Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Kjekshus, John

doi:10.1161/01.res.33.5.489

Cited by 123 publications

(32 citation statements)

References 37 publications

(41 reference statements)

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“…We found no change in inner:outer flow ratio during the volume load even though end diastolic pressure was three times greater than with the open ductus alone (Tables I and 2). These findings are similar to those found in adult animals, where increases in end diastolic pressure up to 25 mm Hg produced negligible changes in subendocardial blood flow in the normally perfused left ventricle (24)(25)(26), but decreased subendocardial flow when perfusion pressure was diminished (25,27). The decreased ditistolic blood pressure found in lambs with a patent ductus arteriosus may be the primary factor causing the decreased subendocardia1 perfusion.…”

Section: Discussionsupporting

confidence: 85%

How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

et al. 1987

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ABSTRACT. A model of patent ductus arteriosus in premature lambs was created to examine the lamb's ability to handle the volume load imposed by a patent ductus arteriosus and to determine the lamb's ability to handle any additional volume load. Fifteen preterm lambs I133 -C 2 ( 2 SD) days gestation, term 145 days], whose ductal diameter could be regulated with a mechanical occluder, were studied to determine the independent effects of ductus patency and a saline volume load (50 ml/kg over 3 min) on left ventricular output and its distribution. During a saline infusion, preterm lambs with a closed ductus could only increase their stroke volume by 40% above baseline stroke volume. When challenged with a saline infusion, lambs with an open ductus still were able to increase their stroke volume significantly; the maximal increase in stroke volume during the saline load with the ductus open was 70% above baseline stroke volume. W e hypothesize that the associated reduced left ventricular afterload plays a significant role in the preterm lamb's ability to increase its stroke volume when challenged with a patent ductus arteriosus. Even with a patent ductus arteriosus, the lamb still has the ability to handle additional volume loads. (Pediatr Res 22: 531-535, 1987) Abbreviations PDA, patent ductus arteriosus LV, left ventricle QLV, left ventricular output Q pulmonary, pulmonary blood flow Q ductus, ductus arteriosus blood flow Q systemic, systemic blood flow R pulmonary, pulmonary vascular resistance R systemic, systemic vascular resistance R ductus, ductus arteriosus resistance R total, total resistance Hbg, hemoglobin GI, gastrointestinalThe PDA represents a significant stress on the premature cardiovascular system. The extent of this stress depends both on the magnitude of the left to right shunt through the PDA and on the ability of the cardiovascular system to adjust to that shunt. Full-term newborn lambs respond to volume loading with a limited increase in stroke volume, compared with adult sheep. The left ventricle of the full-term newborn lamb is capable of developing greater force than the left ventricle of the preterm lamb (with closed ductus) at comparable filling volume and resistance (6). Several studies have shown that the fetal lamb has a limited ability to increase its stroke volume above its baseline value during an acute volume load (8-12).The limited ability of the developing left ventricle to increase its output during a volume load is caused by some degree of myocardial immaturity (13) as well as by the high resting output needed to supply the demand for oxygen after delivery (14). The high resting level of performance demanded of the newborn heart may exhaust any reserve pumping capacity. The purpose of our study was both to examine the premature lamb's ability to handle the volume load imposed by a PDA and to see how the presence of a PDA alters the lamb's ability to tolerate any additional volume load. METHODSPreparafion. Fifteen mixed breed western time-dated pregnant ewes at 128-133 days ge...

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Section: Discussionsupporting

confidence: 85%

How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

et al. 1987

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“…Thus, whereas prior studies have demonstrated that the chronically sympathectomized heart has more collateral reserve (Jones and Scheel, 1980;Scheel and Jones, 1983), these potential salutary mechanisms are masked during the ischemic process in the intact, conscious animal. In support of this concept, as pointed out by Kjekshus (1973), Hoffman (1978), Griggs (1981), and Dunn and Griggs (1983), LV end-diastolic pressure is an important determinant of coronary driving pressure and collateral blood flow. The sustained rise in LV end-diastolic pressure after coronary artery occlusion in conscious animals with total cardiac denervation most likely reduced the pressure gradient for collateral perfusion, inhibited full opening of collateral channels, and resulted in more extensive myocardial necrosis.…”

Section: Discussionmentioning

confidence: 73%

Adverse effects of chronic cardiac denervation in conscious dogs with myocardial ischemia.

Lavallée¹,

Amano²,

Vatner³

et al. 1985

Circulation Research

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SUMMARY. The extent to which total chronic cardiac denervation protects the ischemic myocardium was investigated in conscious dogs. The major hemodynamic difference after coronary artery occlusion was that left ventricular end-diastolic pressure rose significantly more, P < 0.01, in the denervated group (12 ± 1.5 mm Hg) than in the normal group (4.4 ± 1.4 mm Hg). Blood flow (radioactive microspheres) in the ischemic endo-and epicardium fell to similar levels at 3-5 minutes after coronary occlusion, but was significantly less (P < 0.01) in denervated dogs at 3 hours after occlusion in the endo-(0.05 ± 0.01) and epicardium (0.30 ± 0.02 ml/min per g), than in the endo-(0.13 ± 0.03) and epicardium (0.42 ± 0.05 ml/min per g) in the normal group. A subgroup of normal dogs was also studied, with left ventricular end-diastolic pressure increased by volume loading to levels similar to those observed in the denervated group after coronary occlusion; in these dogs, blood flow was similar to that in the other two groups 3-5 minutes after coronary artery occlusion, but, at 3 hours, was significantly more depressed (P < 0.01) than that observed in normal dogs without volume loading in both endo-(0.03 ± 0.01) and epicardial (0.25 ± 0.03 ml/min per g) layers. Infarct size, as a fraction of the area at risk, was significantly greater (P < 0.05) in the denervated group (60 ± 4.3%) and in the subgroup of normal dogs with elevated left ventricular end-diastolic pressure (73 ± 5.8%), compared with the normal group without volume loading (37 ± 8.1%). Thus, in conscious dogs, total chronic cardiac denervation exerts an adverse effect on infarct size which may be related to the sustained elevation in left ventricular end-diastolic pressure and consequent impairment of collateral perfusion. (Circ Res 57: 383-392, 1985)

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“…Despite residual coronary vasodilator reserve, the capacity to direct flow to the subendocardium appeared to be exhausted during severe pulmonary artery constriction in this study. It is likely that the increased right ventricular diastolic pressure further impaired right ventricular subendocardial perfusion in a manner similar to that which occurred in the left ventricle, as demonstrated by Kjekshus (1973).…”

Section: Discussionmentioning

confidence: 79%

Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

Gold¹,

Bache²

1982

Circulation Research

126

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SUMMARY. Right ventricular failure during acute pressure overload has been attributed to ischemia which occurs when maximal coronary vasodilation is achieved so that further increases in myocardial blood flow cannot occur. To test the hypothesis that coronary vasodilator reserve is exhausted during acute right ventricular pressure overload, right and left ventricular myocardial blood flow was measured in 14 awake dogs during progressive pulmonary artery occlusion; coronary vasodilator reserve was tested by infusion of adenosine (4 [iM/kg per min) before and during pulmonary artery occlusion. Right ventricular myocardial blood flow rose from 0.77 ± 0.09 ml/min per g (mean ± SEM) during control conditions to 1.69 ± 0.26 ml/min per g during moderate pulmonary artery occlusion (P < 0.01). With further pulmonary artery occlusion to cause increased right ventricular end-diastolic pressure and decreased aortic pressure, a selective decrease in myocardial blood flow to the right ventricular subendocardium was observed, and the right ventricular subendocardial-tosubepicardial blood flow ratio fell from 1.36 ± 0.14 to 0.77 ± 0.06 (P < 0.05). With restoration of mean aortic pressure to control levels, right ventricular systolic pressure increased, right ventricular end-diastolic pressure decreased, and the right ventricular subendocardial-to-subepicardial ratio increased to 1.36 ± 0.18 (P < 0.01). Adenosine infusion during pulmonary artery occlusion in five dogs caused an increase in mean right ventricular blood flow (1.11 ± 0.10 to 2.25 ± 0.30; P < 0.05). This increase was most marked in the outer layers but, nevertheless, was also significant in the subendocardium. These data indicate that acute severe right ventricular pressure overload may be associated with right ventricular subendocardial hypoperfusion, even when coronary vasodilator reserve is not exhausted. (Circ Res 51: 196-204, 1982 ) DURING increased right ventricular systolic pressure, the determinants of right ventricular oxygen requirements increase (Love et al., 1963;Aukland et al., 1967;Brooks et al., 1971). Since increased systolic compression of the intramural coronary vessels during right ventricular systolic hypertension effectively decreases the perfusion pressure gradient between the aorta and right ventricle, an increase in right ventricular myocardial blood flow can only occur by coronary vasodilation and a decrease in coronary vascular resistance (Cross, 1962;Fixler et al., 1973). Brooks et al., (1971) have proposed that right ventricular myocardial ischemia may occur when maximal coronary vasodilation has been achieved so that further increases in right ventricular myocardial oxygen demands cannot be satisfied by further increases in myocardial blood flow. These investigators demonstrated in open-chest, anesthetized dogs that by mechanically increasing perfusion in the right coronary artery, right ventricular failure due to acute pulmonary artery constriction could be reversed without altering the degree of pulmonary artery constriction. Fixler...

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Mechanism for Flow Distribution in Normal and Ischemic Myocardium during Increased Ventricular Preload in the Dog

Cited by 123 publications

References 37 publications

How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

Adverse effects of chronic cardiac denervation in conscious dogs with myocardial ischemia.

Transmural right ventricular blood flow during acute pulmonary artery hypertension in the sedated dog. Evidence for subendocardial ischemia despite residual vasodilator reserve.

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