The purpose of this study was undertaken to test if alteration of calcium flux across the sarcolemma or sarcoplasmic reticulum change subsequent relaxation of rat aorta in tissue model of ischemia. Thoracic aorta ring segments (2-3mm wide) were
studied
with solution that mimicked real ischemia condition (hypoxia, acidosis, elevated lactate levels and zero substrate). During ischemic condition, the effect of treatments thought to decrease cytosolic calcium were tested. Half time (t1/2) and
degree
of
stabilized relaxation were 2.4±0.9minutes and 17.6±12.1% (NE 10E-7 M precontraction as 100%) for verapamil (10E-6 M), 3.3±0.7 minutes, 22.2±3.9% for low Ca²+ (0.75mM) in ischemic solution Interventions aimed to elevating cytosolic calcium
were
also
tested. 3.8±0.9 minutes and 68.6±8.1% for high (10.0mM) Ca²+ in ischemic solution, 3.7±0.7 minutes, 72.8±3.9% for ryanodine (3×10E-9M). 3.8±0.5 minutes, 53.4±2.6% for isoproterenol. Without any treatment or agents during ischemia, hlaf
time
and
degree of relaxation were 4.0±1.7 minutes, 74.6±13.2%, enothelium and time independent. These data support that treatment or agent thought to reduce influx of cytosolic calcium levels exaggerated the severity of relaxation. The mechanism of
relaxation
in ischemia is not completely clear, but it is suggested that a reduction of calcium influx may involved and directly related.
|