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

Coronary occlusion during cardiopulmonary bypass has been used in place of aortic occlusion to perform coronary artery anastomoses, but this procedure on distal myocardial function has not been evaluated. Regional myocardial function was examined with the use of ultrasonic crystals in 20 dogs subjected to this technique to compare normothermic and hypothermic (30 degrees C) bypass in both beating and fibrillating hearts. We found a significant decline in the velocity of contraction of the distal segment in fibrillating compared to bearing hearts (p less than 0.01). Hypothermia prevented this decline in the beating, but not the fibrillating, hearts. With respect to contractile function in the distal myocardial segment, local occlusion techniques cause an injury similar to that reported for aortic cross-clamping.
 ...
PMID:Alterations in regional contractility following cardiopulmonary bypass with intraoperative ischemia. 66 70

Anesthetized dogs were cooled to a core body temperature of 26 degree C. or maintained at a body temperature of 37 degree C. during periods of 5 and 10 hours of LAD coronary artery occlusion. Subsequent macroscopic dehydrogenase enzyme mapping showed that ischemic injury was 25 per cent less after 5 hours of coronary occlusion and 20 per cent less after 10 hours of occlusion in hypothermic dogs than in normothermic controls. The heart rate and left ventricular minute work in hypothermic dogs decreased to roughly half the levels measured in normothermic animals, while left ventricular contractility was 10 to 40 per cent lower in hypothermic dogs than in normothermic dogs. However, cardiac index and left ventricular end-diastolic pressure were unchanged by whole-body cooling. Thus, hypothermia appeared to diminish the oxygen requirements of the ischemic myocardium without reducing the performance of the heart as a pump. Hypothermia may be useful as a therapeutic adjunct to myocardial revascularization or pharmacologic interventions.
 ...
PMID:Protection of ischemic myocardium by whole-body hypothermia after coronary artery occlusion in dogs. 71 40

Effects of moderate spontaneous hypothermia on left ventricular systolic and diastolic function during acute myocardial infarction were documented in 17 anesthetized dogs with micromanometric pressure and ventriculographic dimension recordings acquired at baseline and at 1 and 3 h after coronary occlusion. In Group 1 (n = 5), core temperature was allowed to decline spontaneously. In Groups 2 (n = 6) and 3 (n = 6), core temperature was maintained at normothermic levels. Hypothermia impaired isovolumic relaxation markedly despite its lack of effect on ventricular volumes or ejection fraction. At 32.3 degrees C, tau 1/2, defined as the time needed for the left ventricular pressure at the time of peak negative rate of change of left ventricular pressure (dP/dt) to fall by 50%, was increased by 129% 3 h after occlusion. In addition, at this temperature significant changes were found in heart rate, cardiac output, minute work, peak positive and peak negative dP/dt, systolic ejection time, mean velocity of circumferential fiber shortening, mean aortic pressure and end-diastolic pressure. Thus, hypothermia evolving under conditions of general anesthesia profoundly alters left ventricular function in the setting of acute myocardial infarction, a phenomenon that requires consideration and control in studies of myocardial ischemia and left ventricular function in experimental animals.
 ...
PMID:Sensitivity of isovolumic relaxation to hypothermia during myocardial infarction. 333 99

Possible use of thermography (AGA Thermovision 750) in heart surgery has been investigated in animal experiments and in human extracorporeal operations as well. In six open-chest isolated dog hearts, coronary circulation had been occluded and antero- and retrograde local cooling was employed. Following coronary occlusion, effective hypothermia was achieved retrograde via the coronary sinus. 22 patients were arranged into three groups according to the operation technique used, and the possibilities for effective cardiac cooling by cold cardioplegic solution were studied. Hearts of the six patients subjected to surgical intervention for valvular lesions (four mitral and two aortic) could be safely cooled by cold cardioplegic solution infused through the aorta or the coronary arteries. The hearts of the twelve patients with coronary artery stenosis could be cooled sufficiently by additional retrograde infusion only. Employing antero- and retrograde hypothermia, in four patients the size of the aneurysm of the left ventricle, and the area which had to be resected was determined by thermography. Thermography is considered to be a suitable non-invasive method to derive information concerning: the efficacy of cold cardioplegic solution in aortocoronary bypass grafting, quantitative changes in nutritive coronary flow, the size of left ventricular aneurysmectomy.
 ...
PMID:[Experiences with thermography in the surgical treatment of ischemic heart disease]. 348 58

Peak current defibrillation thresholds (PCDT), i.e., values with 50% probability of success, were determined after ligation of the left anterior descending coronary artery (LADCA) while, simultaneously, body temperature was slowly decreased until central venous temperature reached an average minimum of 22.8 degrees C (s.d. 3.1). In 14 dogs with over 166 successful defibrillations, the average time elapsed between the moment of ligation and the last defibrillation was 179.1 min. (s.d. 31.9), with an average PCDT of 53.6 mA g-1 of heart (s.d. 20.5). This value was compared by means of the unpaired Student's t test with three previous values obtained, respectively, under hypothermia with no occlusion (HNO), normo-thermia with coronary occlusion (NCO), and normothermia with no occlusion (NNO), that is, HNO 69.5 (s.d. 30.4), NCO 81.1 (s.d. 29.3), and NNO 89.5 (s.d. 32.8), all expressed in mA g-1 of heart. All three differences even after Bonferroni's correction, were statistically significant (P less than 0.3%). We concluded that, (1) defibrillation thresholds were decreased by coronary occlusion and by hypothermia, (2) the decrease due to hypothermia was greater than that due to coronary occlusion, (3) both decrements appeared as additive.
 ...
PMID:Transventricular simple-capacitor discharge defibrillation thresholds after coronary ligation and body hypothermia. 650 54

Hypothermic synchronized retroperfusion was applied during coronary artery occlusion to determine its ability to alleviate junctional derangements of reperfusion and to reduce infarct size. The proximal left anterior descending coronary artery was occluded in 25 closed chest dogs for 3 hours and then reperfused for 7 days. Thirteen dogs with no reperfusion pretreatment served as a control group (Group A). In 12 dogs, hypothermic retroperfusion was applied from 30 minutes up to 3 hours of the occlusion period (Group B). Sequential two-dimensional echocardiographic and hemodynamic as well as metabolic measurements were performed. Compared with untreated control dogs, dogs with hypothermic synchronized retroperfusion had significantly reduced heart rate and rate-pressure product, decreased left ventricular volumes and improved ejection fraction during the occlusion period. Two-dimensional echocardiographically-derived ischemic zone systolic fractional area change and systolic wall thickening indicated significantly improved function as a result of retroperfusion. During the reperfusion period, untreated control dogs (group A) had more severe derangements in hemodynamics and wall motion than dogs treated by hypothermic retroperfusion (group B). Mortality was 30.7% in group A, 16.7% in group B and 7th day infarct size as percent of the left ventricle was 12.0 +/- 6.5 (mean +/- standard deviation) and 4.2 +/- 5.9, respectively (p less than 0.02). It is concluded that hypothermic synchronized retroperfusion applied after coronary occlusion and before reperfusion significantly improves cardiac function during occlusion, minimizes complications of reperfusion and reduces the ultimate infarct size. Because this form of circulatory assistance helps maintain cardiac function and delays the evolution of myocardial necrosis, its application may be beneficial during an evolving acute myocardial infarction before achievement of surgical or nonsurgical reperfusion.
 ...
PMID:Prevention of ischemic injury and early reperfusion derangements by hypothermic retroperfusion. 683 45

Hypothermic synchronized retroperfusion (HSRP) was applied in closed-chest dogs after acute coronary occlusion to determine whether this intervention can significantly retard the otherwise rapidly developing irreversible ischemic injury. The left anterior descending coronary artery (LAD) was occluded for 3 hours in 22 dogs and for 6 hours in 16 dogs. Starting 30 minutes after occlusion, HSRP was applied during maintained coronary occlusion in 21 dogs. The remaining dogs served as untreated controls. Arterial blood was cooled to 20 degrees C and retroperfused in diastole into the regional coronary veins. Hemodynamics, contrast cineangiography and two-dimensional echocardiography were measured sequentially. Glycogen-depleted ischemic areas and necrotic zones were delineated in transverse slices of the left ventricle. Untreated controls dogs further deteriorated; in contrast, HSRP between 30 minutes and 3- and 6-hour LAD occlusion significantly reduced the rate-pressure product (21.3 +/- 4.0% or 26.8 +/- 8.2%) and left ventricular end-diastolic pressure (39.5 +/- 9.5% or 51.4 +/- 7.7%) and increased ejection fraction (28 +/- 17% and 33 +/- 2.0%). HSRP caused no arrhythmias and led to much less necrosis of ischemic myocardium in the treated 3- or 6-hour occlusion series (7.4 +/- 2.7% or 28.9 +/- 12.6%) than in respective untreated controls (47.1 +/- 8.9% and 72.3 +/- 5.9%). Moderately hypothermic closed-chest phased retroperfusion appears to protect reversibly injured ischemic myocardium and improve cardiac function. Such treatment may be particularly suitable in the earliest stages of evolving myocardial infarction, when maintenance of myocardial viability is essential for preservation of jeopardized myocardium while awaiting coronary bypass revascularization or nonsurgical thrombolytic reperfusion.
 ...
PMID:Hypothermic coronary venous phased retroperfusion: a closed-chest treatment of acute regional myocardial ischemia. 707 99

In order to study the metabolic consequences of myocardial stunning, repeated coronary occlusions were performed in dogs. The production of CO2, adenosine triphosphate (ATP), phosphocreatine (PCr), and inorganic phosphate (Pi) by myocardial cells was assessed, along with extracellular and intracellular pH. Our results indicate that regional coronary artery occlusion reduces the ability of the myocardium to produce H+ and CO2 and to replenish ATP post ischemia. These alterations, then, represent the hallmark of metabolic viability during periods of ischemic insult. Decreases in PCr and Pi were completely eliminated during reperfusion and, therefore, are ot reflective of myocardial stunning. When normothermic cardiopulmonary bypass (CPB) is instituted and the coronary artery is occluded three times with reperfusion between each occlusion, alterations in myocardial H+ and high energy phosphates are identical to those observed using only repetitive coronary occlusion. Systemic hypothermia during CPB does not protect against myocardial stunning; however, it is anticipated that interventions that prevent the reduction in H+ and ATP levels may overcome the effects of myocardial stunning that occur during cardiac surgery.
 ...
PMID:Metabolic correlates of myocardial stunning and the effect of cardiopulmonary bypass. 846 15

The present study describes a method for rapidly cooling the whole body via its blood pool and tests whether cooling instituted after ischemia has begun can still limit infarction. We also evaluated whether the cardiac protection seen with cooling could be added to that from ischemic preconditioning. Recently it was reported that lowering myocardial temperature by only several degrees greatly slows the extent of myocardial infarction in the beating heart experiencing regional ischemia. To further explore the potential of hypothermia for myocardial protection, rabbits underwent either a 30-, 45- or 60-min coronary artery occlusion and 3-h reperfusion. Blood from a carotid artery was allowed to circulate through a heat exchanger immersed in ice water and return to a jugular vein until the blood temperature in the left atrium reached the target temperature of 35 or 32 degrees C. Furthermore, to elucidate the mechanism of hypothermia's protection, we also examined its effect on isolated cardiomyocytes. Rewarming began upon reperfusion in all protocols. Cooling to 32 degrees C before a 30-min ischemia reduced infarct size from 37.3 +/- 2.5% (n = 6) of the risk zone in normothermic controls to 3.6 +/- 0.3% (n = 6). When cooling was begun 10 or 20 min after the onset of ischemia infarct size was still significantly smaller [8.1 +/- 1.2% and 22.8 +/- 1.8%, respectively (n = 6 in each group)]. Less but significant protection was also seen with cooling to 35 degrees C. Cooling caused only mild bradycardia and hypotension and no apparent arrhythmias. Forty-five min of regional ischemia caused 50.7 +/- 3.3% (n = 6) of risk zone to infarct in untreated hearts. Preconditioning with 5-min ischemia/10-min reperfusion reduced infarct size to 27.5 +/- 2.5% (n = 6). Cooling to 32 degrees C starting 20 min after the onset of ischemia protected the heart (28.7 +/- 2.6% infarction, n = 8), and this protection could be added to the effect from ischemic preconditioning (6.3 +/- 2.3% infarction, n = 6). In the myocyte model, hypothermia and ischemic preconditioning delayed the progressive increase in osmotic fragility that occurs during simulated ischemia in an additive way, but only hypothermia delayed the appearance of contracture suggesting that different mechanisms are involved. Hence blood pool cooling was easily induced and well tolerated and protected the beating heart against infarction even when hypothermia was started after the onset of coronary occlusion. We conclude that hypothermia might be a simple and useful therapy for patients presenting with acute myocardial infarction.
 ...
PMID:Mild hypothermia reduces infarct size in the beating rabbit heart: a practical intervention for acute myocardial infarction? 983 49

The goals of myocardial protection during cardiac surgery are not only to facilitate the operation by providing a quiet bloodless field, thereby facilitating the precision of the operation, but also to avoid iatrogenic injury induced by cardiopulmonary bypass itself or by surgically imposed ischemia. In addition, myocardial protective strategies are geared to preventing reperfusion injury upon resolution of the coronary occlusion and the ultimate release of the aortic cross clamp. Cardioplegia plays a very important role in myocardial protection strategies. Acting as a selective perfusion agent, cardioplegia solutions can alter or inhibit ischemic injury by virtue of hypothermia and asystole. In addition, cardioplegia can be used to avoid reperfusion injury by altering the conditions of its delivery and the composition of the solution using various adjunctive agents and pharmacologic therapies for which cardioplegia solutions serve as a vector. Future strategies, particularly for off-pump surgical procedures, may incorporate systemic delivery of therapeutic agents to the heart directly either in conjunction with or without cardioplegia.
 ...
PMID:Myocardial protection: an overview. 1094 22


1 2 Next >>