D V Cumming, A M Seymour, C T Bowles, K Nishimura, K Kalsi, S S Shah, R D Pritchard, C W Pattison, J R Pepper, M H Yacoub
{"title":"Metabolic analysis of latissimus dorsi coupled to a mock circulation.","authors":"D V Cumming, A M Seymour, C T Bowles, K Nishimura, K Kalsi, S S Shah, R D Pritchard, C W Pattison, J R Pepper, M H Yacoub","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A mock circulation system has been used to examine the metabolic and hemodynamic responses of untrained and trained latissimus dorsi muscle in a normal animal model. The metabolic response of untrained latissimus dorsi to differing stimulation regimes runs parallel to its mechanical performance. The ratio of power generated to oxidative capacity (a measure of metabolic efficiency) was maintained to a greater extent in muscle trained for 5 months subjected to specific fatigue tests, falling by only 20% (as opposed to 80% observed in untrained control muscle). This approach to studying metabolic and hemodynamic performance may have relevance when skeletal muscle is used for cardiac assistance.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"251-6"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Global myocardial ischemia protects the myocardium from subsequent regional ischemia.","authors":"D M Walker, J M Walker, D M Yellon","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Many investigators use in vitro models of global ischemia to examine the effects of preconditioning, often with recovery of contractile function as the end-point. Such models are relevant to myocardial protection during cardiac surgery. However, there is still debate as to whether preconditioning preserves ventricular contraction secondary to limitation of infarction or by a direct effect on stunning. Since infarct size is the original end-point against which protection by preconditioning is measured, our aims were, first, to validate global ischemic preconditioning by measuring infarct size after subsequent regional ischemia and, second, to correlate limitation of infarct size with mechanical function. After stabilization, seven isolated buffer perfused rabbit hearts were subjected to 5 minutes of global \"no-flow\" ischemia followed by 10 minutes of reperfusion (\"global preconditioning\"). Seven control hearts were allowed to stabilize for an additional 15 minutes at constant flow. Subsequently, regional ischemia was induced in both groups for 45 minutes followed by 2 hours of reperfusion. Left ventricular and coronary perfusion pressures were measured throughout. Myocardial infarct size was measured using triphenyltetrazolium staining and expressed as a percentage of the area at risk outlined with fluorescent microspheres. The ratio of infarct to risk zone was reduced from 47.6 +/- 7.3% in control hearts to 16.4 +/- 5.4% (p = 0.005) in preconditioned hearts, confirming the efficacy of global preconditioning. In addition, preconditioning led to a better preservation of systolic function, which correlated significantly with limitation of infarct size (r = 0.75, p = 0.002). Global preconditioning may account for the successful use of cross-clamp fibrillation during cardiac surgery.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"263-6"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
O Ondrejickova, A Ziegelhoeffer, I Gabauer, R Sotnikova, J Styk, P Gibala, J Sedlak, L Horakova
{"title":"Evaluation of ischemia-reperfusion injury by malondialdehyde, glutathione and gamma-glutamyl transpeptidase: lack of specific local effects in diverse parts of the dog heart following acute coronary occlusion.","authors":"O Ondrejickova, A Ziegelhoeffer, I Gabauer, R Sotnikova, J Styk, P Gibala, J Sedlak, L Horakova","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Alterations in the levels of glutathione, glutathione disulfide, malondialdehyde, and the activity of gamma-glutamyl transpeptidase in nonischemic and ischemic parts of the left ventricle and in the right ventricle were studied in canine hearts after occlusion of the left anterior descending coronary artery for 60 minutes and subsequent reperfusion for 20 minutes. Ischemia caused no significant change in malondialdehyde concentration and gamma-glutamyl transpeptidase activity in ischemic or nonischemic parts of the left ventricle, but it increased the activity of gamma-glutamyl transpeptidase in the continuously perfused right ventricle. Reperfusion of the ischemic areas of the left ventricle was accompanied by accumulation of malondialdehyde and an increase in gamma-glutamyl transpeptidase activity, not only in the reperfused and adjacent areas of the left ventricle, but also in the continuously perfused right ventricle. An increase in the level of glutathione disulfide and decrease in glutathione occurred in all parts of the myocardium during coronary occlusion; these changes were maintained in reperfusion. The findings indicate that the effects of acute occlusion and reperfusion of the left anterior descending coronary artery on myocardial concentrations of glutathione, glutathione disulfide and malondialdehyde or gamma-glutamyl transpeptidase activity are not confined to the local area.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"225-30"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18902132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M G Tozzi-Ciancarelli, C Di Massimo, A Mascioli, E Tozzi, P Gallo, F Fedele, A Dagianti
{"title":"Rheological features of erythrocytes in acute myocardial infarction.","authors":"M G Tozzi-Ciancarelli, C Di Massimo, A Mascioli, E Tozzi, P Gallo, F Fedele, A Dagianti","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>There is evidence that oxidative insult plays a role in the development of acute myocardial infarction. Significance has also been attributed to changes in viscosity of the blood and in the deformability and aggregation of erythrocytes affecting their rheological behavior. In a group of patients with myocardial infarction we found a decreased erythrocyte filtration and an increased blood viscosity with no significant change in plasma viscosity. These changes were accompanied by alterations in the microviscosity of the erythrocyte membrane assessed by measuring the polarization of specific fluorescent molecules. From our data it is evident that there is an increase in the rigidity of the membrane at the lipid/protein boundary, with an associated increase in the fluidity of the deep lipid core of the membrane, while no changes were observed in the dynamic behavior of the membrane proteins. These physico-chemical perturbations in the membrane could be the basis for the decreased filtration of erythrocytes. We found, however, no evidence of lipid peroxidation in the erythrocyte membrane.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"231-4"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Effect of thyroid status on phosphatidylinositols in rat heart.","authors":"G Jakab, E Kiss, E G Kranias, I Edes","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The incorporation of 32Pi into phosphatidylinositols and inositol trisphosphates was studied in Langendorff-perfused hearts from hypothyroid, euthyroid and hyperthyroid rats. The hearts were perfused with modified Krebs buffer containing [32P]orthophosphate and the degree of 32P-labeling of phosphatidylinositol, phosphatidylinositol 4-monophosphate, phosphatidylinositol 4,5-bisphosphate, inositol trisphosphates and phosphatidic acid was measured. Hyperthyroidism was associated with increases in rates of rise and fall of left ventricular systolic pressure, sarcoplasmic reticular Ca(2+)-ATPase activity and 32P-labeling of phosphatidylinositols, inositol trisphosphates and phosphatidic acid. These measurements were significantly decreased in hypothyroid hearts. The tissue levels of inositol 1,4,5-trisphosphate isoform were found to be significantly higher in hyperthyroid hearts and lower in hypothyroid hearts than in euthyroid ones. Examination of phosphoinositide-specific phospholipase C activity in the perfused hearts revealed that hyperthyroidism was associated with an increase in the membrane-associated enzymatic activity, assayed at physiological calcium concentrations, while hypothyroidism was associated with a decrease in this activity as compared with control hearts. These findings indicate that alterations in the thyroid state of the myocardium may be associated with changes in basal phosphoinositide turnover which may contribute to alterations in myocardial contraction.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"257-62"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Metabolism of the failing heart.","authors":"A M Katz","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Our understanding of the pathogenesis and therapy of heart failure has evolved through three paradigms. Organ physiology, the first paradigm, focused therapy of heart failure on salt and water retention and vasoconstriction, which represent major circulatory responses to, cardiac pumping. The second paradigm of cell biochemistry led to the development of powerful inotropic agents designed to increase myocardial contractility. The third paradigm, gene expression (molecular biology), describes regulatory mechanisms that are both primitive and complex; in the setting of heart failure, this paradigm focuses on the roles of altered myocardial cell growth and composition in explaining the accelerated deterioration of the hypertrophied, failing heart. This review focuses on one aspect of the second paradigm: factors that contribute to a state of energy-starvation and the resulting functional consequences in the failing heart.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"199-203"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19285794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Free radical effects on myocardial membrane microviscosity.","authors":"I H Coetzee, A Lochner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Previous studies have shown that myocardial membranes, isolated from ischemic myocardial tissue, showed marked changes in microviscosity. To evaluate the contribution of free radical production and concomitant lipid peroxidation to these changes in microviscosity, the in vitro effects of two radical producing systems (H2O2/FeCl2 and xanthine oxidase/hypoxanthine/FeCl3) were investigated separately on the microviscosity of sarcolemmal, mitochondrial and sarcoplasmic reticulum membranes. In all three membranes both these free radical producing systems caused formation of malondialdehyde as quantitated by the thiobarbituric acid test. The sensitivity of the membranes to free radical damage differed: the sarcolemma was more sensitive to H2O2 damage, while mitochondrial malondialdehyde production was highest with xanthine oxidase. H2O2/FeCl2 caused a reduction in microviscosity (i.e. increased fluidity) of all three membranes, whereas the xanthine oxidase system increased mitochondrial and sarcolemmal microviscosity and reduced that of the sarcoplasmic reticulum. The similarity between ischemia-induced membrane microviscosity changes and those induced in vitro by xanthine oxidase, indicate a possible causal role for superoxide and hydroxyl free radicals produced during ischemia.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"205-15"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19285795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of endocardial endothelium in the modulation of myocardial contraction in the isolated whole heart.","authors":"S Fort, M J Lewis, A M Shah","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Selective damage to the endocardial endothelium in isolated papillary muscle preparations has been shown to produce an abbreviation of contraction, changes which were also observed following an increase in myocardial cyclic GMP in those preparations. In the present study we have investigated the effects of removing the endocardium and increasing myocardial cyclic GMP on contractile parameters in isolated Langendorff perfused ferret hearts, where the myocardial mass underlying the endocardium is much greater. Selective damage to left ventricular endocardial endothelium without damaging the underlying myocardium was achieved by brief exposure to a weak detergent solution (Triton X-100 0.005% v/v). This resulted in a significant abbreviation of the left ventricular pressure-time curve due to the earlier onset of relaxation, but there was little effect on early systole. The direct intraventricular infusion for 15 minutes of 10 microM sodium nitroprusside, a donor of nitric oxide, or of 1 microM substance P, to stimulate release of endothelium-derived relaxing factor, did not increase myocardial cyclic GMP levels or alter left ventricular contractile performance. Myocardial cyclic GMP levels were significantly increased by 15 minute intracoronary infusions of 10 microM nitroprusside and 1 microM substance P, approximately ten-fold and two-fold respectively. Intracoronary nitroprusside induced an abbreviation of the left ventricular pressure-time curve with an earlier onset of relaxation, but contraction was unaltered by intracoronary substance P. These results show that, in the isolated Langendorff perfused ferret heart, both selective removal of endocardial endothelium and an increase in myocardial cyclic GMP cause an abbreviation of left ventricular pressure and an earlier onset of relaxation with little change in early systole.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"217-23"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18514693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M Sakanashi, K Noguchi, T Matsuzaki, Y Ojiri, J Nakasone, T Itomine, M Higuchi, N Shiroma
{"title":"Effects of pilsicainide on systemic hemodynamics and cardiac function of anesthetized dogs.","authors":"M Sakanashi, K Noguchi, T Matsuzaki, Y Ojiri, J Nakasone, T Itomine, M Higuchi, N Shiroma","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The effects of pilsicainide, propafenone and flecainide on systemic hemodynamics and cardiac function were compared in anesthetized open-chest dogs. Pilsicainide, propafenone and flecainide given intravenously at 1 and 3 mg/kg produced dose-dependent decreases in the mean aortic pressure. The heart rate was decreased by pilsicainide and flecainide, but not by propafenone. The three drugs increased the left ventricular end-diastolic pressure and reduced the first derivative of left ventricular pressure and myocardial oxygen consumption. Pilsicainide decreased aortic, vertebral, coronary and renal blood flows in a dose-dependent manner at 1 and 3 mg/kg. Propafenone increased aortic and vertebral blood flows at 1 mg/kg and decreased coronary and renal blood flows at 3 mg/kg. Flecainide did not significantly change blood flow, except for an increase in the aortic blood flow with 3 mg/kg. The total peripheral, vertebral, coronary and renal vascular resistances were increased by pilsicainide, but not by flecainide. Propafenone decreased total peripheral and vertebral vascular resistances, but hardly affected the coronary and renal vascular resistances. The stroke volume was decreased by 1 and 3 mg/kg pilsicainide in a dose-dependent manner, and increased by 1 and 3 mg/kg propafenone, but not significantly changed by 1 or 3 mg/kg flecainide. The stroke work index was decreased by 3 mg/kg pilsicainide and 3 mg/kg flecainide. The effects of pilsicainide correlated with the changes in its plasma concentration with time. The results indicate that pilsicainide has a negative inotropic activity similar to that of propafenone and flecainide. Pilsicainide and flecainide show almost the same effects with a slightly different efficacy, while propafenone exerts different effects upon some cardiovascular functions.</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 4","pages":"241-50"},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19286338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cardiovascular response to triiodothyronine in Sprague-Dawley and spontaneously hypertensive rats.","authors":"H G Zimmer, M Heckmann, S Lortet","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study we have compared the influence of triiodothyronine (T3) on cardiovascular function and heart weight in Sprague-Dawley and spontaneously hypertensive rats. We also investigated whether the effects induced by T3 are reversible. T3 was administered daily (0.2 mg/kg subcutaneously) for 14 days in female Sprague-Dawley and spontaneously hypertensive rats. Treatment was then stopped for 14 days. At the end of the treatment and of the period without T3, hemodynamic measurements were made in the intact, anesthetized animals by catheterization of the left ventricle with a Millar ultraminiature catheter pressure transducer. Cardiac output was measured by thermodilution. The development and regression of myocardial hypertrophy was measured by the ratio of heart to body weight. The systolic pressure in the left ventricle was higher in spontaneously hypertensive rats than in Sprague-Dawley rats matched for body weight. At the end of treatment with T3, the heart rate was increased to exactly the same extent in both groups. Left ventricular systolic pressure was increased by 15% in Sprague-Dawley rats, but was not altered significantly in spontaneously hypertensive rats. T3 induced an increase in left ventricular dp/dtmax by 106% in Sprague-Dawley rats, but by only 32% in spontaneously hypertensive rats. Cardiac output increased by 63% in Sprague-Dawley rats, but by only 31% in spontaneously hypertensive rats (statistically not significant). When T3 treatment was stopped for 14 days, all the functional changes returned to control values.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":9629,"journal":{"name":"Cardioscience","volume":"4 3","pages":"157-62"},"PeriodicalIF":0.0,"publicationDate":"1993-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19385434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}