For the experimental studies on chronic coronary stenosis, an ameroid constrictor was modified to facilitate serial cineangiographic evaluation of the degree of arterial narrowing. A radiolucent plastic ring instead of a stainless frame was used to prevent outward swelling of the ameroid material. Coronary cineangiography was performed 10, 20 and 30 days after the implantation of the modified ameroid constrictor on the left circumflex coronary artery (LCX), which could prove the progressive coronary stenosis of 57, 78 and 88% on the respective days. Collateral channels from the anterior descending branch of the left coronary artery to the LCX were demonstrated angiographically in 5 out of the 6 dogs on the 30th day.
SUMMARY We studied the relationships among collateral flow, regional myocardial shortening and the grade of coronary stenosis during ameroid-induced chronic coronary constriction in 22 conscious dogs. A radiolucent ameroid, a Doppler flow probe and a cuff occluder were placed on the left circumflex coronary artery (LCx). Regional myocardial shortening and regional myocardial blood flow were assessed simultaneously using ultrasonic dimension gauges and the tracer microsphere technique, respectively, during temporary occlusion of the LCx. Regional hypokinesia and ischemia were attenuated as a function of time during progressive coronary stenosis. Fifty percent recovery and full recovery of regional shortening during occlusion were observed 19 3 and 25 4 days after instrumentation, respectively, when the endocardial blood flow recovered from 0.42 + 0.07 ml/min/g at 7 days to 0.56 0.07 and 0.80 0.05 ml/min/g, respectively. Greater than 75% coronary stenosis coincided with collateral development, as estimated from regional shortening rate and the appearance of angiographically opacified collaterals. Our study confirms that the development of collateral vessels reduces regional ischemia and hypokinesia induced during abrupt coronary occlusion in a canine model. GRADUAL coronary occlusion over a period of days, especially in a canine model, leads to the development of collateral channels, which can be evaluated by measuring peripheral coronary pressure, ' retrograde flow,2',3 reactive hyperemia 7 and regional contraction abnormalities that appear during temporary coronary occlusion.A-'0 However, the relationship between the grade of coronary stenosis and the functional reserve of collateral vessels and the relationship between collateral blood flow and regional shortening during progression of collateral development are unclear.The functional state of collateral channels has been estimated according to the degree of reactive hyperemia3,6 and by regional myocardial contraction.81-0 Recently, an inverse linear relation between the reduction of reactive hyperemia and recovery of contraction abnormalities during temporary coronary occlusion was noted after the implantation of an ameroid constrictor.'0 However, the grade of coronary stenosis is a major determinant of reactive hyperemia.", 12 Therefore, to define the extent to which reactive hyperemia reflects collateral function per se, it may be important to assess both the grade of coronary stenosis and collateral function. In a previous study, we devised a radio-
The inhibitory effects of disopyramide on electromechanical responses were investigated in guinea‐pig papillary muscles driven by electrical stimuli. Disopyramide up to 10−5 m did not cause a negative inotropic effect, while the maximum upstroke velocity of the action potential (dV/dtmax) was significantly decreased. At higher concentrations, this drug dose‐dependently inhibited the contraction, and dV/dtmax was further decreased. This inhibition of contraction was accompanied by a depression of the slow action potential in partially depolarized preparations by increasing [K+]o (26 mm). In preparations pretreated with nifedipine (10−6 m) and ryanodine (10−6 m), the contraction was almost completely inhibited. In such preparations, ouabain (2 × 10−6 m) markedly increased the contraction, probably through the Na+‐Ca2+ exchange mechanism. This contraction was inhibited by disopyramide above 10−8 m, and an almost complete inhibition was caused at 3 × 10−5 m. A similar inhibitory effect was observed on the contraction increased by the lowering of [Na+]o (36 mm). These results suggest that disopyramide at high concentrations inhibits Ca influx through slow Ca2+ channels and at low concentrations, it reduces the contraction increased through the Na+‐Ca2+ exchange mechanism. Disopyramide had a greater effect on cardiac contractility mediated by the Na+‐Ca2+ exchange mechanism.
SUMMAThe effects of chronic instrumentation on regional myocardial performance and regional myocardial blood flow were studied in 8 mongrel dogs. Regional segment lengths were measured by an ultrasonic dimension gauge technique at two areas of the left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX). Regional myocardial blood flow was measured by a tracer microsphere technique. These measurements were repeated while the animals were conscious on the 4th, 11th, 21st and 28th days after instrumentation.On the 4th day, the heart rate was rather high and regional shortening at both the LAD and LCX areas remained suppressed. After the 11th day, hemodynamic variables such as heart rate, left ventricular pressure and regional wall motion were fairly constant. Regional myocardial blood flow and its distribution were also constant throughout the experimental period. Fibrosis of the epicardium invariably induced by surgical procedures did not affect the distribution of regional blood flow as compared with that of the interventricular septum.Thus, a stable hemodynamic state was recorded after the 11th day following surgical manipulation and the implantation of sensors and catheters did not affect the level of regional myocardial blood flow or its distribution at rest. Such long term reproducible measurements of regional wall motion and regional myocardial blood flow may facilitate chronic studies of cardiovascular physiology.
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