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.

We report a case of reoperation for proximal and distal pseudoaneurysmal formations of the ascending aorta with aortic regurgitation (AR) after an ascending aorta replacement for acute type A aortic dissection. The patient was a 69-year-old woman who had undergone ascending aorta replacement for acute type A aortic dissection six years previously. Subsequent development of pseudoaneurysms of the ascending aorta and aortic regurgitation were revealed by computed tomography and echocardiography respectively. We chose debranch Thoracic Endovascular Aortic Repair (TEVAR) with a staged approach. First, aortic valve replacement, patch closure of proximal pseudoaneurysmal formation, coronary artery bypass, and ascending aorta-axillary artery bypass were performed. Two weeks later, debranching and TEVAR were performed. Cardiac reoperation for proximal and distal pseudoaneurysmal formations of the ascending aorta with aortic regurgitation after an ascending aorta replacement is known to be high risk. Nevertheless we performed the operation safely in two-stage surgery.

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.

Here, we report a patient who underwent surgery for acute aortic regurgitation (AR) due to rupture of an aortic valve commissure. The patient was a 51-year-old man who had undergone ascending aorta replacement for acute type A aortic dissection 6 years previously. He presented with a 2-day-history of headache and insomnia. Echocardiography showed only AR initially. However, 2 days later, a vegetation-like mass was noted at the aortic valve commissure on transesophageal echocardiography. We diagnosed AR associated with infective endocarditis, and decided to perform aortic valve replacement immediately. During surgery, we found that the cause of AR was rupture of the aortic valve commissure without infection. The cause of rupture in this case was suspected to be traumatic or myxomatous degeneration.

The patient was a 48-year-old woman who had been taking oral steroids for dermatomyositis since age 39. The patient experienced an episode of sudden chest tightness at age 48, and acute myocardial infarction was suspected. Coronary angiography revealed a right coronary artery occlusion ; emboli (thrombi) were collected from the same site. Left cardiac ventriculography revealed the presence of a mobile thrombotic mass in the ascending aorta. Although heparin therapy was initiated considering the possibility of thrombosis, no shrinkage of the mass was observed, and surgery was planned as per treatment guidelines. The mass was a rod-shaped thrombus measuring 20 mm×7 mm×7 mm attached to the aortic wall, approximately 2.5 cm distal from the entrance to the right coronary artery. Since the aortic wall at the site of the tumor attachment was normal, surgery involved only removal of the mass. A histopathological assessment revealed that the mass was a mixed thrombus containing both white and red thrombotic components. The patient was started on postoperative oral antiplatelet and anticoagulant drug therapy to prevent additional thrombosis, and no recurrence has been noted at 1 year postoperative.