Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous investigations have shown that calcitonin gene-related peptide (CGRP) protects against myocardial ischemia-reperfusion injury and that rutaecarpine activates vanilloid receptors to evoke CGRP release. In the present study, we examined whether rutaecarpine enhances preservation with cardioplegia in guinea-pig hearts, and whether the protective effects of rutaecarpine are related to stimulation of endogenous CGRP release via activating vanilloid receptors. The isolated guinea-pig heart was arrested using St. Thomas Hospital solution, and then reperfused with normothermic Krebs-Henseleit solution for 30 min after a 4-h hypothermic ischemic period. Hypothermic ischemia caused a decline in cardiac function (left ventricular pressure, +/-dp/dt(max), heart rate and coronary flow) and an increased release of creatine kinase during reperfusion. Rutaecarpine at the concentration of 1.0 microM significantly improved the recovery of cardiac function and reduced the release of creatine kinase during reperfusion after hypothermic ischemia. Rutaecarpine at the concentration of 3.0 microM significantly reduced the release of creatine kinase and increased the coronary flow, but only caused a slight improvement of left ventricular pressure, +/-dp/dt(max), heart rate during reperfusion. The cardioprotective effects of rutaecarpine were abolished by capsazepine, a competitive vanilloid receptor antagonist, or by CGRP (8-37), a selective CGRP receptor antagonist. Rutaecarpine at the concentration of 1.0 or 3.0 microM significantly increased the release of CGRP, which was also abolished by capsazepine. These results suggest that rutaecarpine enhances preservation with cardioplegia in guinea-pig hearts and that the protective effects of rutaecarpine are due to stimulation of endogenous CGRP release via activating vanilloid receptors.
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PMID:The cardioprotection of rutaecarpine is mediated by endogenous calcitonin related-gene peptide through activation of vanilloid receptors in guinea-pig hearts. 1222 92

The purpose of the study is to comparatively evaluate the impact of normo- and hypothermic perfusion on acid-base balance (ABB), gas blood composition, metabolic parameters, and hemostasis. Fifty patients undergone multiple aortocoronary bypass under extracorporeal circulation (EC) were examined. Twenty four patients and 26 (Groups 1 and 2, respectively) had been operated on under normo- and hypothermia. The groups did not differ in age, body weight, the duration of an operation, the number of shunts, the time of EC, and myocardial ischemia. ABB, gas blood composition, the concentrations of hemoglobin, lactate, fibrinogen, prothrombin time, thrombin time, activated partial thromboplastin time, activated coagulation time, blood coagulation time as described by Leigh-White, the count of platelets, and ADP-induced platelet aggregation in the early postperfusion and postoperative periods, following 24 and 48 hours after surgery. There were no significant differences in the values of ABB, gas blood composition, blood lactate levels in patients from both groups. However, metabolic acidosis, elevated blood lactate concentrations were more frequently encountered in Group 2 patients, which suggests that hypothermia prduces a more aggressive effect on systemic homeostasis. Impact of normo- and hypothermia on the coagulative link of homeostasis was not revealed. Nevertheless, hypothermic EC halved the functional activity of platelets, which has a substantial effect on the size of postoperative blood loss.
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PMID:[Temperature regimen of extracorporeal circulation during aortocoronary bypass surgery]. 1261 Dec 98

Whether the ATP-sensitive potassium channel opener pinacidil can provide myocardial protective effects in prolonged isolated global ischemic rat heart was investigated. On modified isolated rat working heart model, 40 hearts were divided into four groups randomly: Hyperpolarized arrest H-K solution containing pinacidil (50 mumol/L) (P1 and P2) and depolarized arrest St. Thomas' solution (S1 and S2) subjected to 15 degrees C hypothermia, 60 min (P1 and S1) or 120 min (P1 and S2) of ischemia and 30 min reperfusion. The experimental indices included cardioplegic efficiency, cardiac function, coronary blood flow, myocardial enzyme release, myocardial water and ATP content. Hyperpolarized arrest provided significantly better recovery of cardiac function than depolarized arrest. Postischemic coronary flow and myocardial ATP content were higher. The arrest time of electro-mechanical activities were longer than depolarized arrest. There were no differences among the groups in myocardial water contents. The hyperpolarized arrest solution containing pinacidil can provide a marked myocardial protective effect during prolonged hypothermic myocardial ischemia.
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PMID:Protective effects of hyperpolarizing cardioplegia with pinacidil on myocardium in rats. 1265 77

The relative role of different adhesion molecules in the ischemia-reperfusion injury after cardioplegic arrest in the clinical setting is unknown, because of protective effects of cardioplegia and hypothermia. The aim of this study is to determine the relationship between the method of the cardioplegia and endothelial derived soluble adhesion molecules; soluble vascular adhesion molecule-1 (sVCAM-1) and soluble intercellular adhesion molecule-1 (sICAM-1) in myocardial ischemia- reperfusion injury. Fourteen male patients who underwent aortocoronary bypass surgery with cardiopulmonary bypass were included in this study. They were randomised to be given blood or crystalloid cardioplegia for myocardial protection. Group I (n=7) received blood cardioplegia and group II (n=7) received crystalloid cardioplegia. The cross-clamp times were not significantly different between the two groups, 49.4+/-4.6 min for group I and 54.8+/-2.5 min for group II. Mean age of patients was 58+/-2.1 years for group I and 54+/-2.6 years for group II. Blood samples were taken from both the aorta and coronary sinuses of all patients before cross-clamp, after cross-clamping and at 30th min of reperfusion. Plasma were obtained from blood samples and then stored at -70 degrees C. sVCAM-1 and sICAM-1 levels were measured by ELISA in the samples. There were no significant differences in the levels of sICAM-1 and sVCAM-1 at the beginning of reperfusion and at 30th min of reperfusion in coronary sinus of group I patients. But, increased sICAM-1 and sVCAM-1 levels were observed at 30th min of reperfusion in blood taken from coronary sinuses of group II patients compared with beginning of reperfusion (respectively p=0.01, p=0.03). In conclusion, these results have shown that ischemia-reperfusion injury is more likely to occur in patients protected by crystalloid cardioplegia, and suggest that blood cardioplegia may be preferred especially in borderline myocardial functioned patients.
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PMID:The relationship between the method of cardioplegia and vascular endothelial cell derived soluble adhesion molecules in myocardial ischemia-reperfusion injury. 1266 54

Arrhythmia is the most common perioperative cardiac complication during noncardiac surgery. Most perioperative arrhythmia is benign, but fatal arrhythmia can occur, requiring emergency care. Arrhythmia is divided into tachycardia and bradycardia. Both arrhythmias often result in cardiac failure. Ischemic heart disease often causes premature ventricular contraction or ventricular tachycardia. Hypertensive heart disease or valvular heart disease can lead to atrial fibrillation or supraventricular tachycardia. Although patients may not have cardiac disease, hypoxia, hypovolemia, electrolyte disturbance, acidosis, and hypothermia can also cause arrhythmia. Patients with pacemakers or implantable cardiodefibrillators (ICDs) are affected by electric cauterization, which interferes with the sensing and inhibits the pacing of pacemakers as well as ICDs If this occurs, the mode of pacemakers and ICDs must be reset during surgery.
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PMID:[Non-cardiac surgery for patients with arrhythmia]. 1593 53

A 68-year-old woman with anti-phospholipid antigen syndrome (APS) was proposed to undergo partial pulmonary resection for lung cancer. She suffered from mild cerebellar ataxia. Exercised 201Tl myocardial scintigraphy was performed due to abnormal Q wave in preoperative electrocardiography and showed old myocardial infarction in inferior-to-posterior area without myocardial ischemia. Cardiac function was marginally decreased in cardiac echographic evaluation. Arterial thrombosis by APS might cause cerebellar ataxia and myocardial infarction. Low molecular weight heparin (LMWH) was continuously infused from 1 hour prior to arrival in an operation room. Elastic stockings (ES) were worn from the morning of the operation in combination with the use of intermittent pneumatic compression apparatus (IPC). Significant bleeding was not observed perioperatively. Hypothermia was avoided by forced-air-warming therapy. She was transferred to ICU after the end of the operation. She was returned to her ward without IPC on the first postoperative day. Warfarin was given with the beginning of ambulation on the second postoperative day to keep PT-INR about 2. On the third postoperative day LMWH was discontinued and ES were taken off. The postoperative course was uneventful.
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PMID:[Prophylaxis of perioperative pulmonary thromboembolism in a patient with anti-phospholipid antigen syndrome]. 1629 75

A large proportion of deaths in the Western World are caused by ischaemic heart disease. Among these patients a majority die outside hospital due to sudden cardiac death. The prognosis among these patients is in general, poor. However, a significant proportion are admitted to a hospital ward alive. The proportion of patients who survive the hospital phase of an out of hospital cardiac arrest varies considerably. Several treatment strategies are applicable during the post resuscitation care phase, but the level of evidence is weak for most of them. Four treatments are recommended for selected patients based on relatively good clinical evidence: therapeutic hypothermia, beta-blockers, coronary artery bypass grafting, and an implantable cardioverter defibrillator. The patient's cerebral function might influence implementation of the latter two alternatives. There is some evidence for revascularisation treatment in patients with suspected myocardial infarction. On pathophysiological grounds, an early coronary angiogram is a reasonable alternative. Further randomised clinical trials of other post resuscitation therapies are essential.
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PMID:Post resuscitation care: what are the therapeutic alternatives and what do we know? 1648 70

Although hypothermia is one of the most powerful modulators that can reduce ischemic injury, the effects of hypothermia on the function of the cardiac autonomic nerves in vivo are not well understood. We examined the effects of hypothermia on the myocardial interstitial norepinephrine (NE) and ACh releases in response to acute myocardial ischemia and to efferent sympathetic or vagal nerve stimulation in anesthetized cats. We induced acute myocardial ischemia by coronary artery occlusion. Compared with normothermia (n = 8), hypothermia at 33 degrees C (n = 6) suppressed the ischemia-induced NE release [63 nM (SD 39) vs. 18 nM (SD 25), P < 0.01] and ACh release [11.6 nM (SD 7.6) vs. 2.4 nM (SD 1.3), P < 0.01] in the ischemic region. Under hypothermia, the coronary occlusion increased the ACh level from 0.67 nM (SD 0.44) to 6.0 nM (SD 6.0) (P < 0.05) and decreased the NE level from 0.63 nM (SD 0.19) to 0.40 nM (SD 0.25) (P < 0.05) in the nonischemic region. Hypothermia attenuated the nerve stimulation-induced NE release from 1.05 nM (SD 0.85) to 0.73 nM (SD 0.73) (P < 0.05, n = 6) and ACh release from 10.2 nM (SD 5.1) to 7.1 nM (SD 3.4) (P < 0.05, n = 5). In conclusion, hypothermia attenuated the ischemia-induced NE and ACh releases in the ischemic region. Moreover, hypothermia also attenuated the nerve stimulation-induced NE and ACh releases. The Bezold-Jarisch reflex evoked by the left anterior descending coronary artery occlusion, however, did not appear to be affected under hypothermia.
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PMID:Hypothermia reduces ischemia- and stimulation-induced myocardial interstitial norepinephrine and acetylcholine releases. 1708 72

A 79-year-old man underwent aortic arch replacement for thoracic aortic aneurysm. He had a history of smoking, coronary stenting for ischemic heart disease and replacement with artificial blood vessel for abdominal aortic aneurysm. Anesthesia was induced and maintained with midazolam, fentanyl, sevoflurane, and vecuronium. A 20 gage catheter was placed in the right radial artery and a 22 gage catheter in the left posterior tibial artery. Total circulatory arrest under profound hypothermia and retrograde cerebral perfusion were performed using extracorporeal circulation. After finishing anastomosis with artificial blood vessel, he was weaned from extracorporeal circulation. The pressure in the left posterior tibial artery was maintained at 15 mmHg, although the blood pressure in the right radial artery increased gradually. Then, the pressure in the left femoral artery in the operative field was the same as the pressure in the right radial artery. Therefore, we suspected the arterial line occlusion of the left posterior tibial artery. After the operation, we found the left leg and foot pale and cold with no pulsation on the left popliteal, dorsal pedis, and posterior tibial arteries. Further, acute left popliteal arterial occlusion was assessed by means of Doppler and left lower extremity angiography. We immediately performed the balloon-catheter embolectomy. However, as he developed compartment syndrome on the left lower limb due to reperfusion injury postoperatively, fascitomy was performed. On the 58th postoperative day, he was discharged from our hospital. Measurement by Doppler is useful for the early diagnosis of the lower leg arterial occlusion.
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PMID:[Acute popliteal arterial occlusion during extracorporeal circulation]. 1713 97

The purpose of this study was to determine whether ketanserin protects the globally ischemic canine heart and whether such protection, if present, is independent of that provided by hypothermia or calcium channel blockade with lidoflazine. Forty mongrel dogs, anesthetized with halothane, were divided into eight groups of five and subjected to one hour of global myocardial ischemia during hypothermic (30 degrees C; groups 1 to 4) or normothermic (37 degrees C; groups 5 to 8) cardiopulmonary bypass (CPB). Dogs in groups 1 and 5 served as controls with respect to prebypass myocardial protective therapy, and received only placebo (a normal saline bolus) prior to CPB. Before bypass, dogs in groups 2 and 6 received lidoflazine, 1.25 mg/kg intravenously (IV); those in groups 3 and 7 received ketanserin, 5 mg IV bolus, followed by a continuous infusion at 33 microg/min during bypass. Animals in groups 4 and 8 were given both lidoflazine and ketanserin according to the dosing schedules above. No type of pharmacologic or mechanical cardiovascular support was provided after termination of CPB. Postbypass hemodynamic performance and survival of the unsupported animal were assumed to reflect the degree of myocardial protection during CPB. One minute after bypass, mean arterial pressure and cardiac output were decreased in all groups. Cardiac output was lower in groups 5 to 8 (normothermic CPB) than in groups 1 to 4 (hypothermic CPB). After CPB, left ventricular filling pressures were elevated in all groups kept normothermic and in group 3 (hypothermic CPB plus ketanserin). By 15 minutes after CPB, there were no survivors in groups 5, 7, and 8. Sixty percent of animals in group 6 (normothermic CPB plus lidoflazine) survived to the end of the study. Relative odds of survival were increased 110-fold by hypothermia and sevenfold by lidoflazine. Conversely, treatment with ketanserin was associated with an increased likelihood of nonsurvival. It is concluded that, at the doses studied, ketanserin does not protect the canine myocardium against ischemic injury and may exert a detrimental effect when combined with calcium channel blockade in this setting.
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PMID:Preservation of the ischemic canine myocardium: a comparison of hypothermia, lidoflazine, and ketanserin. 1717 69


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