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

We investigated changes in myocardial pH during cardioplegic arrest with five methods of preservation at 15 degrees +/- 1 degree C. Twenty-five dogs were subjected to cardiopulmonary bypass for 150 minutes. Group I (control) had hypothermia only. Group II received THAM-buffered blood cardioplegia, group III a bicarbonate-buffered blood cardioplegic solution, group IV infusions of hyperkalemic blood, and group V oxygenated St. Thomas 2 solution. After 120 minutes of ischemia, interstitial pH in group I was markedly depressed (6.4 +/- 0.07; p < 0.01). The pH in groups II and IV was well maintained (7.23 +/- 0.05 and 7.27 +/- 0.07) and differed significantly (p < 0.05) from that of the remaining groups. The pH in groups III and V was less well maintained (7.14 +/- 0.02 and 7.01 +/- 0.05), with no significant difference (p > 0.05) between these two groups. Postreperfusion functional recovery after 45 minutes was 24% +/- 6% in group I, 92% +/- 3% in group II, 82% +/- 5% in group III, 84% +/- 4% in group IV, and 66% +/- 6% in group V. Creatine kinase levels were significantly (p < 0.01) increased and ultrastructural damage was more prominent in group I compared with the remaining groups. Myocardial water content significantly increased in all groups. We conclude that a strongly buffered blood-based cardioplegic solution is more effective in preventing interstitial acidosis during moderate hypothermia and that maintenance of an optimal tissue pH plays an important role in postischemic functional recovery.
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PMID:Interstitial pH during myocardial preservation: assessment of five methods of myocardial preservation. 843 Oct 54

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

Thirty-five isolated rabbit hearts were subjected to 60 minutes of storage after cardiac arrest with high K+ crystalloid cardioplegic solution at 5 degrees C. They were divided into five groups (n = 7 per group) according to the preservative protocol: group I (simple immersion in 0 degrees C normal saline solution), group II (simple immersion in 30 degrees C blood cardioplegic solution), group III (immersion and perfusion in 30 degrees C blood cardioplegic solution), group IV (simple immersion in 10 degrees C blood cardioplegic solution), and group V (immersion and perfusion in 10 degrees C blood cardioplegic solution). After storage for 1 hour, cardiac function, tissue water content, and the number of hearts capable of ejecting against a 100 cm H2O column afterload were recorded and compared among the five groups. Cardiac function in group II was not different from group I. Aortic pulse pressure and left ventricular developed pressure were lower in group II than in group III, IV, or V. Aortic developed pressure was higher in groups III and V (p < 0.05). Tissue water content in group I was significantly higher than in groups II, III, and V (p < 0.05). All hearts in groups III and V could eject against a 100 cm H2O afterload after preservation (p < 0.05 versus groups I, II, and IV). Factorial analysis among the groups using blood cardioplegic solution showed that either hypothermia or perfusion alone or the combination was a protective factor in providing functional recovery of stored hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Functional recovery in rabbit heart after preservation with a blood cardioplegic solution and perfusion. 847

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

Ischemic preconditioning has not been assessed in an experimental model for myocardial preservation during heart transplantation. Using isolated working rat hearts, ischemic preconditioning was investigated as an adjunct to isolated hypothermic (group 1), crystalloid (group 2: University of Wisconsin solution; group 3: St. Thomas' Hospital cardioplegic solution II; group 4: Bretschneiders' cardioplegic solution), and noncrystalloid (group 5: cold blood cardioplegia) preservation during a 10-hr period of global ischemia at 4 degrees C. After acquisition of functional baseline data, ischemic preconditioning was induced with one cycle of 5 min of normothermic ischemia and 5 min of reperfusion before induction of global hypothermic ischemia (n= 10/group). Nonpreconditioned hearts (n= 10/group) were assessed for control. Ischemic preconditioning improved postischemic: functional recovery. Thus, aortic flow after 60 min of reperfusion recovered to 0%, 8%, 0%, 1% and 0% in control groups 1 to 5 without ischemic preconditioning and 21%, 25%, 10%, 8%, and 3% in groups 1 to 5 with ischemic preconditioning. The same pattern of recovery was observed in regard to postischemic maximum developed left ventricular pressure, which recovered to 21%, 56%, 30%, 36%, and 19% in groups 1 to 5 without preconditioning and 46%, 75%, 49%, 40%, and 47% in the corresponding groups with ischemic preconditioning. High-energy phosphate contents were not significantly different between preconditioned hearts and corresponding nonpreconditioned control hearts. Creatine kinase leakage during early reperfusion was found to be reduced with ischemic preconditioning. Thus, we have demonstrated that ischemic preconditioning can improve contractile function after global hypothermic ischemia in the isolated rat heart and we have shown that this protection is additive to that of hypothermia-induced protection during global ischemia at 4 degrees C. This endogenous mechanism of cardioprotection was effective regardless of whether preservation was accomplished using cardioplegic solution or topical hypothermia alone. This may have clinical implications in myocardial preservation for heart transplantation.
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PMID:Ischemic preconditioning enhances donor heart preservation. 869 37

Glycolysis, glucose oxidation, palmitate oxidation, and cardiac function were measured in isolated working hearts from ground squirrels and rats subjected to a hypothermia-rewarming protocol. Hearts were perfused initially for 30 min at 37 degrees C, followed by 2 h of hypothermic perfusion at 15 degrees C, after which hearts were rewarmed to 37 degrees C and further perfused for 30 min. Functional recovery in ground squirrel hearts was greater than in rat hearts after rewarming. Hypothermia-rewarming had a similar general effect on the various metabolic pathways in both species. Despite these similarities, total energy substrate metabolic rates were greater in rat than ground squirrel hearts during hypothermia despite a lower level of work being performed by the rat hearts, indicating that rat hearts are less efficient than ground squirrel hearts during hypothermia. After rewarming, energy substrate metabolism recovered completely in both species, although cardiac work remained depressed in rat hearts. The difference in functional recovery between rat and ground squirrel hearts after rewarming cannot be explained by general differences in energy substrate metabolism during hypothermia or after rewarming.
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PMID:Effects of hypothermia on energy metabolism in rat and Richardson's ground squirrel hearts. 910 58

From January 1989 through June 1996, 29 patients underwent surgical repair of type A acute aortic dissection. Mean age was 59 +/- 13.5 years (range 25-76 yrs) and 21 patients (72.4%) were male. Nineteen patients (65.5%) had systemic hypertension and 3 (10.3%) Marfan syndrome. One patient (3.4%) had prior surgical repair of descending aortic dissection and CABG. Six patients (20.7%) were operated on in shock. The dissection was limited to the ascending aorta (DeBakey type II) in 12 patients (41.4%). Eleven patients (37.9%) had severe aortic regurgitation. Replacement of the ascending aorta was performed in all cases and extended to include the transverse arch in one. Twenty-three patients (79.3%) were operated upon using a tubular graft (sacron-21, homograft-2) with aortic valve resuspension. In the remaining 6 (20.7%) the aortic valve and root were replaced using a Bentall procedure, modified with a homograft in 3 cases. Five patients (17.2%) had associated surgery: CABG (4) and closure of aortic-atrial fistula (1). Mean cardiopulmonary bypass time was 134 minutes (range 70 to 285 min) and aortic cross-clamp time was 58 minutes (range 23 to 93 min). Hypothermic circulatory arrest for open distal anastomosis was used in 26 patients (89.7%) (mean time 22 min; range 10 to 32 min), with retrograde cerebral perfusion in the last 4 years (18 cases; 62.1%). Hospital mortality was 17.2% (5 patients). Eight patients (27.6%) had hospital morbidity: reexploration for bleeding (4 cases), CVA (3), A-V block necessitating permanent pacemaker (1). The mean time of hospitalization was 18 days (range 9 to 81 days). In the follow-up period (mean 38 mths; range 4 to 94 mths), 2 patients died (CVA and gastrointestinal bleeding) and 4 required hospitalization (perforated duodenal ulcer, peritonitis, suspected endocarditis, supraventricular tachyarrhythmia-1 patient each). All 22 survivors (75.9%) returned to the functional status they had prior to the dissection and 18 of them (81.8%) are in NYHA functional class I. Type A acute aortic dissection is a complex pathology and the postoperative mortality remains significant, but surgery permits good functional recovery and an active life for the survivors.
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PMID:[Surgery for acute type-A aortic dissection]. 930 6

Hypothermia protects ischemic tissues by reducing ATP utilization and accumulation of harmful metabolites. However, it also reduces ATP production, which might cause deterioration in the energy supply/demand ratio. Modulation of energy supply/demand according to temperature has not been previously studied in detail. In this study, isolated, perfused rabbit hearts (n = 60) were used to determine the effects of various temperatures on myocardial energy metabolism and function during cardioplegic arrest. Ischemia was induced by crystalloid cardioplegic solution at 4, 18, 30, and 34 degrees C for 120 min, respectively. At each temperature, the hearts were divided into a glucose-treated group which contained 22 mM glucose in cardioplegic solution as the only substrate and a control group which contained 22 mM mannitol to keep same osmolarity. Following 15 min reperfusion, recovery of left ventricular developed pressure (DP), +/- dP/dtmax, and the product of heart rate and DP were significantly higher in 30, 18, and 4 degrees C groups than those in 34 degrees C control group. The functional recovery was also significantly higher in the 34 degrees C glucose-treated group than that in the 34 degrees C control group, but there was no difference between those groups at 30 degrees C and the temperature below 30 degrees C. Myocardial ATP concentration was significantly lower in 34 degrees C control group than those in other groups. There is a close relationship between myocardial ATP concentration and functional recovery (R2 = 0.90). The accumulations of lactate and CO2 were significantly higher at 34 degrees C in glucose-treated group than those in the control group. However, there was no significant difference between these two groups at 30 degrees C and the temperature below 30 degrees C. These results indicate that under these study conditions: (1) a marked decrease in energy supply/demand occurs above 30 degrees C, implying that a temperature threshold exists; and (2) this can be ameliorated by provision of glucose as substrate in cardioplegia solution.
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PMID:Temperature threshold and modulation of energy metabolism in the cardioplegic arrested rabbit heart. 950 Sep 28

The retrospective results of external lumbar drainage in 7 adult patients with severe closed head injury and intracranial pressure (ICP) refractory to aggressive management strategies are presented. All patients had Glasgow Coma Scale (GCS) scores of 8 or less within 24 hours after admission and were treated by a staircase protocol including sedation, ventricular drainage, hyperventilation and mannitol. In three cases barbiturate drugs and an artificially induced hypothermia were used. Four patients required surgical evacuation of mass lesions. Three patients made a good functional recovery, 2 were severely disabled and 2 patients died. In none of the patients clinical signs of cerebral herniation occurred. We recommend additional external lumbar drainage in adults with severe head injury unresponsive to aggressive ICP control with open basilar cisterns and absent focal mass lesions on computerized-tomography scan before drainage.
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PMID:External lumbar drainage in uncontrollable intracranial pressure in adults with severe head injury: a report of 7 cases. 977 37

Traumatic brain injury in the United States is a serious health problem: it is a significant factor in approximately half of all trauma-related deaths, and, leads to persistent, long-term neurologic dysfunction in survivors. Physiological changes that accompany brain trauma such as cardiovascular alterations, hypercapnia, hypoxiaischemia, metabolic dysfunction, and alterations in the endogenous neurochemical systems are associated with poor clinical outcome. Using a variety of animal models, experimental studies have begun to elucidate these neurochemical disturbances that underlie the behavioral deficits and the pathologic outcome. Modification of the post-traumatic neurochemical milieu can promote functional recovery. While a number of currently available pharmaceutical compounds have been reported to be effective in various animal models of TBI, their utility in the clinical setting has been disappointing [119]. New hope has arisen for the treatment of TBI, based upon new research findings regarding the development of novel pharmacological therapies for brain trauma. Reduction of brain temperature can maintain relative tissue homeostasis by lowering metabolic activity. Hypothermia has been attempted in patients over the past 50 years and recent experimental evidence suggests that posttraumatic hypothermia can attenuate EAA release and free-radical production [120]. In animal models, hypothermic treatment has attenuated post-traumatic neurologic motor dysfunction [121,122], improved histopathologic damage [123,124], and reduced the extent of cytoskeletal damage [120]. In addition, the armamentarium of potentially neuroprotective compounds, which has increased rapidly in the recent years, provides promising pharmacological therapies for the treatment of TBI.
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PMID:Pharmacotherapy for traumatic brain injury: a review. 983


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