To investigate the time-dependent effects of ischemia, as modified by muscle fiber type composition, on sarcoplasmic reticulum (SR) function, Ca(2+)-ATPase activity (total minus basal) was measured in homogenates prepared from samples obtained from rat soleus and extensor digitorum longus (EDL) muscle of ischemic and contralateral controls. Ischemia was induced by occlusion of blood flow to one hindlimb for periods of 1, 2, and 3 h (n = 10 per group). In EDL, maximal Ca(2+)-ATPase activity (expressed in mumol.g wet wt-1.min-1) was higher (P < 0.05) in ischemic than in control at 1 h (80 +/- 10 vs. 56.5 +/- 5.3) and increased progressively with ischemia at both 2 h (88 +/- 4.6 vs. 53.1 +/- 2.8) and 3 h (116 +/- 3.8 vs. 67.8 +/- 3.2). In contrast, in soleus, increases (P < 0.05) in Ca(2+)-ATPase activity with ischemia were observed at 2 h (19.2 +/- 0.86 vs. 14.0 +/- 0.56) and 3 h (19.9 +/- 1.4 vs. 12.4 +/- 0.62) but not at 1 h (10.7 +/- 1.5 vs. 10.0 +/- 0.83). In both EDL and soleus, basal Mg(2+)-ATPase was unchanged with ischemia. On the basis of these findings, it can be concluded that ischemia results in an increase in the maximal SR Ca(2+)-ATPase activity but that the time course of the change is dependent on the fiber type composition of the muscle.
Although bipolar cautery was designed to minimize trauma to the central nervous system, little is known about the effects of bipolar cautery on peripheral nerve tissue. This experiment was designed to study the effect of direct bipolar cautery on a peripheral nerve and the muscles innervated by that nerve. Lewis rats (n = 200) were assigned to five different groups: control, sham, and three cautery groups (duration of either 0.5, 1.0, or 1.5 seconds). The hind limb tibial nerves were isolated in the sham group and isolated and cauterized in the cautery groups. Assessments performed at 2 hours, 2 weeks, 4 weeks, and 8 weeks postoperatively included isometric contractile function studies of both a fast- and a slow-twitch muscle, muscle weights, and nerve histology/morphometry. Significant muscle weight loss and reduced muscle function were found in the cautery groups at 2, 4, and 8 weeks (p < 0.05). Histologically, the nerves of the cautery groups showed nerve damage consistent with Sunderland's type 4 nerve injury when examined at 2 weeks and showed nerve regeneration at 4 and 8 weeks. Both the fast-twitch muscle and the shorter duration cautery were associated with faster recovery relative to the slow-twitch muscles and longer duration cautery, respectively. Bipolar cautery, as administered to rat tibial nerves in this experiment, is associated with a significant injury to the nerve and loss of function of the muscles innervated by the nerve.
To investigate the significance of fibre type and the duration of ischemia on changes in sarcoplasmic reticulum Ca2+ ATPase activity (SR Ca2+ ATPase), blood flow was occluded to the rat hind limb for 1, 2, or 3 h (n = 10 per group) and the soleus and extensor digitorum longus (EDL) muscles were examined following 2 h of reperfusion. When compared with the contralateral control muscles, calcium-dependent (total tau basal) SR Ca2+ ATPase activity in soleus was reduced (p < 0.05) to 75.9% by 1 h of ischemia and 2 h of reperfusion (13.1 +/- 0.6 vs. 9.95 +/- 0.85 mumol.mg-1 wet weight.min-1; X +/- SE) with no further reduction (p > 0.05) observed at either 2 h (9.75 +/- 0.57) or 3 h (9.40 +/- 0.64) of ischemia and 2 h of reperfusion. For the EDL muscles, SR Ca2+ ATPase activity with 2 h reperfusion was not reduced (p > 0.05) with 1 h of ischemia (80.4 +/- 3.0 vs. 70.7 +/- 2.9 mumol.mg-1 wet weight.min-1) but was reduced (66.7 +/- 2.3 mumol.mg-1 wet weight.min-1; p < 0.05) in the 2-h ischemia group, with further reductions (53.2 +/- 3.4 mumol.mg-1 wet weight.min-1; p < 0.05) in the 3-h ischemia group. No changes (p > 0.05) in basal or SR Mg2+ ATPase were found for either muscle group with ischemia and reperfusion, regardless of the duration of ischemia. When these results are interpreted in the context of the increases in SR Ca2+ ATPase activity that occur with ischemia, it appears that two components are involved in the reductions in SR Ca2+ ATPase activity noted during reperfusion: one that reduces the SR Ca2+ ATPase activity to below normal and one that simply reverses the ischemic-induced increase in SR Ca2+ ATPase activity. The former component appears to be more pronounced in the EDL muscle.
Complete occlusion of blood flow to rat hind limb by tourniquet was used to study the effects of total ischemia for 1, 2, and 3 h on contractile function and metabolic behaviour of two muscles composed predominantly of either fast-twitch (extensor digitorum longus, EDL) or slow-twitch (soleus, SOL) fibres. Percent loss in twitch force (Pt) was greater (p < 0.05) in SOL than EDL during the first 45 min of ischemia. Following 1 h of ischemia, ATP concentration was lower (p < 0.05) than in the contralateral control (20.8 +/- 2.0 vs. 26.4 +/- 1.5 mmol/kg dry weight). Thereafter, the decline in ATP was greater, with approximately 95% depleted by 3 h of ischemia (1.46 +/- 0.46 mmol/kg dry weight). The effect of ischemia on ATP levels in the SOL was similar to ATP levels in the EDL, 1 h of ischemia also resulted in a large decrement in PCr, from 50.1 +/- 2.9 to 11.7 +/- 2.4 mmol/kg dry weight, and a large increase in lactate, from 25.0 +/- 3.0 to 114 +/- 10 mmol/kg dry weight. As ischemia was prolonged, only lactate was increased (p < 0.05) both at 2 h (171 +/- 12 mmol/kg dry weight) and 3 h (208 +/- 5.4 mmol/kg dry weight). Similar trends were found for SOL. By 3 h of ischemia, glycogen was depleted (p < 0.05) by 88% in EDL and 92% in SOL, respectively. These results support the hypothesis that both high energy phosphate transfer and anerobic glycolysis are of major importance in defending ATP hemostasis, particularly during the 1st h of ischemia, and that the resulting metabolic disturbances are responsible for the large fatigability observed. The mechanisms underlying the greater resistance to fatigue observed for the SOL compared with the EDL during the earlier period of ischemia remain uncertain.
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