Collateral Circulation and Survival Related to Gradual Occlusion of the Right Coronary Artery in the Pig

Lumb, George; Hardy, Lawrence B.

doi:10.1161/01.cir.27.4.717

Cited by 64 publications

(13 citation statements)

References 9 publications

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“…Depressed tension development (Carey et al, 1978), as well as depressed shortening velocity (Maughan et al, 1979;Capasso et al, 1982) in hypertrophied myocardium of smaller mammals, is associated with depressed myosin ATPase activity; however, the rodent myosin isozyme patterns differ from that of man. The pig, whose overall size, heartto-body weight ratio (Schaper et al, 1971), and coronary artery distribution (Lumb and Hardy, 1963) resemble those of man, may be a more appropriate model for pressure overload hypertrophy. In adult pig as well as adult human left ventricle (Lompre et al, 1981), there is only one isomyosin seen after native gel electrophoresis, and that isomyosin co-migrates with the V 3 isozyme of the rat.…”

Section: Discussionmentioning

confidence: 99%

Contractile function, myosin ATPase activity and isozymes in the hypertrophied pig left ventricle after a chronic progressive pressure overload.

Wisenbaugh¹,

Allen

th³

et al. 1983

Circulation Research

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SUMMARY. Experimental right ventricular pressure-overload hypertrophy in small mammals is associated with early muscle dysfunction, even before the onset of overt pump failure. Experimental results are quite heterogeneous regarding muscle function of the pressure hypertrophied left ventricle. Muscle dysfunction of the right or left ventricle, when found, may be causally related to alterations of myosin ATPase activity and isozyme type. However, the effect of a gradual pressure overload, analogous to that which occurs in human aortic stenosis, on myocardial contractile function and myosin ATPase activity has not been studied in a large animal whose normal myosin isozyme pattern resembles that of man. We therefore studied pump performance, myocardial contractile function, and myosin ATPase activity and isozyme pattern in pigs with severe, gradually applied left ventricular pressure overload. Thirteen weeks after supravalvular aortic banding, 10 pigs grew more than 7-fold in body weight and were found to have an aortic stenosis area of 0.5 ±0.1 cm 2 with a gradient of 93 ± 12 mm Hg. Compared with nine control animals, the banded animals had a 67% increase in left ventricular mass relative to body weight without overt pump failure as measured by cardiac index and pulmonary artery wedge pressure. Left ventricular ejection performance, measured as shortening fraction, was maintained except in three animals with extreme hypertrophy, in which depressed ejection performance may have been due to an afterload mismatch, myocardial dysfunction, or both. Myocardial contractile function, determined from the end-systolic stress-diameter relationship, was normal except in two pigs in which ejection performance was depressed and left ventricular mass was more than doubled. Only the slow V 3 isozyme of myosin ATPase was found in both normal and hypertrophied pig myocardium, and the ATPase activity was normal in pigs with all degrees of hypertrophy. Thus, in a large animal model of severe, gradual left ventricular pressure overload, in which myosin isozyme pattern remains apparently unaltered, moderate hypertrophy can be associated with normal myosin ATPase activity and contractile function that is normal by current methods of evaluation. (Circ Res 53: 332-341, 1983)

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Section: Discussionmentioning

confidence: 99%

Contractile function, myosin ATPase activity and isozymes in the hypertrophied pig left ventricle after a chronic progressive pressure overload.

Wisenbaugh¹,

Allen

th³

et al. 1983

Circulation Research

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“…Also, the swine has a coronary artery distribution similar to that of the normal human (Lumb and Hardy, 1963), a limited coronary collateral circulation (Blumgart et al, 1950), and a similar ratio of heart weight to body weight to that of man (Schaper, 1971). Therefore it is an appropriate model for comparison to man (Blumgart et al, 1950; Lumb andSingletary, 1961;1962;Lumb and Hardy, 1963;Kong et al, 1969). However quantitative ultrastructural studies of the normal and hypertrophic heart have been conducted mainly in smaller species, e.g., rats (Page et al, 1971;Anversa et al, 1976Anversa et al, , 1978Legato, 1976; Wendt-Gallitelli and Jacob, 1977;McCallister et al, 1979;Tomanek et al, 1979), rabbits (Anversa et al, 1971;Goldstein et al, 1974), hamsters (Colgan et al, 1978), cats (Sheridan et al, 1977), and ferrets (Breisch et aL, 1980).…”

Section: Discussionmentioning

confidence: 99%

“…We nave used swine as a model of cardiac hypertrophy (White et al, 1979) since its response to exercise stress is similar to that in humans. Also, the swine has a coronary artery distribution similar to that of the normal human (Lumb and Hardy, 1963), a limited coronary collateral circulation (Blumgart et al, 1950), and a similar ratio of heart weight to body weight to that of man (Schaper, 1971). Therefore it is an appropriate model for comparison to man (Blumgart et al, 1950; Lumb andSingletary, 1961;1962;Lumb and Hardy, 1963;Kong et al, 1969).…”

mentioning

confidence: 99%

Myocardial morphometric characteristics in swine.

Singh¹,

White²,

Bloor³

1981

Circulation Research

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SUMMARYWe have quantified the ultrastructure of myocardial cells in tissue samples obtained from six adult normal Yucatan swine, tissue samples were obtained from 20 different sites in the left ventricle, right ventricle, and interventricular septum. The samples were processed for electron microscopy and quantitative morphometric analysis. The percent relative volumes of myoflbrils, mitochondria, transverse tubular system, sarcoplasmic reticulum, and clear intracellular space were determined using stereologic&l morphometric methods. Overall, the data were distributed homogenously among the 20 individual sites. However, when certain eubcellular components were examined regionally, some differences appeared. The mitochondrial:myofibril volume ratios were significantly increased in the left ventricle and interventricular septum compared to the right ventricle. They also were greater in the endocardial region compared to the epicardium, which is consistent with higher metabolic activity of these zones. Similarly, the sarcoplasmic reticulum :myofibril ratio was greater in the endocardial region vs. the epicardial region and the basal layer compared to the mid-layer, suggesting the greater need for provision of calcium ions in these particular cones. Since the swine is a convenient large animal fur physiological studies, these results indicate that swine can also be used for quantitative morphometric measurements of myocardial changes in normal and pathologic hearts, and for the study of regional changes in various layers and regions of heart walls. Circ Res 49: 434-441, 1981 MANY experimental models of cardiac hypertrophy have been used to describe the different functional, structural, and biochemical alterations that occur during the development of hypertrophy and failure in the heart. We nave used swine as a model of cardiac hypertrophy (White et al., 1979) since its response to exercise stress is similar to that in humans. Also, the swine has a coronary artery distribution similar to that of the normal human (Lumb and Hardy, 1963), a limited coronary collateral circulation (Blumgart et al., 1950), and a similar ratio of heart weight to body weight to that of man (Schaper, 1971). Therefore it is an appropriate model for comparison to man (Blumgart et al., 1950; Lumb andSingletary, 1961;1962;Lumb and Hardy, 1963;Kong et al., 1969). However quantitative ultrastructural studies of the normal and hypertrophic heart have been conducted mainly in smaller species, e.g., rats (Page et al., 1971;Anversa et al., 1976Anversa et al., , 1978Legato, 1976; Wendt-Gallitelli and Jacob, 1977;McCallister et al., 1979;Tomanek et al., 1979), rabbits (Anversa et al., 1971;Goldstein et al., 1974), hamsters (Colgan et al., 1978), cats (Sheridan et al., 1977), and ferrets (Breisch et aL, 1980). Although ultrastructural studies have been conducted on the hearts of dogs (Vitali-Mazza and Anversa, 1972;Winkler et al., 1977;McCallister et al., 1978;Legato, 1979), it was not known whether the percentages of cell volume of ultrastructural ...

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“…32 The porcine model obviates effects due to coronary collateral blood flow. [16][17][18][19] Pump perfusion was used to accurately measure the net effect of heart rate changes on regional function and myocardial blood flow without the need for assumptions concerning the stability of a mechanical, occlusive device or hydraulic occluder or variations in the degree of the coronary stenosis during different interventions.…”

Section: Other Mechanismsmentioning

confidence: 99%

“…5 Thus, bradycardia could favorably influence contraction through beneficial changes in both supply and demand. Accordingly, the present study was designed to examine the effects of bradycardia on relations between regional myocardial blood flow distribution and left ventricular regional contractile function in a porcine model, in which collateral blood flow is negligible, [16][17][18][19] and in which coronary stenosis is replaced by reduced coronary inflow that is held constant by pump perfusion. The negative inotropic actions of fl-blocking agents were avoided by using a bradycardic drug (UL-FS 49) shown to have no direct cardiodepressant action, 20 23 and thereby allowing assessment of the role of slowed heart rate on contraction at different levels of ischemia under controlled conditions.…”

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confidence: 99%

Mechanisms of improved ischemic regional dysfunction by bradycardia. Studies on UL-FS 49 in swine.

et al. 1989

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In anesthetized swine, the left anterior descending coronary artery was cannulated and perfused at constant blood flow levels during two grades of ischemia. In one group (n = 10), moderate ischemia reduced percent systolic wall thickening (by sonomicrometry) from 25+±7% to 6±2%, whereas in the other group (n =7), severe ischemia reduced percent wall thickening from 24+6% to -0.5+4%. Heart rate was paced in both groups at 91 beats/min. After reperfusion and complete return to control conditions, administration of the bradycardic agent UL-FS 49 (0.37 mg/kg i.v.) decreased the heart rate to 55±5 beats/min. During subsequent ischemia at the same coronary inflow as before bradycardia, percent wall thickening in the ischemic zone during moderate ischemia was increased from 6+2% to 25 ±6% (p<0.01) (not significantly different from control without ischemia), and during severe ischemia, percent wall thickening increased from -0.5±4% to 13 ±7% (p <0.01). During moderate ischemia, bradycardia caused an increase in the subendocardial blood flow from 0.24+±0.60 to 0.42+±0.17 (ml/min)/g (p<0.009) and during severe ischemia, bradycardia caused an increase from 0.14±0.08 to 0.2+0.1 (ml/min)/g (p<0.001). At each level of ischemia, a more marked improvement occurred in subendocardial blood flow per beat ([(ml/min)/g]/heart rate). The relation between myocardial blood flow and wall function at a heart rate of 55 beats/min (n = 14) was plotted and compared with that studied at a heart rate of 122 beats/min in another group of pigs (n = 14). The increase in subendocardial blood flow per minute during bradycardia was not sufflicient to explain the striking increase in function; thus, an independent relation (p<0.05) between blood flow per minute and contractile function (percent wall thickening) was found for each heart rate. In contrast, when myocardial blood flow was normalized for heart rate and expressed per beat, data from both heart rate groups could be described by a single relation. Thus, the subendocardial blood flow per beat predicted wall function independently of heart rate and accounted for changes in both oxygen supply and demand. (Circulation 1989;80:983-993) I ncreased heart rate aggravates myocardial ischemia,1-4 and pharmacologic reduction of heart rate by ,B-adrenergic blockade has been an important form of therapy in patients with coronary artery disease. Mechanisms involved in the

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Collateral Circulation and Survival Related to Gradual Occlusion of the Right Coronary Artery in the Pig

Cited by 64 publications

References 9 publications

Contractile function, myosin ATPase activity and isozymes in the hypertrophied pig left ventricle after a chronic progressive pressure overload.

Contractile function, myosin ATPase activity and isozymes in the hypertrophied pig left ventricle after a chronic progressive pressure overload.

Myocardial morphometric characteristics in swine.

Mechanisms of improved ischemic regional dysfunction by bradycardia. Studies on UL-FS 49 in swine.

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