To investigate the hypothesis that ischemia and reperfusion would impair sa
rcoplasmic reticulum (SR) Ca2+ regulation in skeletal muscle, Sprague-Dawle
y rats (n = 20) weighing 290 +/- 3.5 g were randomly assigned to either a c
ontrol control (CC) group, in which only the effects of anesthetization wer
e studied, or to a group in which the muscles in one hindlimb were made isc
hemic for 4 h and allowed to recover for 1 h (I). The nonischemic, contrala
teral muscles served as control (C). Measurements of Ca2+-ATPase properties
in homogenates and SR vesicles, in mixed gastrocnemius and tibialis anteri
or muscles, indicated no differences between groups on maximal activity, th
e Hill coefficient, and Ca-50, defined as the Ca2+ concentration needed to
elicit 50% of maximal activity. In homogenates, Ca2+ uptake was lower (P <
0.05) by 20-25%, measured at 0.5 and 1.0 <mu>M of free Ca2+ ([Ca2+](f)) in
C compared with CC. In SR vesicles, Ca2+ uptake was lower (P < 0.05) by 30-
38% in I compared with CC at [Ca2+](f). between 0.5 and 1.5 <mu>M. Silver n
itrate induced Ca2+ release, assessed during both the initial, early rapid
(phase 1), and slower, prolonged late (phase 2) phases, in homogenates and
SR vesicles, indicated a higher (P < 0.05) release only in phase 1 in SR ve
sicles in I compared with CC. These results indicate that the alterations i
n SR Ca2+ regulation, previously observed after prolonged ischemia by our g
roup, are reversed within 1 h of reperfusion. However, the lower Ca2+ uptak
e observed in long-term, nonischemic homogenates suggests that altered regu
lation may occur in the absence of ischemia.