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.

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.

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.

Several substitutes have been utilized for pericardial closure after open heart surgery. A 55-year-old man was admitted to our hospital with a diagnosis of constrictive pericarditis 13 years after open mitral commissurotomy. At reoperation, the thickened pericardium was peeled off and the epicardium was covered with 0.1mm expanded polytetrafluoroethylene surgical membrane (Gore-tex^®, sheet thickness 0.1mm). At the 7th postoperative day, he complained of fatigue and dyspnea. Physical examination revealed jugular venous distension, hepatomegaly, ascites and peripheral edema. Cardiac catheterization suggested the suspicion of pericardial or epicardial constriction. On the 3rd-operation, the Gore-tex^® sheet was removed and multiple longitudinal and transverse incisions were made in the thickened epicardium, that is the waffle procedure, while protecting the myocardium and the coronary arteries. Perioperative hemodynamics improved remarkably. His cardiac index increased from 3.0 to 4.5l/min/m². The postoperative course was uneventful.

The patient was a 61-year-old male, who underwent thoracoabdominal aortic aneurysm repair with Gelseal Triaxial prosthetic graft 2 years previously. False-aneurysm due to prosthetic graft dilatation was diagnosed. The direct closure of the ostium of the disruption of the anastomosis was successfully performed by an emergency operation. The postoperative course was uneventful. This case suggests that prosthetic graft dilatation may cause false-aneurysm at the site of end-to-side anastomosis.

A 65-year-old woman was admitted with a diagnosis of unstable angina after PTCA. She was diagnosed with acromegaly 8 years ago. She underwent an emergency coronary artery bypass grafting (LITA-LAD, SVG-HL-Cx). Serum growth hormone (GH) levels were 65.5ng/ml (normal limit<5ng/ml) before the operation. During a cardiopulmonary bypass GH levels elevated to 92.7ng/ml, but decreased to 15.9ng/ml after the operation. After 3 postoperative days GH levels increased gradually again and blood sugar levels became unstable. Finally it was necessary to increase the dose of bromocriptine. To our knowledge, there are only a few patients who have undergone coronary artery bypass grafting associated with acromegaly. This case suggests it is important to control GH levels at the operation and during the postoperative period.

A 40-year-old woman visited our emergency room (ER) with fever and shaking chills. Blood cultures for suspicion of urinary tract infection revealed bacteremia two days later. Since Streptococcus mitis was detected, infective endocarditis was strongly suspected. In addition to her history of dental calculus removal, careful cardiac auscultation revealed a continuous murmur, leading to the existence of patent ductus arteriosus (PDA). PDA was confirmed by echocardiography and 3D-CT angiography. The patient was successfully treated by antibiotics and then received transcatheter PDA closure. Careful auscultation after detection of bacteremia led to a diagnosis of PDA.

We evaluated 13 patients (4 men & 9 women, mean age: 61 years-old) who required steroid treatment for more than 1 month before open heart surgery. The subjects included 3 patients with collagen diseases, 3 with dermatopathy, 2 with bronchial asthma, one each with Takayasu's disease, autoimmune hemolytic anemia, paroxysmal nocturnal hemoglobinuria, brain tumor and post-renal transplantation. Surgical procedures were performed with an AC bypass in 9 cases, one each with AVR, MVR, reMVR and ASD patch closure. The steroid treatment before open heart surgery had been continued for a mean of 4 years and 11 months at a mean dose of 9.4mg/day equivalent of prednisolone. We evaluated the adrenocortical function on the rapid ACTH test and found hypoadrenalism in 5 of 8 cases (63%). In these cases we gave either 100mg of hydrocortisone or 1, 000mg of methylprednisolone before open heart surgery. The total perioperative dosage of steroid was a mean of 2, 488mg equivalent of prednisolone, including 4mg/kg of betamethasone during the extra corporeal circulation. Postoperatively we lost one case due to ventricular rupture after MVR. Other major complications were seen in one case each, cardiac tamponade, temporary clamp, wound infection and lumbar vertebral fracture. For steroid treated patients, it is important to select the patient who really need steroid by the rapid ACTH test, and to use the minimum dosage of steroids in open heart surgery.