Effects of sodium tanshinone II-A sulfonate and propranolol on coronary collaterals in acutely infracted dogs
Abstract
In 22 mongrel dogs acute myocardial ischemia was made by severing the left anterior descending coronary artery (LAD). Effects of sodium tanshinone II-A sulfonate (DS-201) and propranolol on epicardial S-T segment elevation, hemodynamic parameters in the acute stage, and myocardial collateral anastomosis were assessed by vinyl casts of coronary arteries after 5 h.
In 7 control dogs, the epicardial S-T segment showed a significant elevation, but heart rate, left atrial pressure and mean blood pressure showed only minimal changes after LAD occusion. All 7 coronary vascular casts revealed huge clear-cut deficit areas corresponding to the venterolateral portion of left ventricle and no visible collaterals were found in the boundary regions between nonischemic and ischemic areas except in 1 cast in which a small anastomosis was seen above the occluded level.
DS-201 (8 mg/kg iv) exerted no significant effects on the hemodynamic parameters but reduced significantly the S-T elevations in 10 dogs. In these hearts the vascular deficit areas were markedly diminished or abolished by retrograde filling of vinyl material via the bridgelike collaterals with inner diameters of 100-150 microm. This result suggests that the salutary effects of DS-201 on ischemic hearts both experimentally and clinically may possibly be related to its acceleration of the opening of coronary collaterals.
In 5 dogs propranolol (1 mg/kg iv) protected the S-T elevation, exerted a negative chronotropic effect, and raised the left atrial pressure. In 3 casts the vascular deficit areas were reduced to some extent, and collaterals from left circumflex or posterior coronary arteries were observed. This hints the possibility of blood redistribution from nonischemic to ischemic myocardium after propranolol therapy.
Keywords:
In 7 control dogs, the epicardial S-T segment showed a significant elevation, but heart rate, left atrial pressure and mean blood pressure showed only minimal changes after LAD occusion. All 7 coronary vascular casts revealed huge clear-cut deficit areas corresponding to the venterolateral portion of left ventricle and no visible collaterals were found in the boundary regions between nonischemic and ischemic areas except in 1 cast in which a small anastomosis was seen above the occluded level.
DS-201 (8 mg/kg iv) exerted no significant effects on the hemodynamic parameters but reduced significantly the S-T elevations in 10 dogs. In these hearts the vascular deficit areas were markedly diminished or abolished by retrograde filling of vinyl material via the bridgelike collaterals with inner diameters of 100-150 microm. This result suggests that the salutary effects of DS-201 on ischemic hearts both experimentally and clinically may possibly be related to its acceleration of the opening of coronary collaterals.
In 5 dogs propranolol (1 mg/kg iv) protected the S-T elevation, exerted a negative chronotropic effect, and raised the left atrial pressure. In 3 casts the vascular deficit areas were reduced to some extent, and collaterals from left circumflex or posterior coronary arteries were observed. This hints the possibility of blood redistribution from nonischemic to ischemic myocardium after propranolol therapy.