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

We compared moderate (29 degrees C.) and profound (5 degrees C.) (ice chips) cardiac hypothermia for myocardial preservation during aortic cross-clamping for 30 or 60 minutes in a canine right heart bypass preparation. Ventricular function deteriorated significantly at 29 degrees C. but not at 5 degrees C. Maximum dp/dt declined only after 60 minutes of ischemia at 29 degrees C., and Vmax decreased after one hour at either temperature. Lactate and pyruvate washout were greater after 29 degrees C., and pyruvate production persisted after 60 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C. Reactive hyperemia was greater after 30 minutes of ischemia at 29 degrees C., and total coronary flow remained elevated after 60 minutes of ischemia at 29 degrees C. Coronary flow distribution was not altered by hypothermia. Ultrastructural changes were primarily time dependent and not temperature dependent. Ice-induced subepicardial injury was not evident in the ultrastructure or by flow distribution. Sixty minutes of profound topical cardiac hypothermia is moderately well tolerated by the canine heart, but functional and structural alterations are evident.
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PMID:Topical cardiac hypothermia for myocardial preservation. 87 Jul 64

Four cases of gunshot wounds to the suprarenal abdominal aorta are described. All required prosthetic graft replacement including one or more visceral arterial branches. Two patients survived. Factors important in survival were rapid transportation permitting early resuscitation and retroperitoneal tamponade which delayed exsanguination and permitted stabilization with systematic management. The major problem in management of gunshot wounds of the suprarenal abdominal aorta is limitation of visceral ischemia, particularly hepatic and renal. Special adjuncts such as local renal hypothermia, as used in these cases, or bypass techniques are necessary and should be available before exploration of a periaortic hematoma due to gunshot wound in this area.
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PMID:Gunshot wounds of the suprarenal abdominal aorta. 93 49

Recent studies have shown that after total coronary artery occlusion, there is impaired "reflow" of blood accompanied by myocardial and capillary endothelial cell swelling. To investigate the effect of prolonged low flow myocardial ischemia on coronary vascular resistance, regional hypoperfusion of the distal left anterior descending coronary artery was studied in 31 autonomically blocked dogs on right heart bypass. Heart rate, aortic pressure, and, during ischemia, left ventricular end-diastolic pressure were held constant. The distal left anterior descending coronary artery was perfused at a substantially reduced perfusion pressure which resulted in an antegrade coronary blood flow that usually was between 3% and 7% (0.5-1 ml/min) of control. When relative hypothermia (33-34 degrees C) was induced in nine dogs, left anterior descending coronary artery vascular resistance did not change during 2.5-3 hours of low flow ischemia. Under euthermic conditions (37-40 degrees C) in 17 dogs there was a consistent progressive increase in distal left anterior descending coronary artery vascular resistance starting at 90 minutes (median) after onset of ischemia. By 110-140 minutes ischemic antegrade flow decreased by 35 +/- 4% (SEM) (P less than 0.01). Directionally similar flow changes were observed in six euthermic experiments using the krypton-85 washout technique. Light microscopy did not reveal hemorrhage as a cause of the increased vascular resistance. The perfusion impairment did not occur in two euthermic, nonischemic hearts. In five dogs elevation of serum osmolality by 23 +/- 11 mOsmol/liter with mannitol attenuated the progressive decrease in flow. Thus, a progressive perfusion defect exists in the ischemic low flow state in the heart which presumably contributes to the extent of eventual necrosis.
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PMID:Progressive perfusion impairment during prolonged low flow myocardial ischemia in dogs. 93 13

An isolated perfused working rat heart model was used to investigate the extent to which various protective agents, used either singly or in combination, were able to increase the resistance of the heart to periods of transient ischemia. The aim of the studies was to develop a solution which, if infused into the coronary vessels just prior to the onset of ischemia, would rapidly induce arrest and would also counteract several of the deleterious cellular changes known to occur during myocardial ischemia. Agents with induce cardiac arrest, modify cellular ion loss, affect substrate utilization, energy production and energy stores, affect coronary vessel diameter and cell swelling, prevent dysrhythmias, and affect metabolic rate were investigated. The additive effects of these agents were evaluated. An aqueous solution was formulated which contained high concentrations of potassium and magnesium, in combination with adenosine triphosphate, creatine phosphate and procaine. This solution increased the recovery of the ischemic (37 degrees C for 30 min) rat heart from 0% to 93%. The safe period of ischemia could be further increased by the use of hypothermia.
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PMID:Cellular protection during myocardial ischemia: the development and characterization of a procedure for the induction of reversible ischemic arrest. 93 20

Experimental examinations were performed in 22 dogs to find out the mechanism which leads to a permanent or a reversible damage of the renal parenchyma after normo- and hypothermic ischemia. For this reason the perfusion and the distribution were examined with 133Xe, the vascular changes by angiography, and the parenchymal function with 131I-Hippuran. After normothermic ischemia a short-term reactive hyperemia appeared, which however could not compensate the damage of the renal tubular cells and the resulting excretory insufficiency. After hypothermic ischemia the perfusion was reduced, probably as a consequence of a vasconstriction by cold, however, the function of the tubular cells remained intact, because of the protective mechanism of the hypothermia. The importance of these findings for the development of the so-called "shock-kidney" (acute tubular necrosis) and for the conservative renal surgery in hypothermia is discussed and the application of measures beneficial to perfusion, are suggested.
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PMID:[Changes in perfusion and blood flow distribution following normo- and hypothermic ischemia of the kidneys]. 98 Jul 93

The clinic of such injuries is characterized by marked local manifestations (solid progressive edema of the injured limb leading frequently to decompensated ischemia) and a high incidence of acute renal insufficiency. Hemostatic disorders are manifested in hyperkalemia, hyponatremia, hypocalcemia, cell-extracell transfer of electrolytes, metabolic disorders in the myocardium, as evidenced by EEG findings. It is the authors' opinion that therapeutic measures should be aimed at liquidation of the progressive edema (hypothermia, fasciotomy), prevention of acute renal insufficiency and correction of metabolic disorders.
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PMID:[Postural crush syndrome]. 101 97

Different methods of preservation are examined in long-lasting extremity ischemia in dogs. After preservation of 10 h duration by hypothermia and perfusion the status of energy-rich phosphates and pH was equivalent to the status after 2 h of ischemia under control conditions.
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PMID:[Preservation of dog limbs through hypothermic perfusion]. 103 22

Three patients with severe hypertension secondary to renal artery stenosis were treated by renal autotransplantation. Of these 3 patients 2 had solitary kidneys and 1 had 2 renal arteries to each kidney, all of which were stenosed. Renal autotransplantation with hypothermia of the kidney was performed in all 3 patients rather than the more conventional arterial bypass or endarterectomy because 1) hypothermic preservation permitted a prolonged ischemia time and 2) there was improved exposure for the vascular anastomosis. Postoperatively 2 patients remained normotensive without drugs for 9 and 12 months and 1 patient died of septicemia not directly related to the autotransplant. All 3 patients required expansion of the intravascular volume postoperatively to overcome the loss of vasoconstrictor substances following restoration of renal blood flow.
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PMID:Renal autotransplantation using hypothermic storage and pulsatile perfusion. 109 39

Hypothermic arrest, potassium arrest, and ischemic arrest, either singly or in combination, with or without coronary perfusion were studied in an isolated perfused rat heart preparation. Procedures that permitted the maintenance of high cellular levels of adenosine triphosphate (ATP) and creatine phosphate during arrest, e.g., coronary perfusion with hypothermic solutions or solutions containing 16.0 mM potassium, produced a fully reversible arrest with complete cardiac recovery. Cardiac arrest and coronary flow were related to the degree of hypothermia and the concentration of potassium in the coronary perfusate, and the minimum conditions required to induce complete cardiac arrest were ascertained. The effects of hypothermia and potassium were additive; total cardiac arrest could be obtained by combining small evaluations of potassium with moderate hypothermia. Under these conditions, cellular high-energy phosphates were maintained, and complete recovery was possible. Under conditions in which arrest was obtained without maintaing coronary perfusion, e.g., ischemic arrest, cellular high-energy phosphates declined rapidly, and the hearts exhibited poor recoveries. Some protection could be afforded to the ischemic myocardium by topical hypothermia or by combining the ischemia with potassium arrest. In both instances, ATP and creatine phosphate were maintained at higher levels, and improved recoveries were observed.
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PMID:Hypothermic arrest and potassium arrest: metabolic and myocardial protection during elective cardiac arrest. 111 43

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.
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PMID:The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia. 113 99


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