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Fiber shortening, blood flow and high-energy phosphate content in various layers of the left ventricular wall at the onset of ischemia
19 ITIJZEFFECT OF RYPERIENSION ON 'ITIE PXSEQNSE OF 'IRE MYCCARDIUMTo NOIMYIHE%IIC GLOBAL ISCRAELIIA. W.G. Nayler, IT. Sturrock. Department of Medicine, University of Melbourne Austin Hospital, Heidelberg, Victoria, Australia. Ischaemia of the myocardium is accompanied by a rapid decline in contractility. \Ye have investigated whether pre-existing hypertension influences this decline. 'Ihe experiments were perforn-ed on hearts isolated from adult, age and weight-matched rats, Nomtensive Sprague Dawley and Wistar Kyoto rats (mean systolic B.P. 110-130 mn Hg), stroke prone hypertensive (SPR), spontaneously hypertensive (SBR) and genetically hypertensive (GSR) rats (mean systolic B.P. 180-210 mn Hg) were used. 'lhe hearts were isolated and perfused by the non-recirculating Iangendorff technique at 37oC. After 30 min equilibration the hearts were either assayed for ATP and ('P, or made globaIl\ ischaemic at 37oC. Peak developed tension was monitored. Cn scme occasions after GO min of normothenaic ischaemia the hearts were reperfused. Irrespective of their origin cessation of coronary flow resulted in an abrupt decline in peak developed tension. The rate of decline was greater (~~0.01) in the nomtensive series. Cpon reperfusion the percentage recovery of tension generating capacity was linearly related to the rate of decline in tension generation during the first 30 seconds of ischaemia.
20 FIBER SHUKTEI~IN~~, BLJUD FLUW AND HIGH-ENERtiY PHUSPHATE CUdTENT IN VARIUUS LAYERS 3F THE LEFT VENTRICULAR WALL AT THE ONSET OF ISCHEMIA. F.W. Prinzen, T. Arts, G.J. van der VUSSE, R.S. Reneman, Depts of Physiology and Biophysics, University of Limburg, Maastricht, The Netherlands. In open-chest dogs (n=30) coronary artery stenosis caused a decrease of mean post-stenotic perfusion pressure to 3.3 kPa (median value). Epicardial deformation was measured during the ejection phase with an inductive technique, allowinq the calculation of epicardial minimal (emin) and maximal shortening (emax). W?thin seconds after onset of stenosis e reflecting fiber shortening in the inner layers, fell from 2.6% to negative &?&s, indicating lengthening in this direction. This lengthening was maximal (-4.0%) after 20 s, and then diminished to -0.3% after in the inner layers blood flow had decreased by 68% 60 s of stenosis. At this moment, no change in ATP content could be and creatine phosphate (CP) content by 46%; observed. In the outer layers, blood flow decreased by 36% after 60 s, whereas CP and reflecting fiber shortening in the ATP contents were unchanged. Nevertheless e outer layers decreased, from 7.1% to 2.3% at'w;. These results suggest that during early ischemia fiber shortening in the outer layers is impaired by the loss of function in the inner layers. (Supported by FUNtiO through ZWO)
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PREDICTION OF FIBER SHORTENING IN THE INNER LAYERS OF THE LEFT VENTRICULAR WALL FROM EPICARDIAL DEFORMATION MEASUREMENTS DURING NORMOXIA AND ISCHEMIA. F.W. Prinzen, T. Arts, G.J. van der Vusse, R.S. Reneman. Departments of Physioloqy _. and Biophysics, University of Limburg, Maastricht, The Netherlands. Muscle fiber shortening across the left ventricular wall was assessed by determining For this purpose circumferential deformation of the epicardial surface. shortening (e ), base-to-apex (e ) shortening and shear anterior freeCwall of the left Ifentricle simultaneously the direction and magnitude of maximal using an inductive method. From e Their direction ) and minimal (e . ) epicafiiz? were calculated. (e apvP6ximately coincide?$kh the fiber orientation in the outer and inner layers of the myocardium, respectively. After onset of coronary artery occlusion in open-chest indicating indogs (n=13), e decreased earlier and more pronounced than e crease of the !!'ransmural difference in fiber shortening. This d?&rence decreased Separately the relation between e . and shortening again after 30 s of occlusion. ) was assessed measuP1Rg mutual motion parallel to e in the inner layers (e and angulatio#'& three needles pierced ??&J the nlyocardial wall. During normoxia and e and ischemia (n=6, 12 occlusions) e were correlated significantly (r=O.Y3), indicating that emin is clo@& relat&fipdeo fiber shortening in the inner layers. (Supported by FUNGO through ZWO)
20 FIBER SHUKTEI~IN~~, BLJUD FLUW AND HIGH-ENERtiY PHUSPHATE CUdTENT IN VARIUUS LAYERS 3F THE LEFT VENTRICULAR WALL AT THE ONSET OF ISCHEMIA. F.W. Prinzen, T. Arts, G.J. van der VUSSE, R.S. Reneman, Depts of Physiology and Biophysics, University of Limburg, Maastricht, The Netherlands. In open-chest dogs (n=30) coronary artery stenosis caused a decrease of mean post-stenotic perfusion pressure to 3.3 kPa (median value). Epicardial deformation was measured during the ejection phase with an inductive technique, allowinq the calculation of epicardial minimal (emin) and maximal shortening (emax). W?thin seconds after onset of stenosis e reflecting fiber shortening in the inner layers, fell from 2.6% to negative &?&s, indicating lengthening in this direction. This lengthening was maximal (-4.0%) after 20 s, and then diminished to -0.3% after in the inner layers blood flow had decreased by 68% 60 s of stenosis. At this moment, no change in ATP content could be and creatine phosphate (CP) content by 46%; observed. In the outer layers, blood flow decreased by 36% after 60 s, whereas CP and reflecting fiber shortening in the ATP contents were unchanged. Nevertheless e outer layers decreased, from 7.1% to 2.3% at'w;. These results suggest that during early ischemia fiber shortening in the outer layers is impaired by the loss of function in the inner layers. (Supported by FUNtiO through ZWO)
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PREDICTION OF FIBER SHORTENING IN THE INNER LAYERS OF THE LEFT VENTRICULAR WALL FROM EPICARDIAL DEFORMATION MEASUREMENTS DURING NORMOXIA AND ISCHEMIA. F.W. Prinzen, T. Arts, G.J. van der Vusse, R.S. Reneman. Departments of Physioloqy _. and Biophysics, University of Limburg, Maastricht, The Netherlands. Muscle fiber shortening across the left ventricular wall was assessed by determining For this purpose circumferential deformation of the epicardial surface. shortening (e ), base-to-apex (e ) shortening and shear anterior freeCwall of the left Ifentricle simultaneously the direction and magnitude of maximal using an inductive method. From e Their direction ) and minimal (e . ) epicafiiz? were calculated. (e apvP6ximately coincide?$kh the fiber orientation in the outer and inner layers of the myocardium, respectively. After onset of coronary artery occlusion in open-chest indicating indogs (n=13), e decreased earlier and more pronounced than e crease of the !!'ransmural difference in fiber shortening. This d?&rence decreased Separately the relation between e . and shortening again after 30 s of occlusion. ) was assessed measuP1Rg mutual motion parallel to e in the inner layers (e and angulatio#'& three needles pierced ??&J the nlyocardial wall. During normoxia and e and ischemia (n=6, 12 occlusions) e were correlated significantly (r=O.Y3), indicating that emin is clo@& relat&fipdeo fiber shortening in the inner layers. (Supported by FUNGO through ZWO)