Krebs bicarbonate buffer in protecting chronically hypoxemic (PaO2 = 34 +/- 11 mmHg, SaO2 = 63% +/- 3%) versus normoxemic (PaO2 = 76 +/- 11 mmHg, SaO2 = 92% +/- 3%) immature hearts (7 to 12 days old) during ischemia. Hearts (n = 6 per group) underwent aerobic 'working' perfusion with Krebs bicarbonate buffer and cardiac function was measured. The hearts were then arrested with a 3 minute infusion of either cold (14 degrees C) Krebs buffer (1.8 mmol calcium/L) as hypothermia alone or modified St. Thomas' II solution before 6 hours of hypothermic (14 degrees C) global ischemia. Hearts were reperfused and postischemic enzyme leakage and recovery of function were measured. A bell-shaped dose-response profile was observed for recovery of postischemic aortic flow but not for postischemic creatine kinase leakage, with improved protection occurring at lower calcium concentrations. Optimal myocardial protection occurred at a calcium content of 0.4 mmol/L, which was significantly better than with hypothermia alone or standard St. Thomas' II solution. We conclude that the existing calcium concentration of St. Thomas' II solution is responsible, in part, for its inadequate protection of immature myocardium hypoxemic from birth during ischemia.
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PMID:Calcium and cardioplegic protection of the ischemic immature heart: impact of hypoxemia from birth. 794 63

A key element of neonatal regionalization is the establishment of transport links between centres of tertiary care and subregional centres. During the 11-year period 1982-92, 186 transports were undertaken from the neonatal unit, Vestfold Central Hospital, for a total of 180 patients, or 0.8% of all live born infants (n = 23,652). 64 patients (36%) were referred for prematurity/respiratory distress syndrome (IRDS), 81 (45%) for congenital malformations, and 35 (19%) for other conditions. Transports for prematurity/IRDS declined significantly from the the first 6-year period 1982-87 to the last 5-year period 1988-92 (3.6 vs. 1.8 per 1,000 live born infants; p < 0.01), owing to the establishment of a local respirator treatment programme for severe IRDS. In 71 (38%) transports the infants were mechanically ventilated. Seven (10%) suffered in-transport complications related to the endotracheal tube. At arrival, significantly more patients were anaemic (Hb < 14 g%; transports before 48 hours after birth), alcalotic (pH > 7.50), hypocapnic (PCO2 < 4 kPa) or had a base excess < -10 mmol/l than before transportation (p < 0.05). There was a tendency towards more patients with hypothermia (tp < 36 degrees C), acidosis (pH (< 7.20) and hypercapnia (PCO2 > 10 kPa) at arrival than before transportation (p > 0.05). No deaths occurred during transport. However, two infants died within two hours after arrival, giving a transport-related mortality rate of 1%. Transporting critically ill neonates implies discontinuity of treatment and monitoring of these infants. Optimal stabilization before transportation, and scrupulous work on technical details are of utmost importance.
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PMID:[Transport from a subregional neonatal unit. Experiences from Vestfold Central Hospital during an 11-year period 1982-92]. 825 80

Hypothermic alkaline pharmacologic cardioplegia used in pediatric cardiac surgery may be less than satisfactory despite its benefits in adults. We determined whether the pH (7.8) of standard St. Thomas' II cardioplegic solution contributes to inadequate protection of the ischemic immature heart and whether the effect is age-related. Modified hypothermic St. Thomas' II solution (pH range, 4.8 to 8.8) was compared with hypothermic bicarbonate buffer alone (pH 7.25) in protecting the ischemic immature (7 to 10 days old) and mature (12 months old) rabbit heart. Isolated hearts (n = 6 per group) were perfused with bicarbonate buffer, and aortic flow was measured before hypothermic (14 degrees C) ischemia (immature hearts: 4 hours; mature hearts: 3 hours). Hearts were reperfused, and enzyme leakage and recovery of function were measured. In the immature heart, a bell-shaped dose-response profile was observed for pH and recovery of aortic flow but not for postischemic creatine kinase leakage. Optimal recovery of aortic flow (98% +/- 3%) occurred at pH 6.8, which was greater than protection with hypothermia alone (82% +/- 4%; p < 0.05) and standard St. Thomas' II solution (72% +/- 2%; p < 0.05). In the mature heart, a bell-shaped dose-response curve existed for recovery of aortic flow and a U-shaped curve existed for creatine kinase leakage. Again, optimal recovery of aortic flow (84% +/- 5%), which was superior to that with standard St. Thomas' II solution (60% +/- 8%; p < 0.05), and minimal enzyme leakage also occurred at pH 6.8, as did the least enzyme leakage (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age and protection of the ischemic myocardium: is alkaline cardioplegia appropriate? 845 42

Mild hypothermia (33 degrees C to 35.5 degrees C) is reported to improve oxygenation and survival in patients with lung failure (1). Although hypermetabolism may account for about 50% of the ventilatory demand in ARDS patients, the concept of reducing oxygen consumption (VO2) by lowering metabolic rate, has only recently gained attention (2). Our study was aimed to test whether mild hypothermia established by continuous veno-venous haemofiltration (CVVHF), could optimize values for oxygen kinetics in ARDS patients. Overall, we recruited 27 patients with ARDS and sepsis. Prior initiation of CVVHF patients had to meet the following criteria: a) Murray score > 2.5, and hypoxaemia with PaO2/FIO2 < 200, b) hyperthermia of > 38 degrees C, c) cardiovascular instability requiring inotropic support. Evaluation of cardio-respiratory data was performed within four different phases (I = before, II + III during and IV = after CVVHF) every 6 hours. Core temperature as derived from the thermistor of pulmonary artery catheter was aimed to be between 35.0 degrees C and 36.5 degrees C. Optimal values for oxygen delivery (DO2) (> 550 mL/min/m2) and VO2 (> 160 mL/min/m2) were defined according to Shoemaker and achieved by fluid loading, transfusion and inotropic support (3). Septic shock occurred in 10 of 14 nonsurvivors (nons) and 2 of 13 survivors (surv). Mean values for DO2 and VO2 were calculated at different body temperature ranges. While at 37 degrees C DO2 was identical between surv and nons, (663 +/- 128 versus 666 +/- 127 means +/- SD) moderate hypothermia led to a small decrease of DO2 in surv and a significant decrease in nons (632 +/- 134 versus 605 +/- 128 mL/min/m2) at 35 degrees C. Concerning VO2 during hypothermia, there was a significant drop in nonsurvivors while in survivors the decrease was less pronounced. We could demonstrate a decrease in DO2 and VO2 during mild hypothermia during CVVHF. However, decreases in nonsurvivors were more pronounced than in survivors. These results suggest that the inability to achieve optimal values for DO2 and VO2 during mild hypothermia induced by CVVHF could serve as a prognostic sign for fatal outcome. Although oxygen consumption is decreased during hypothermia, hypoxaemia may result due to alterations of the oxygen transport on a cellular basis. The relationship between oxygen transport and temperature during CVVHF therefore deserves further studies.
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PMID:Optimal values for oxygen transport during hypothermia in sepsis and ARDS. 859 83

Resuscitative (postinsult) hypothermia is less well studied than protective-preservative (pre- and intra-arrest) hypothermia. The latter is in wide clinical use, particularly for protecting the brain during cardiac surgery. Resuscitative hypothermia was explored in the 1950s and then lay dormant until the 1980s when it was revived. This change occurred through the discoveries of brain damage mitigating effects after cardiac arrest in dogs, and after forebrain ischemia in rats, of mild (34 degrees C) hypothermia (which is safe), and of benefits derived from moderate hypothermia (30 degrees C) after traumatic brain injury or focal brain ischemia in various species. The idea that protection-preservation or resuscitation by hypothermia is mainly explained by its ability to reduce cerebral oxygen demand has been replaced by an increasingly documented synergism of many beneficial mechanisms. Deleterious chemical cascades during and after these insults are suppressed even by mild hypothermia. Prolonged moderate hypothermia carries some risks, e.g., arrhythmias, infection and coagulopathies. These side effects need further study. In global brain ischemia, protective-preservative mild hypothermia provides lasting mitigation of brain damage. Resuscitative mild hypothermia, however, may be beneficial in terms of long-term outcome or may merely delay the inevitable loss of selectively vulnerable neurons. Even if the latter is true, mild hypothermia may extend the therapeutic window for other interventions. This extension of the therapeutic window requires further documentation. After normothermic cardiac arrest of 11 mins in dogs, mild resuscitative hypothermia from 15 mins to 12 hours after reperfusion plus cerebral blood flow promotion normalized functional recovery with the least histologic damage seen thus far. Optimal duration of, and rewarming methods from, resuscitative hypothermia need clarification. The earliest possible induction of mild hypothermia after cardiac arrest seems desirable. Head-neck surface cooling alone is too slow. Among many clinically feasible rapid cooling methods, carotid cold flush and peritoneal cooling look promising. After traumatic brain injury or focal brain ischemia, which seem to still benefit from even later cooling, surface cooling methods may be adequate. Resuscitative hypothermia after cardiac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.
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PMID:Resuscitative hypothermia. 860 9

Optimal use of hypothermic circulatory arrest during aortic surgery requires understanding of its physiology. Research in laboratory animals and clinical observations have now documented that considerable residual cerebral metabolism remains with cooling to levels of 15-18 degrees C, especially if cooling intervals are short, reflected by persistent jugular venous desaturation. Cooling should be continued to below 15 degrees C if the duration of HCA is expected to exceed 20 minutes, and continued until jugular venous saturations exceed 95%. There is considerable laboratory evidence that even short durations of HCA are followed by a prolonged interval of increased cerebral vascular resistance during which cerebral metabolism is maintained at normal levels by markedly increased oxygen extraction. Clinical observations have now confirmed that considerable jugular venous desaturation is present in patients following HCA: it is more pronounced with prolonged HCA, and is still present as late as six hours after the start of rewarming. This reinforces the concept of a prolonged postoperative vulnerable interval following HCA, during which any compromise in oxygen delivery has the potential for producing cerebral injury. Several adjunctive measures have been shown to improve outcome following HCA. The simplest and most important is topical hypothermia: packing the head in ice during the interval of HCA. Retrograde cerebral perfusion (RCP) has also been shown to improve EEG recovery as well as histological and behavioral outcome in laboratory animals following prolonged HCA, but some of its effect may be secondary to its efficacy in keeping the brain cold, since RCP provides very low rates of flow and supports metabolism at a much lower level than antegrade perfusion at the same temperature. But despite the clear superiority of antegrade perfusion, and the documentation of some benefits of RCP in laboratory measures of cerebral protection, clinical results using RCP and ACP have not yet demonstrated the superiority of these methods over use of HCA alone, perhaps because these modalities are usually employed in patients with unusually high risk of neurological injury: those with dissection or with clot or atheroma in the aorta. Nevertheless, recent years have seen considerable reduction in mortality following aortic surgery, especially in older patients, and a trend toward a lower incidence of permanent neurologic dysfunction. The presence of preoperative rupture or hemodynamic compromise, and of clot or atheroma in the aorta, remain the most significant risk factors both for death and occurrence of stroke.
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PMID:Use of hypothermic circulatory arrest for cerebral protection during aortic surgery. 927 61

Hypothermia is commonly used to prevent ischemic renal damage during complex nephron-sparing surgical procedures requiring temporary renal artery occlusion. We developed a novel Cooling Sheath device, which is compatible with laparoscopy, to protect the kidney hypothermically during 60 minutes of temporary arterial occlusion in a laparoscopic swine model. Comparison of temperature curves and histology to control groups undergoing open slush surface cooling and laparoscopic warm ischemia for similar time periods was performed. Optimal hypothermic temperatures were reached rapidly and maintained with the use of the Cooling Sheath. Ischemic damage, present in all kidneys subjected to warm ischemia, was not found on histopathologic examination of the cooled kidneys. This new device provides hypothermic protection of the kidney during ischemia. The use of the Cooling Sheath combined with temporary arterial occlusion will allow more complex nephron-sparing renal surgery to be performed using laparoscopy.
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PMID:The laparoscopic cooling sheath: novel device for hypothermic preservation of kidney during temporary renal artery occlusion. 960 43


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