Distribution of the Coronary Blood Flow across the Canine Heart Wall during Systole

Downey, James M.; Kirk, Edward S.

doi:10.1161/01.res.34.2.251

Cited by 140 publications

(39 citation statements)

References 24 publications

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“…In our recent study, we observed that increased RVP in newborn infants with critical pulmonary stenosis severely restricts RCA flow (37). The extravascular compression factor of total coronary resistance has been estimated as 29% of total coronary vascular resistance (38). The decrease in ventricular pressure leads to a decrease in the intramural tension.…”

Section: Discussionmentioning

confidence: 98%

Circulatory Effects of Inhaled Iloprost in the Newborn Preterm Lamb

et al. 2009

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Inhaled NO (iNO) has an established role in the treatment of pulmonary hypertension (PH) in the newborn. However, costs and potential toxicity associated with iNO have generated interest in alternative inhaled selective pulmonary vasodilators such as iloprost. In a preterm lamb model of respiratory distress syndrome, we studied effects of increasing doses of iloprost followed by iNO on right ventricular pressure (RVP) and circulation including cerebral oxygenation. Fetal sheep were randomized to three doses (0.2-4 mg/kg) of iloprost (n ϭ 9) or saline (n ϭ 10), administered as 15-min inhalations with 15-min intervals after a 60-min postnatal stabilization. No differences were found in RVP, arterial PO 2 , or cardiac index according to treatment. The cerebral oxygenation, measured with near-infrared spectroscopy, deteriorated in control lambs, but not in iloprost lambs. Iloprost treatment followed by iNO resulted in a larger decrease (p ϭ 0.007) in RVP than saline treatment followed by iNO. In conclusion, iloprost stabilized cerebral oxygenation and when followed by iNO had a larger effect on RVP than iNO alone. Although species differences may be relevant, these results suggest that iloprost should be studied in newborn infants for the treatment of PH. circulation, the pulmonary vascular resistance decreases rapidly. The vascular tone in pulmonary arteries is regulated by a balance of vasoconstrictors and vasodilators. Endothelin, hypoxemia, and acidemia have strong constrictor effects on pulmonary arterioles (1). The main endogenous vasodilators are the endothelial-derived substances NO and prostacyclin, which increase endothelial cell production of cGMP and cAMP, respectively (1). When the transition is disturbed, the pulmonary arterial resistance remains elevated resulting in considerable hypoxemia and low-oxygen delivery to tissue. As arterial O 2 tension does not necessarily reflect the oxygen delivery to tissue because of low perfusion or extraction, near-infrared spectroscopy (NIRS) has been applied to monitoring tissue oxygenation (2).Inhaled NO (iNO) exerts a rapid pulmonary vasodilatation and is an established treatment of pulmonary hypertension (PH) in newborn infants (3). iNO has, however, several disadvantages, such as unpredictable and nonsustained effect, and rebound PH after withdrawal (4). The toxic NO product peroxynitrite inhibits prostacyclin synthase (5), the key enzyme of prostacyclin synthesis. Further, NO causes an increased endothelin-1 release (6). Thus, other effective agents with fewer side effects are sought for the treatment of PH in the newborn.Prostanoids have been administered in the clinical setting mainly in adults as i.v. infusions of prostacyclin, s.c. infusion of treprostinil, and inhalations of iloprost (7). I.v. prostacyclin causes severe systemic hypotension in newborns (8). Inhaled prostacyclin decreases pulmonary vascular resistance without decreasing systemic blood pressure. The prostacyclin analogue iloprost has a longer half-life (almost 30 min) than prostac...

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Section: Discussionmentioning

confidence: 98%

Circulatory Effects of Inhaled Iloprost in the Newborn Preterm Lamb

et al. 2009

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“…This finding is consistent with differences in the left and right coronary artery phasic flow patterns. 17 Intramyocardial pressure in the left ventricle is sufficiently high to impede flow to subendocardium during systole, 18 so most left coronary flow occurs during diastole." With left coronary dilation in the presence of hypotension, the transmural gradient of vascular tone required to compensate for subendocardial underperfusion during systole is compromised, and ischemia becomes more severe in subendocardial tissue.…”

Section: Discussionmentioning

confidence: 99%

Transmural variation in autoregulation of right ventricular blood flow.

Yonekura

Watanabe

Downey

1988

Circulation Research

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We examined transmurally the right coronary autoregulatory flow response to varied perfusion pressures in 11 anesthetized, open-chest dogs. Right coronary artery flow was measured electromagneticalry, and its transmural distribution was denned with 15-(im radioactive microspheres. Heart rate, mean aortic blood pressure, right ventricular systolic pressure, end-diastolic pressure, and dP/dt_ were constant. At 100 mm Hg, subepicardial flow averaged 0.48 ±0.04 ml/min/g, and subendocardial flow averaged 0.56 ± 0.05 ml/min/g. In contrast to the left coronary circulation, right coronary hypotension did not cause preferential subendocardial ischemia. As right coronary perfusion pressure was decreased from 100 to 40 mm Hg in five dogs, subepicardial and subendocardial flows were reduced similarly by 35-36%. As right coronary perfusion pressure was elevated from 100 to 150 mm Hg in six dogs, right ventricular subepicardial blood flow increased by 31%, whereas 5 a phenomenon known as autoregulation.6 When left coronary perfusion pressure is decreased below the autoregulatory pressure range, regional flow falls more precipitously in subendocardium, 7 "9 and the subendocardial-to-subepicardial flow ratio (endo/epi) reaches approximately 0.3 at complete occlusion of the left coronary artery.8 When left coronary perfusion pressure is increased above the autoregulatory pressure range, the endo/epi ratio increases, 10 indicating that left coronary autoregulation fails first in subendocardium. To date, there have been no reports of regional autoregulatory capability in the right coronary circulation, although we recently found that right coronary artery autoregulation was less potent than left coronary autoregulation." It is possible that the blunted autoregulatory capability of the right coronary circulation has a regional basis like that of the blunted capability Received June 8, 1987; accepted November 2, 1987. of the hyperperfused left coronary circulation. 10 Thus, this investigation was conducted to define transmurally right coronary autoregulatory capability over a wide range of right coronary perfusion pressures. Materials and MethodsEleven mongrel dogs of either sex, weighing 15 to 24 kg, were anesthetized with sodium pentobarbital, 30 mg/kg i.v. initially, and supplemented as needed to maintain stable anesthesia. After tracheotomy, the dogs were ventilated by a respirator (Harvard Apparatus, South Natick, Massachusetts) with room air supplemented with oxygen to maintain normal arterial oxygen tension. A vinyl catheter was positioned in the inferior vena cava through a femoral vein for administration of supplementary anesthetic, heparin, and fluids. A second vinyl catheter was advanced into the thoracic aorta through a femoral artery to monitor aortic pressure. Right ventricular pressure was measured with a catheter-tipped transducer (Millar Instruments, Houston, Texas) inserted through the right jugular vein and across the tricuspid valve. The right ventricular pressure signal was differentiated electronically, and ...

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“…Nevertheless, it is likely that increased impedance to subendocardial blood flow during systole contributed to the decrease in ENDO/EPI ratio during severe pulmonary artery occlusion (Walston et al, 1978;Monroe et al, 1972). Myocardial blood flow during systole is principally determined by the dynamic interaction of perfusion pressure, vasomotor tone, and intramyocardial presure (Downey and Kirk, 1974;Hess and Bache, 1976;Hess and Bache, 1979;Bellamy and Lowensohn, 1980). Unlike the left ventricle, during normal intraventricular pressures, right coronary artery blood flow occurs equally throughout the cardiac cycle (Lowensohn et al, 1976).…”

Section: Discussionmentioning

confidence: 99%

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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Distribution of the Coronary Blood Flow across the Canine Heart Wall during Systole

Cited by 140 publications

References 24 publications

Circulatory Effects of Inhaled Iloprost in the Newborn Preterm Lamb

Circulatory Effects of Inhaled Iloprost in the Newborn Preterm Lamb

Transmural variation in autoregulation of right ventricular blood flow.

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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