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

Between January 1991 and February 1993, 14 patients (3 female, 11 male) aged between 21 and 79 years (mean 50 years) underwent reconstruction of the thoracic (n = 7) and thoracoabdominal aorta (n = 7). Four patients had previously undergone operation of the ascending aorta, in 3 patients coronary artery by pass grafting was performed before. All patients were operated using cardiopulmonary bypass with continuous blood cardioplegia, hypothermic circulatory arrest (11 degrees C nasopharyngeal temperature, 0-EEG) and posterolateral exposure. All patent lower intercostal and lumbar arteries (Th3-L5) were reimplanted. The 30-day mortality after repair of the thoracic aorta was 0, after replacement of the thoracoabdominal aorta 28.5% (n = 2). One patient died 70 days after replacement of the thoracic aorta as a consequence of a perioperative stroke. None of the surviving 11 patients developed a permanent neurologic deficit, renal or cardiac dysfunction. The average intensive care stay was 6 days for patients after replacement of the thoracic and 18 days for patients after replacement of the thoracoabdominal aorta. Our results indicate the method of elective hypothermia and circulatory arrest effective in spinal cord protection. The increase in the tolerable duration of spinal cord ischemia supports the reimplantation of all intercostal and lumbar vessels.
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PMID:[Surgery of thoracic and thoraco-abdominal aneurysms using deep hypothermia and cardiovascular arrest with continuous administration of blood cardioplegia]. 758 59

Microcystin-LR, a cyclic peptide from the cyanobacterium Microcystis aeruginosa, given at acutely toxic doses causes severe hepatic interstitial hemorrhage. Hemodynamic, calorimetric and acid-base balance changes after i.v. microcystin were measured. The effect of isoproterenol, dopamine, methylprednisolone and whole-blood volume expansion on the immediate hemodynamic effects after toxin administration were also evaluated. A dose of 100 micrograms kg-1 was invariably lethal for rats in all studies. Pathophysiological changes included: a sustained, rapid decline in cardiac output and stroke volume; an acute hypotension responsive to volume expansion with whole blood; a decreased heart rate, responsive to both isoproterenol and dopamine; an early decline in oxygen consumption, carbon dioxide production and metabolic rate accompanied by progressive hypothermia; and acid-base balance changes indicating partially compensated metabolic acidosis. The lethal effects of microcystin-LR were previously attributed to hypovolemic shock as a result of hepatic interstitial hemorrhage. These results indicate that, in addition, there may be a cardiogenic component that limits the physiological cardiac reserve, compromising a normal response to circulatory inadequacy.
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PMID:Hemodynamic and calorimetric changes induced by microcystin-LR in the rat. 759

In ten patients we treated with distal arch aneurysms exposed through left posterolateral incisions, we induced profound hypothermia and circulatory arrest. Before circulatory arrest, thiopental, nicardipine and glycerol were used to protect the brain. The brain function was objectively evaluated through continuous recording of EEG and PO2 tension of the internal jugular vein. A cardiopulmonary bypass was introduced via the left atrium, pulmonary artery and left femoral artery cannulation. After proximal anastomosis between the graft and transverse aorta, graft cannulation was added. The distal aortic arch was replaced in all patients, with the entire descending thoracic aorta additionally replaced in two. No patients died in hospital. Two suffered neurological deficit, i.e., one having slight memory impairment and the other having a left-sided stroke due to right cerebral infarction, but recovering completely within a week. Our results indicate that profound hypothermia and circulatory arrest can be implemented safely when treating patients with distal arch aneurysm.
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PMID:[The treatment of patients with distal arch aneurysms--hypothermic circulatory arrest and left posterolateral exposure]. 759 44

The infusion of esmolol during hypothermic cardiopulmonary bypass (CPB) has no negative myocardial effects after CPB, despite increased esmolol levels during CPB due to hypothermia. The purpose of this randomized, double-blind, prospective study was to measure the effects of esmolol infused during CPB on cardiac function as measured by calculated indices of cardiac work and by transesophageal echocardiography (TEE). Patients scheduled for CPB were randomized to receive intravenous esmolol (300 micrograms.kg-1.min-1 during CPB after bolus of 2 mg/kg prior to CPB) or placebo. Infusion was stopped at 10 min after release of aortic cross-clamp. Hemodynamics and TEE were recorded during the procedure. Fractional area of contraction (FAC), an approximation of left ventricular ejection fraction, was calculated from end-diastolic and end-systolic areas. Esmolol was administered to 15 patients and placebo to 14. Heart rates in the esmolol group were lower during infusion and prior to CPB (P < 0.05). Stroke volume index and left ventricular stroke work index were higher in the esmolol group at 15 min post-CPB (P < 0.05). FAC was higher in the esmolol group at 15 and 30 min post-CPB (P < 0.05), but no difference was observed between groups at 1 h post-CPB. Esmolol infused during CPB in this series of patients was associated with better left ventricular function during the first 0.5 h post-CPB.
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PMID:Effect of esmolol given during cardiopulmonary bypass on fractional area of contraction from transesophageal echocardiography. 761 5

Conflicting results have been reported as to the extent that cardiovascular function can be reestablished after rewarming from hypothermia. We measured hemodynamic function, myocardial metabolism and tissue water content in dogs core-cooled to 25 degrees C and later rewarmed. At 25 degrees C left ventricular (LV) systolic pressure (LVSP) was 54% +/- 4%, maximum rate of LV pressure rise (LV dP/dtmax) 44% +/- 5%, aortic pressure (AOP) 50% +/- 6%, heart rate (HR) 40% +/- 0%, cardiac output (CO) 37% +/- 5%, myocardial blood flow (MBF) 34% +/- 5%, and myocardial oxygen consumption (MVO2) 8% +/- 1%, compared to precooling. Stroke volume (SV) and LV end-diastolic pressure (LVEDP) were unchanged. As normothermia (37 degrees C) was reestablished, the depression of cardiac function and myocardial metabolism remained the same as that at 25 degrees C: LVSP 71% +/- 6%, LV dP/dtmax 73% +/- 7%, SV 60% +/- 9%, AOP 70% +/- 6%, CO 57% +/- 9%, MBF 53% +/- 8%, and MVO2 44% +/- 8% HR, in contrast, recovered to precooling values. The arterial concentrations of glucose and free fatty acids (FFA) did not change significantly during the experimental period, whereas an increase in lactate of nonmyocardial origin appeared after rewarming. Increased myocardial contents of creatine phosphate and water were found during both hypothermia and rewarming. The present study demonstrates a persistent depression of cardiac function after hypothermia and rewarming in spite of adequate energy stores. Thus, a direct influence on myocardial contractile function by the cooling and rewarming process is suggested.
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PMID:Experimental hypothermia: effects of core cooling and rewarming on hemodynamics, coronary blood flow, and myocardial metabolism in dogs. 763 53

We have used retrograde arterial perfusion of the superior vena cava as an adjunct to deep hypothermia and systemic circulatory arrest for intraoperative cerebral protection in 43 adult patients (18 of whom were 70 years old or older). The indications for the use of circulatory arrest were thoracic aortic operations (37 patients) and atherosclerosis or calcification of the ascending aorta (6 patients) in patients needing aortic valve or coronary operations. In all patients systemic hypothermia (16 degrees to 18 degrees C) was achieved with cardiopulmonary bypass and the systemic arterial circulation was arrested. Retrograde arterial perfusion of the superior vena cava was established through a wire-reinforced venous cannula (with a superior vena cava tourniquet) at a temperature of 15 degrees C. In 36 patients a separate roller pump system was used for the retrograde cerebral perfusion. Central venous pressure was monitored at 25 to 30 mm Hg; mean flow rate was 250 ml/min. Periods of circulatory arrest and retrograde cerebral perfusion ranged from 4 to 110 minutes (mean 38 minutes), and for seven patients the period of circulatory arrest was longer than 60 minutes. Four postoperative deaths occurred, one related to stroke in a patient who had an aortic dissection during coronary surgery and the others related to noncerebral complications. Three nonfatal cerebral complications occurred, although all had completely resolved by late follow-up. Advantages of retrograde cerebral perfusion are (1) simplicity of use and avoidance of vascular trauma, (2) excellent exposure, (3) retrograde flow that minimizes embolization of air and atherosclerotic debris, and (4) effective cerebral oxygen delivery. Retrograde cerebral perfusion appears to be an important adjunct to hypothermia and circulatory arrest not only for patients undergoing operation for ascending aorta and aortic arch disease but also for patients with diffuse aortic atherosclerosis undergoing coronary or valve operations.
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PMID:Systemic hypothermia and circulatory arrest combined with arterial perfusion of the superior vena cava. Effective intraoperative cerebral protection. 771 22

The increasing number of patients with extensive aortic and peripheral vascular atherosclerosis or aneurysms who are undergoing cardiac operations present difficult decisions as to the optimal site of arterial cannulation for cardiopulmonary bypass. Femoral artery cannulation is the most common alternative to ascending aortic cannulation, but severe iliofemoral disease or the danger of atheroemboli caused by retrograde perfusion through an atherosclerotic or aneurysmal descending aorta may make this approach impossible or undesirable. We have used axillary artery cannulation for cardiac operations in 35 patients for indications including severe aortic atherosclerosis (n = 16), extensive aortic aneurysms (n = 11), and aortic dissection (n = 8). The cardiac operations performed were coronary artery bypass grafting (n = 9) aortic valve replacement (n = 1), aortic valve replacement and coronary artery bypass grafting (n = 5), repair of mitral valve periprosthetic leak (n = 1), and resection of ascending and/or aortic arch (n = 19). Deep hypothermia with circulatory arrest was used in 26 patients and retrograde cerebral perfusion in 18. All patients awoke from the operation and no patient had a cerebrovascular accident. One patient required axillary artery thrombectomy and one patient had a mild ipsilateral brachial plexus paresis after the operation. Four patients died in the hospital. We conclude that axillary artery cannulation is a safe and effective means of providing antegrade arterial flow during cardiopulmonary bypass in patients with severe atherosclerotic or aneurysmal disease. This strategy may lower the prevalence of stroke associated with cardiopulmonary bypass in these patients.
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PMID:Axillary artery: an alternative site of arterial cannulation for patients with extensive aortic and peripheral vascular disease. 852 96

Thrombolysis with tissue plasminogen activator (tPA) and hypothermia are two potential treatment modalities for acute ischemic stroke. Many investigators are studying these modalities both in the laboratory and in clinical trials. Because these modalities each appear to show benefit in animal models, there is considerable interest in studying combined therapy with both thrombolysis and hypothermia. However, it is known that alterations in the coagulation system can occur with decreased body temperature. Clinicians have frequently observed bleeding problems when patients are subjected to hypothermia for a variety of reasons. Hypothermia induced coagulopathy has been attributed to a variety of factors. Hypothermia can cause platelet dysfunction, inhibition of clotting factors, increased fibrinolysis and endogenous production of a heparin-like factor. Groups who studied fibrinolysis and temperature, however, found the opposite to be the case. Clot lysis studies with streptokinase showed increased fibrinolysis at higher temperatures. Data by Mumme suggested that the peak fibrinolytic activity of streptokinase was at 40 degrees C, but at 43 degrees C fibrinolytic activity was decreased. Rijken et al studied plasminogen activation with tissue plasminogen activator (tPA), urokinase and streptokinase at extremely low temperatures. They found less plasminogen activation and fibrinogen degradation at 25 degrees C compared to 37 degrees C, but negligible differences at 10 degrees C, 0 degrees C and -8 degrees C. To our knowledge, there is no data studying the fibrinolytic activity of tissue plasminogen activator (tPA) at temperature ranges between 25-37 degrees C which is the range of temperatures used clinically for therapeutic purposes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Thrombolysis with tissue plasminogen activator (tPA) is temperature dependent. 777 62

Experimental observations in our laboratory indicate that myocardial recovery is similar following warm or cold antegrade blood cardioplegia when the core temperature is maintained at 37 degrees C. To determine the effects of hypothermia on myocardial recovery, 15 adult mongrel dogs were randomized to normothermic or hypothermic bypass (28 degrees C) during 60 min of continuous warm antegrade blood cardioplegia. The hypothermic group was rewarmed after releasing the aortic cross-clamp and bypass was discontinued at 30 min in both groups. Myocardial recovery was assessed at 60, 90, and 120 min after the arrest. Core temperature was maintained in the normothermic group but gradually decreased after bypass in the hypothermic group, reaching a low of 33.8 +/- 1 degrees C at 120 min. Myocardial functional recovery was preserved after normothermic bypass. The decrease in core temperature, however, that was observed after systemic hypothermia, was paralleled by significant decreases in the maximum rate of left ventricular pressure rise (dp/dt), the maximum elastance of the left ventricle, and preload recruitable stroke work. Diastolic function decreased slightly, but not significantly, during reperfusion following systemic hypothermia but was unaltered after normothermic bypass. Myocardial oxygen consumption was unchanged in both groups. Myocardial ultrastructure was preserved after normothermic bypass. In contrast, cellular oedema and mild ultrastructural changes were evident after systemic hypothermia. We therefore conclude that the use of systemic hypothermia during bypass is associated with lower core temperatures during early recovery which results in impaired functional recovery.
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PMID:Influence of systemic hypothermia on systolic and diastolic functional recovery after continuous warm antegrade blood cardioplegia. 781 84

The effect of thrombolytic therapy is well-documented in acute myocardial infarction. In acute cerebral infarction, thrombolytic therapy has been evaluated in small series of patients. The point of thrombolytic therapy is to avoid or reduce ischemic damage of neuronal tissue by rapid arterial recanalization. In thrombolytic therapy of cerebral vascular occlusion, the pathophysiology of reperfusion needs further investigation and documentation. This review describes studies of thrombolysis in embolic stroke using animals embolized by intracarotid injections of blood clots. Vascular occlusion was demonstrated by angiography and measurement of cerebral blood flow. Thrombolytic therapy with recombinant tissue-type plasminogen activator was initiated after varying periods of time. Reperfusion, cellular function, and brain damage were examined by angiography and by clinical and pathoanatomical examination. Based mainly on results from our own investigations, the following theses concerning ischemic stroke were made: (a) Cerebral infarction caused by arterial occlusion is due to delayed, incomplete, or no reperfusion. Spasms, or hemodynamic mechanisms, seem to be of only minor importance. (b) Early thrombolytic therapy in animal models increases the degree of reperfusion and reduces brain damage, clinical deficits, and mortality. (c) Early arterial reperfusion reduces cerebral infarction and related edema. With early reperfusion, the extent of brain damage correlates to the length of the delay from onset of ischemia. (d) Cerebral stunning is caused by arterial occlusion followed by very early spontaneous or induced reperfusion, as neurons temporarily lose their functional capabilities without dying. (e) Multiple embolic microclots in experimental stroke result in more brain damage than a single macroclot, and with clots the extent of brain damage is dependent on the structural composition and volume of emboli. (f) The ability to recanalization in experimental embolic stroke is related to the amount of red cells in the emboli and inversely related to the volume of emboli and to the fibrin content and density of the clots. (g) Infarct-limiting effects in experimental stroke can be obtained by ischemic neuroprotectants or by hypothermia, either alone or with thrombolytic therapy, which then reduces brain damage further.
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PMID:Thrombolytic therapy in experimental embolic stroke. 781 66


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