Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the open chest dog model, the response of the left ventricle exposed to acute mechanical hypertension was evaluated while the animals were receiving various concentrations of halothane, enflurane, and isoflurane. Myocardial contractility was quantified by the end-systolic pressure-length relation (ESPL). When the mean aortic pressure was increased by 40% above the control value for a given concentration of inhalation agent, the end-diastolic volume increased and thereby maintained stroke work. However, as the end-tidal concentrations of the anesthetics increased, this compensatory mechanism became progressively more ineffective as a result of myocardial depression caused by the anesthetics. No evidence could be found of an improvement in myocardial contractility as the aortic pressure was increased. Mild depression of myocardial contractility could be demonstrated for 1.1 MAC halothane, 0.6 MAC enflurane, and 1.0 MAC isoflurane. Severe depression of contractility occurred at 2.3 MAC halothane, 1.2 MAC enflurane, and 1.5 MAC isoflurane.
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PMID:Response of the heart to acute hypertension during halothane, enflurane, and isoflurane anesthesia. 368 92

This study was undertaken to evaluate the chronic, long-term effect of global ischemia produced by cold potassium cardioplegia during cardiopulmonary bypass. Fifteen dogs underwent either control thoracotomy and chronic instrumentation(Group A) or cardiopulmonary bypass and 60 minutes of cold cardioplegic arrest (Group B). With the dogs conscious, hemodynamic variables and left ventricular studies were recorded weekly for 12 weeks postoperatively, both at rest and during volume overload with saline solution. At rest, the heart rate in Group B was 18% higher and stroke volume was 14% lower than Group A. With volume overload, cardiac output and maximum rate of rise of left ventricular pressure in Group B rose only from 3.7 +/- 0.6 to 7.1 +/- 0.8 liters per minute and 2,410 +/- 220 to 2,730 +/- 130 mm Hg per second, respectively, compared with 3.9 +/- 0.6 to 10.4 +/- 0.8 liters per minute and 2,740 +/- 230 to 3,890 +/- 350 mm Hg, respectively, in Group A (p less than 0.01). In Group B, the other variables reached a plateau sooner than in Group A (48 versus 110 seconds). The left ventricular function curve showed a mild decrease in functional capacity and depressed contractility. Therefore, one hour of cardioplegic cardiac arrest caused no depression of function at rest. Mild depression of left ventricular function was demonstrated up to 7 weeks postoperatively during acute volume overload.
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PMID:Does cardioplegic arrest compromise long-term left ventricular function? 738 47