Ultrastructural changes in myocardial cells of rats fed a low protein diet.

Ultrastructural changes in the ventricular myocardial cells in rats fed a low protein diet were examined by electron microscopy. The most striking changes were observed in the I-band region of the sarcomeres, which occurred very occasionally in myofibrils. In the sarcomere affected the I-band region was often fractured and/or disintegrated on one side, leaving an extended space, while the opposing I-band region disappeared along with dislocation of the intact A-band toward the adjacent Z-line. This dislocation was presumably attributed to the elasticity of titins connecting between the end of thick filaments and the Z-line. Fractured I-band regions were often accompanied by the dilated sarcoplasmic reticulum in the close vicinity of them. In some myofibrils the streaming and/or disruption of the Z-line were occasionally observed where disarrangement of thick and thin myofilaments were usually present. The study suggests that the fracture of the I-band region, consisting of actin and titin filaments, and the streaming of the Z-line of myofibrils are due to a proteolytic action of calpain and/or cathepsin L, which are activated by leaked Ca2+ ion and/or by modification of internal circumstances of the cytoplasm induced by a low protein diet, thus resulting in a low cardiac output.

Late results of acute medial necrosis in rabbit aorta.

To clarify whether acute medial necrosis of the aorta induces aneurysms and intimal thickening at a later stage, we first attempted to induce acute aortic medial necrosis in 47 normal rabbits by the administration of Russell's viper venom intraperitoneally and of angiotensin II intravenously as used in a previous study and then followed the rabbits for 1 and 2 months respectively. As a control, 18 adult normal rabbits were used. Six control and 20 treated rabbits were sacrificed after aortagraphy at the end of one month, while the remaining 12 control and 27 treated rabbits were sacrificed at the end of 2 months. We evaluated the aortic lesions by gross observations and both light and electron microscopic examinations. In addition, at the end of one month, aortagraphy was performed to measure the luminal diameter of the aorta of the 6 control and 20 treated rabbits. We macroscopically found the saccular lesions to be surrounded by small crater like lesions mainly at the thoracic aortas in 18 out of 47 treated rabbits. These lesions consisted of the necrosis and calcification of the aortic media and the destruction of the elastic fiber along with intimal thickening. However, no aneurysmal dilatation was found in the aortagraphy findings. We thus conclude that acute medial necrosis produced saccular and crater like lesions but these lesions were not confirmed by aortagraphy.

How amino acids control the binding of Cu(II) ions to DNA. Part III. A novel interaction of a histidine complex with DNA.

L-Histidine Cu(II) complex bound to DNA showed broad EPR signals characteristic of the aggregated Cu(II) species, which could be observed even when the molar ratio of L-histidine to Cu(II) ion was smaller than unity. The signal for the DNA fibers changed with the orientation of the fibers in the static magnetic field. Based on these results, the signal was assigned to a mono-histidine Cu(II) complex stereospecifically aggregated in a groove or along a phosphodiester chain of the double helical DNA. In contrast to the L-histidine complex, the D-histidine complex bound to DNA did not show such broad signals and the observed spectra for the complex on B-form DNA fibers at -150 degrees C were simulated assuming that the g1 axis of the mono-D-histidine complex tilts by about 55 degrees from the DNA-fiber axis. Addition of some deoxy-nucleotides, but not deoxy-nucleosides, to a solution of a mono-histidine complex resulted in the formation of a dinuclear ternary complex with different structures for L- or D-histidine, suggesting the possibility that the stereospecific aggregation of the L-histidine complex on a double helical DNA was mediated by the phosphodiester backbones.

[Surgical management of infective endocarditis in childhood].

From 1971 to 1993, four patients, 7 to 13 years of age, underwent intracardiac operation for infective endocarditis. Two patients underwent mitral valve replacements, one was tricuspid replacement and one received tricuspid valvulectomy. There was no operative death but one late death occurred (correction of occurred) due to cerebral bleeding. Surgical treatment of infective endocarditis in childhood could be performed safely by adequate selection of operative methods.

[A successful surgical treatment of WPW syndrome associated with tricuspid atresia].

The occurrence of both tricuspid atresia and WPW syndrome is quite rare. To our knowledge, only two operated cases have been reported. In this report, a 8-year-old boy with this combination was reported. Tachycardia via the right side accessory pathway was for the first time pointed out after Kreutzer's operation. Epicardial mapping showed the earliest excitation at the right free wall. When fatty tissue around this area was removed by CUSA, a large cardiac vein appeared. By holding this vein with a forceps, the delta wave disappeared temporarily. ACP seemed to be present near this vein. Permanent disappearance of the delta wave was obtained after ligation and division. Four months after surgery, he is free from tachycardia attacks.

[Surgical management of vascular ring in 5 cases].

Five cases of vascular ring are presented. Three cases have double aortic arch and two cases have right aortic arch with aberrant left subclavian artery. Other congenital heart diseases are complicated in four cases. MRI was useful for the evaluation of tracheal and esophageal compression.

[Aortic root replacement after operation for the ascending aorta and/or aortic valve].

We reviewed ten cases who underwent aortic root replacement after operation for the ascending aorta and/or aortic valve. As initial operation, aortic valve replacement (AVR) was performed in five patients, replacement of the ascending aorta in two, original Bentall operation in two, and entry closure and suspension of the aortic valve in one. At reoperation, three patients were diagnosed as aneurysm of the ascending aorta, two were annulo-aortic ectasia, and one was acute aortic dissection, chronic dissecting aneusym, pseudoaneurysm of the ascending aorta, prosthetic valve endocarditis, and massive aortic regurgitation. Aortic root replacement was performed using mechanical valved composite graft in all cases. One patient who underwent repeat aortic root replacement for prosthetic valve endocarditis was died of septemia and ventricular fibrillation. Five patients had nine complications (two low output syndrome, respiratory failure and cerebral infarction, one gastrointestinal bleeding, septemia and ventricular fibrillation). In conclusion, aortic root replacement after operation for the ascending aorta and/or aortic valve was performed with acceptable morbidity and mortality.

[A case report: successful treatment of acute type B aortic dissection with renal and leg ischemia].

A 56-year-old patient of acute type B aortic dissection with renal and leg ischemia successfully underwent emergency replacement of the descending thoracic aorta. Prior to this operation, we reperfused the ischemic legs in a controlled manner using a cardiopulmonary bypass circuit. This controlled limb reperfusion method could reduce reperfusion injury. Postoperatively, the patient also suffered from renovascular hypertension due to stenosis of the right renal artery. Renal stent angioplasty, performed 10 days after the operation, stabilized his blood pressure. Controlled limb reperfusion and renal stent angioplasty may be useful for managing branch complications associated with aortic dissection.

[Recent surgical treatment for patients with true aortic arch aneurysm].

From december 1996 to april 1999, 25 patients with true aortic arch aneurysm underwent aortic arch aneurysm repair using selective cerebral perfusion. There were 17 males and 8 females ranging in age from 62 to 79 years (mean 71 years). Orikaesi method was used in the procedure of distal anastomosis for complete aortic arch replacement with a prosthetic graft. This technique allowed us a simple approach to the lesion and the easy additional stitch. The average duration of extracorporeal circulation, aortic crossclamping, selective cerebral perfusion were 269 minutes, 140 minutes, and 122 minutes, respectively, under 19.3 degrees C of lowest esophageal temperature. There were no cases complicated with postoperative low output syndrome and cerebrovascular accident, and no hospital mortality. Replacement of the aortic arch using selective cerebral perfusion is a safe procedure with acceptable hospital mortality.

A scanning electron microscope study on the effects of different bile salts on the epithelial lining of jejunal mucosa.

Deconjugation of bile salts may occur in the jejunum under conditions of bacterial proliferation in the upper small intestine. We studied the morphological changes of jejunal mucosa induced by different conjugated (taurocholate, taurodeoxycholate, taurochenodeoxycholate, tauroursodeoxycholate) and unconjugated (cholate, deoxycholate, chenodeoxycholate, ursodeoxycholate) bile salts as compared by scanning electron microscopy. The epithelial lining of the jejunum was not affected in structural appearance below 40 mM concentration of the conjugated bile salts examined. On the other hand, the unconjugated bile salts examined induced morphological changes in varying degree and severity from crack formation at the tip to complete denudation of the jejunal villi, depending on the kind and dose of bile salts given. Among the unconjugated bile salts examined, the most robust in action was deoxycholate, which induced crack formation at 1.0 mM concentration, and the weakest was cholate. The study suggests that deconjugated bile salts produced by bacterial overgrowth in the upper small intestine can induce breakdown of the junctional integrity of the epithelial lining in varying degree and severity, ultimately leading to exfoliation of the epithelium.

The ultrastructure of skeletal and smooth muscle in experimental protein malnutrition in rats fed a low protein diet.

Light microscopy of the pectoralis muscle of rats on a low protein diet did not show such morphological alterations as atrophy, degeneration, or sarcoplasmic edema, but electron microscopy occasionally demonstrated ultrastructural changes only in the sarcomeres of myofibrils. In the affected sarcomeres, the Z-line was disrupted and often showed a jagged structure. The Z-substance with electron opacity was frequently present flowing along the long axis of myofibrils, here referred to as the streaming of Z-lines. In addition, regular striations formed by the reciprocal arrangement of thick and thin filaments disappeared from the affected sarcomeres, though these filaments were still discernible. Two or more consecutive sarcomeres in a single myofibril were occasionally involved in these changes. A further two or more neighboring sarcomeres at the same level of myofibrils were affected transversely by these structural alterations. On the other hand, the ultrastructure of the intestinal smooth muscle was not affected by protein deficiency. The study suggests that the ultrastructural damage induced by a low protein diet is attributed to the activation of endogenous protease by the excess leaking of Ca2+ into the cytosol as a result of lipid peroxidation of cell membrane by raised free radicals, owing to the depletion of glutathione production by protein deficiency. It also suggests that the smooth muscle cells differ in their susceptibility to protein deficiency from the skeletal muscle cells.

Ultrastructural changes and glutathione depletion in the skeletal muscle induced by protein malnutrition.

Ultrastructural changes and glutathione level were investigated in the pectoralis muscle of rats fed a low-protein diet. Electron microscopy demonstrated the ultrastructural changes of occasional myofibrils affected with protein deficiency that were characterized with the streaming and/or disruption of the Z-line and disintegration of sarcomeric striation. In the affected sarcomeres, sarcomere length was often elongated and fragmented thick filaments were present together with dense amorphous materials flowing from the damaged Z-line. Glutathione level of muscle in the low-protein diet group (5% casein) was reduced to about one-third of that in the control diet group (20% casein). The study suggests that depletion of glutathione by protein malnutrition is responsible for inducing myofibrillar damage through the excess leaking of Ca2+ into the cytosol.