The effect of hyperthyroidism on the contractile properties and Ca²⁺ sequestering abilities by the sarcoplasmic reticulum (SR) in the soleus muscles was examined in rats treated with thyroid hormone (3, 5, 3'-triiodo-L-thyronine, T₃) (300μg/kg body weight) for 3, 7 and 21 days. At the end of a given treatment period, the right or left soleus muscle was mounted isometrically at 30°C, and stimulated directly using supramaximal current intensity. A twitch contraction was elicited by a 1 msec square-wave pulse and a tetanic contraction by 20 Hz stimulation for 600 msec. To evaluate fatigue resistance, muscles were stimulated at 40 Hz for 350 msec with tetani repeated at an interval of 2 sec during a 4-min period. Another soleus muscle was used, for analysis of SR Ca²⁺ -uptake rate and SR Ca²⁺ -ATPase activity. Pronounced increases in SR Ca²⁺ -uptake rate and ATPase activity were observed after T₃ treatment periods longer than 6 days. These alterations were accompanied by decreases in twitch and tetanic tension, half-relaxation time, and fatigue resistance. The T₃-treated muscles stimulated at 20 Hz relaxed during the interval between successive stimuli, indicating that the mechanical fusion of tetanic contractions was incomplete. SR Ca²⁺ uptake rate was significantly correlated both to tetanic tension and to fatigue resistance. These data suggest that there may be a causal relationship between changes in SR Ca²⁺ uptake and the loss of muscular strength in the hyperthyroid soleus.

Effects of amrinone and dibutyryl cyclic AMP (DBcAMP) on hemodynamics and myocardial metabolism were studied in 16 patients in the early postoperative period following open-heart surgery. Amrinone was administered continously at 10μg/kg/min for 5 hours and DBcAMP at 12μg/kg/min was infused concomitantly for the last 1 hour. Amrinone increased SVI, and decreased HR, PCWP, arterial systolic blood pressure, double product and central temperature difference significantly. Following concomitant administration of DBcAMP for 1 hour, further increase of CI, O₂ delivery, blood sugar and insulin were observed. Significant decrease of excess lactate from 9.31±3.27 to -1.31±1.83mg/dl (p<0.05) showed that anaerobic metabolism improved in the myocardium after amrinone administration, and the effect improved further to -3.64±1.8mg/dl following concomitant administration of DBcAMP. These data demonstrate that amrinone has beneficial effects on hemodynamics and myocardial metabolism, and following supplementary administration of DBcAMP, further improvement in hemodynamics was observed.

Repeated contractions of skeletal muscle cause fatigue, as manifested by a reduced ability to produce force and slowed contraction. During studies of muscle fatigue, a phenomenon known as low-frequency fatigue (LFF) was observed in human skeletal muscles. It is characterized by a greater loss of force in response to low- versus high-frequency muscle stimulation and a long period of time for full recovery. This force deficit is most likely to be owing to disturbances in sarcoplasmic reticulum (SR) Ca²⁺ release and/or reductions in myofibrillar Ca²⁺ sensitivity. Studies on metabolites have implied that inorganic phosphate and Mg²⁺ might have some role in reduced SR Ca²⁺ release that occurs immediately after fatiguing contraction. In addition, recent experiments have shown that impaired myofibril function may relate to increased nitric oxide and hydroxyl radical production, whereas deterioration of SR function may be attributable to increased superoxide production, elevation of cytoplasmic Ca²⁺ concentration and/or decreased muscle glycogen. Finally, we will discuss possible proteins which are affected and contribute to the development of LFF.

We report a case of redo aortic valve replacement by right minithoracotomy approach for aortic stenosis after coronary artery bypass grafting (CABG). An 81-year-old man was followed-up once a year for 9 years after CABG. He complained of increasing respiratory distress, showed narrowing of the aortic valve area, elevation of the aortic valve pressure gradient, and tricuspid valve regurgitation by echocardiography. He was admitted for surgery. We considered minimally invasive operation would be better for him and performed aortic valve replacement (Carpentier-Edwards Perimaunt valve 19 mm) by a right minithoracotomy approach because graft injury could occur by median sternotomy after CABG, and he had the risks of advanced age, low activities of daily living, and mild dementia. His postoperative course was uneventful. On echocardiography performed at postoperative days 9, the ejection fraction recovered to 75% from 53% before surgery and the mean aortic valve pressure gradient was 8 mmHg. He was discharged on postoperative day 12. Right minithoracotomy approach with port access is a good option for redo operation for aortic valve stenosis after CABG.

The purpose of this study was to investigate changes in sarcoplasmic reticulum (SR) Ca²⁺-sequestering capacity in rat fast-twitch plantaris (PL) and slow-twitch soleus (SOL) muscles during recovery after high-intensity exercise. The rats were subjected to treadmill runs to exhaustion at the intensity (10% incline at 50 m/min) estimated to require 100% of maximal O₂ consumption. The muscles were excised immediately after exercise, and 15, 30 and 60 min after exercise. Acute high-intensity exercise evoked a 27 % and 38 % depression (P<0.05) in SR Ca²⁺-uptake rate in the PL and SOL, respectively. In the PL, uptake rate remained lower (P<0.05) at 30 min of recovery but recovered 60 min after exercise. These alterations were paralleled by those of SR Ca²⁺-ATPase activity. On the other hand, SR Ca²⁺-uptake rate in the SOL recovered 15 min after exercise. Unlike the PL, discordant time-course changes between SR Ca²⁺-ATPase activity and uptake occurred in the SOL during recovery. SR Ca²⁺-ATPase activities were unaltered with exercise and elevated (P<0.05) by 25, 30 and 30% at 15, 30 and 60 min of recovery, respectively. These results demonstrate that SR Ca²⁺-sequestering ability is restored faster in slow-twitch than in fast-twitch muscle during recovery periods following a single bout of high-intensity exercise and suggest that the rapid restoration of SR Ca²⁺-sequestering ability in slow-twitch muscle could contribute to inhibition of disturbances in contractile and structural properties that are known to occur with raised myoplasmic Ca²⁺ concentrations.

To investigate the influences of high-intensity training and/or a single bout of exercise on in vitro Ca²⁺-sequestering function of the sarcoplasmic reticulum (SR), the rats were subjected to 8 weeks of an interval running program (final training : 2.5-min running×4 sets per day, 50 m/min at 10% incline). Following training, both trained and untrained rats were run at a 10% incline, 50 m/min for 2.5 min or to exhaustion. SR Ca²⁺-ATPase activity, SR Ca²⁺-uptake rate and carbonyl group contents comprised in SR Ca²⁺-ATPase activity were examined in the superficial portions of the gastrocnemius and vastus lateralis muscles. For rested muscles, a 12.7% elevation in the SR Ca²⁺-uptake rate was induced by training. Training led to improved running performance (avg time to exhaustion : untrained-191.1 vs trained-270.9 sec ; P<0.01). Regardless of training status, a single bout of exercise caused progressive reductions in SR Ca²⁺-ATPase activity and SR Ca²⁺-uptake rate. Increases in carbonyl content only occurred after exhaustive exercise (P<0.05). At both point of 2.5-min and exhaustion, no differences existed in SR Ca²⁺-sequestering capacity and carbonyl content between untrained and trained muscles. These findings confirm the previous findings that oxidative modifications may account, at least partly, for exercise-induced deterioration in SR Ca²⁺-sequestering function ; and raise the possibility that in the final phase of acute exercise, high-intensity training could delay the progression of protein oxidation of SR Ca²⁺-ATPase.

Effects of hypothermia on corticoidogenesis (CG) were investigated in primary cultured bovine adrenocortical cells. In order to evoke CG, adrenocorticotropic hormone (ACTH), dibutyryl cyclic AMP (db-cAMP), and high K⁺ were used. In the presence of the above mentioned secretagogues, cells were incubated at 37°C, 27°C, and 20°C for 1 hour. Although there was no difference between the ACTH-induced CGs at 37°C and 27°C, CG was significantly lower at 20°C. Both db-cAMP and high K⁺-induced CGs were significantly lower at 27°C, and were not observed at 20°C.
These results indicate that CG is not affected by moderate hypothermia, and is not eliminated even by deep hypothermia. It is also suggested that ACTH influences not only adenylate cyclase and Ca²⁺ channels, but also various processes of glucocorticoid production and could evoke CG at 20°C in bovine adrenocortical cells.

Myocardial oxidative stress during retrograde continuous blood cardioplegia (RCBC) was evaluated in 35 patients undergoing elective aortocoronary bypass surgery. The patients were divided into three groups: Group C (n=12) received cold (20°C) RCBC, Group T (n=11) received tepid (30°C) RCBC, and Group W (n=12) received warm (36°C) RCBC. Myocardial oxidative stress was assessed by measuring the release of oxidized glutathione (GSSG), malondialdehyde (MDA), and myeloperoxidase (MPO) in the coronary sinus plasma before aortic clamping, at 1, 5, and 10min after unclamping. Myocardial oxygen uptake and lactate release were assessed at the same times. Both the hemodynamic recovery and the creatine kinase MB (CKMB) activity were measured perioperatively until 24h after unclamping. In Group C, a significant coronary sinus release of GSSG was found in the early reperfusion period in comparison to Groups T and W. However, the peak CK-MB activity was significantly lower in Group T than in Group W. No significant difference in the release of MDA or MPO was noted in the three groups. The recovery of oxygen uptake after unclamping was rapid in Group T. The recovery in the left and right ventricular functions and the myocardial lactate release were similar in the three groups. In conclusion, tepid RCBC is considered to protect the myocardium from ischemia-reperfusion injury better than cold or warm blood cardioplegia under retrograde continuous perfusion.

We tested the hypothesis that a force reduction in soleus muscles from hyperthyroid rats would be associated with oxidative modification of myofibrillar proteins. Daily injection of thyroid hormone [3, 5, 3’-triiodo-_L-thyronine (T₃)] for 21 days depressed isometric forces in whole soleus muscle across a range of stimulus frequencies (1, 10, 20, 40, 75 and 100 Hz) (P<0.05). In fiber bundles, hyperthyroidism also led to pronounced reductions (P<0.05) in both K⁺- and 4-chloro-m-cresol-induced contracture forces. The degrees of the reductions were similar between these two contractures. These reductions in force production were accompanied by a remarkable increment (103% ; P<0.05) in carbonyl groups comprised in myofibrillar proteins. In additional experiments, we have also tested the efficacy of carvedilol, a non-selective β₁-β₂-blocker that possesses anti-oxidative properties. Treatment with carvedilol prevented T₃-induced oxidation of myofibrillar proteins. However, carvedilol did not improve the hyperthyroid-induced reductions in force production. These data suggest that oxidative modification of myofibrillar proteins may not account for the reductions in force production of hyperthyroid rat soleus muscle.