Abstract
We determined the ventricular fibrillation threshold (VFT) changes in response to graded coronary sinus (CS) obstruction in 13 chloralose-anesthetized dogs with fixed heart rate (150 min −1, mean systemic arterial pressure (80 mm Hg), and cardiac index (100 ml/min · kg −1 body weight). VFT in milliamperes (VFT mA) increased linearily with CS pressure (CSP) increases up to 41.2 ± 1.4 mm Hg (VFT mA = 6.5 + 0.14 CSP mm Hg, p < 0.01). Total coronary venous effluent (CBF) did not change significantly, suggesting compensatory coronary vasodilation. Myocardial O 2 consumption also remained unchanged. At higher CSP, both CBF and VFT declined precipitously (VFT mA = 20.9 − 0.27 CSP mm Hg, p < 0.02). With simultaneous increases of systemic arterial along with CSP, VFT increased again along with the CSP-induced reduction of gradient until it reached 42.8 ± 3.2 mm Hg. We conclude that with coronary venous obstruction, despite coronary perfusion gradient reduction to about 40 mm Hg, CBF remains constant. This constant flow vasodilation is associated with substantial (82%) VFT increase. The mechanism may involve enhanced homogeneity of CBF distribution and increased extracellular fluid.
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