Right atrial admixture in coronary venous blood

Koberstein, RC; De, Pittman; Klocke, F. J.

doi:10.1152/ajplegacy.1969.216.3.531

Cited by 52 publications

(17 citation statements)

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“…Moreover, fluoroscopic monitoring of the catheter within the sinus at the onset of pacing failed to demonstrate any change in catheter position. In addition, the tip of the catheter was positioned at least 3 cm from the coronary sinus ostium in all patients, making right atrial admixture unlikely as a source of error (39).…”

Section: Resultsmentioning

confidence: 99%

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Orlick¹,

Ricci²,

Alderman³

et al. 1978

J. Clin. Invest.

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A B S T R A C T The effect of alpha adrenergic blockade on coronary blood flow regulation at rest was studied in 11 normally innervated patients and 8 cardiac allograft recipients by measuring arterial pressure and coronary sinus blood flow by thermodilution before and after alpha adrenergic blockade with phentolamine. Coronary vascular resistance was calculated by using coronary sinus blood flow and mean arterial pressure, and metabolic demand was estimated by the product of systolic arterial pressure and heart rate. In addition, the coronary sinus blood flow response to tachycardia was examined in 9 innervated patients and 12 denervated patients, with measurements repeated after phentolamine in 8 of the 9 innvervated patients and 6 of the 12 denervated patients. There was a 7.3+4.4% increase in coronary sinus blood flow in the innervated patients in response to alpha blockade, whereas the transplanted patients had an 8.2±1.8% fall in coronary sinus blood flow, despite equivalent changes in rate pressure product. The innervated patients also demonstrated a significantly greater increase in coronary sinus blood flow than did the transplanted patients during the first 5 s of an abrupt increase in heart rate (26±4 vs. 8±2.5 ml/min, P < 0.001). This early response was blunted after alpha adrenergic blockade. We conclude that there is basal alpha adrenergic tone present on the coronary vasculature in man that is withdrawn by a sudden increase in heart rate.

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Section: Resultsmentioning

confidence: 99%

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Orlick¹,

Ricci²,

Alderman³

et al. 1978

J. Clin. Invest.

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“…As mentioned above, the possibility that right atrial blood "contaminates" blood sampled from the great cardiac vein in the dog has been excluded by a previous investigation (10). The data presented for patients indicate that right atrial admixture is unlikely in the distal coronary sinus and great cardiac vein but is frequent in the proximal coronary sinus.…”

Section: Discussion Saturationmentioning

confidence: 96%

Effects of heterogeneous myocardial perfusion on coronary venous H2 desaturation curves and calculations of coronary flow

Klocke¹,

Koberstein²,

Pittman³

et al. 1968

J. Clin. Invest.

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A B S T R A C T The present investigation was intended to evaluate myocardial inert gas desaturation curves for manifestations of heterogeneous coronary perfusion. The test gas was hydrogen (H2) and blood H, analyses were performed with a gas chromatograph capable of detecting small but prolonged venous-arterial H2 differences produced bv areas of reduced flow. Curves were initially obtained after 4-min left ventricular infusions of H11-saturated saline in six patients with arteriographically proven coronary artery disease, three patients with normal coronary arteries, and nine closed-chest dogs. The dogs were studied before and after embolic occlusion of a portion of the left coronary artery. Although the slopes of their semilogarithmically plotted venous desaturation curves varied with time before embolization, they showed more distinct deviations from single exponentials after embolization (after H2 concentrations had fallen below 15% of their initial values). The human curves divided similarly, those from coronary artery patients deviating appreciably from single exponentials. A similar separation wlas also evident in studies of coronary venous-arterial H2 differences after 20 min of breathing 2%11 H; data were obtained in four dogs before and after coronary embolization, and in three normal patients, and five patients with coronary artery disease. Additional data indicated that the This work was presented in part at the 40th Annual

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“…Blood was withdrawn at a rate of less than 10 ml/min to avoid right atrial venous admixture (Koberstein et al, 1969).…”

Section: Coronary Sinus Cannulationmentioning

confidence: 99%

Carotid baroreceptor reflex coronary vasodilation in the dog.

Ito

Feigl²

1985

Circulation Research

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SUMMARY. The hypothesis that neurally mediated coronary vasodilation occurs as part of the carotid baroreceptor reflex was investigated. The left main coronary artery was cannulated and perfused at constant pressure (100 mm Hg) in closed-chest, chloralose-anesthetized dogs. The heart was paced at a constant rate between 60 and 70 beats/min after atrioventricular heart block. Propranolol (1 mg/kg) was given to prevent j3-receptor-mediated alterations in contractility. Aortic blood pressure was stabilized with a blood reservoir. The aortic depressor nerves were cut bilaterally to prevent the buffering influence of aortic arch baroreceptors on the carotid baroreceptor reflex. The carotid sinuses were vascularly isolated and perfused with arterial blood at controlled pressures. Under these conditions, a step change in carotid sinus pressure from 70 to 210 mm Hg produced a 0.29 ml/min per g increase in coronary flow above control and a 10 mm Hg increase in coronary sinus blood oxygen tension. A step in carotid sinus pressure from 70 to 150 mm Hg resulted in a flow increase of 0.13 ml/min per g and a coronary sinus oxygen tension increase of 5.3 mm Hg relative to prestimulation values. Atropine (0.5 mg/kg, iv) blocked most of the reflex coronary vasodilation, indicating a parasympathetic component, and the addition of adrenergic a-receptor blockade with phenoxybenzamine (0.25 mg/kg, ic) abolished the remaining response, demonstrating sympathetic participation. The reflex nature of the coronary response was confirmed with carotid sinus denervation and vagotomy. It is concluded that carotid sinus hypertension results in a graded reflex neural coronary vasodilation independent of myocardial metabolic factors. The major component is due to activation of parasympathetic coronary vasodilator fibers, but there is also inhibition of sympathetic vasoconstrictor fibers. (Circ Res 56: 486-495, 1985) PREVIOUS studies have demonstrated that adrenergic a-receptor coronary vasoconstriction can be reflexly elicited by carotid sinus hypotension (Feigl, 1968(Feigl, , 1983DiSalvo et al., 1971;Limet et al., 1975;Powell and Feigl, 1979;Ely et al., 1981). However, the reflex response to carotid sinus hypertension is less clear. Both coronary vasoconstriction (DiSalvo et al., 1971) and coronary vasodilation (Limet et al., 1975) have been observed during acute elevations in carotid sinus pressure. Coronary vasodilation during the elevation of aortic pressure has also been attributed to the carotid baroreflex (White et al., 1976). Electrical stimulation of the afferent carotid sinus nerve has been employed to mimic carotid sinus hypertension, and either coronary vasoconstriction (Falicov et al., 1970) or vasodilation (Vatner et al., 1970;Hackett et al., 1972;Religa et al., 1972;Solti et al., 1975) has been observed. However, it is difficult to equate a given nerve stimulation frequency with a carotid sinus pressure stimulus that physiologically activates baroreceptors. Furthermore, electrical stimulation of carotid sinus baroreceptor affe...

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Right atrial admixture in coronary venous blood

Cited by 52 publications

References 0 publications

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Effects of Alpha Adrenergic Blockade upon Coronary Hemodynamics

Effects of heterogeneous myocardial perfusion on coronary venous H2 desaturation curves and calculations of coronary flow

Carotid baroreceptor reflex coronary vasodilation in the dog.

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