[A case of mitral stenosis associated with coronary embolism and review of the literature].
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Biomedical subjects
Publications and source records attributed to K Ohishi.
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Lidocaine, W49091, procaine and benzocaine inhibited mast cell secretion induced by concanavalin A and A23187. They inhibited Ca influx stimulated by concanavalin A, suggesting that they inactivate Ca channel of mast cells. Lidocaine and procaine inhibited Ca influx stimulated by A23187, but W49091 and benzocaine did not.
Cationic drugs that interact with calmodulin such as chlorpromazine, trifluoperazine, W-7 and lidocaine caused dose-dependent release of mediator from rat mast cells. A significant correlation was observed between the effects of test drugs with different structure in causing mediator release and calmodulin inhibition.
We report the complete 8714-nucleotide sequence of the integrated bovine leukemia virus genome and deduce the following genomic organization: 5' LTR-gag-pol-env-pXBL-3' LTR, where LTR represents a long terminal repeat and pXBL represents a region containing unidentified open reading frames. This genomic structure is similar to that of human T-cell leukemia virus. The LTR contains a putative splice donor site in the R region. The gag gene encodes a precursor protein with the form NH2-p15-p24-p12-COOH. The NH2- and COOH-terminal regions of the pol product show stronger homologies with those of avian, rather than murine, type C retrovirus, and its structure is identical to that of avian virus. The env gene encodes a surface glycoprotein (gp51) and a transmembrane protein (gp30). In contrast to the pol product, the gp30 shows stronger sequence homology with a murine, rather than avian homologue, indicating the chimeric nature of the bovine leukemia virus genome. Comparisons of the best conserved pol sequences and overall genomic organizations between several major oncoviruses allow us to propose that bovine leukemia and human T-cell leukemia viruses constitute a group, designated as type "E," of Oncovirinae.
Forty kinds of bufotoxins and related compounds were tested for inhibition of Na+, K+ -adenosine triphosphatase from guinea pig heart, and the structure-activity relationship has been discussed. The inhibitory activities of bufotoxins were dependent upon the dicarboxylic acid and amino acid components. The compounds having both the arginine and suberic acid moieties showed the higher inhibitory activities. The sulfates and glucuronides of cardiac steroids exhibited much less potency than the parent genins. The mode of inhibition was determined by means of the Dixon and Lineweaver-Burk plots.
A new method for the assay of Na+, K+-adenosine triphosphatase (Na+, K+-ATPase) inhibition has been devised involving the determination of enzymatically produced adenosine diphosphate (ADP) and unchanged adenosine triphosphate (ATP) by high-performance liquid chromatography (HPLC). The substrate, ATP, was incubated with the enzyme preparation in the presence of an inhibitor. The incubation mixture was filtered through a membrane filter, and ADP and ATP in the filtrate were separated by (HPLC). The inhibitory effect of a cardiac steroid on the enzymic reaction was estimated by measuring the peak area ratio of ADP to ADP plus ATP on the chromatogram. The proposed assay method has proved to be satisfactory with respects to simplicity, sensitivity, and reproducibility.
We studied on operative indication, operative problem, and operative result in patients with valvular lesion with coronary disease. In 650 cases, 51 cases combined with coronary stenosis and ACBG (9 cases) or OTCA (6 cases) were performed in 15 cases of them. For operative indication, ACBG was applied in case with proximal stenosis of more than 70% and OTCA was applied in case with mild localized stenosis. Cardioplegia during operation was important and heart temperature should be kept less than 15 degrees C. In those cases with combined operation, there were no early deaths but one late death (3 years after operation). After operation, chest pain disappeared and clinical symptom and ability for exercise were improved. According to NYHA classification, the improvement before and after operation were class I, none and 11 cases; class II, one case and three cases; class III, 12 cases and none and class IV, two cases and none.
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We have compared the sequence of the entire genomes of bovine leukemia virus (BLV) and human T-cell leukemia virus type I (HTLV-I). Both the gag and pol genes show overall strong homologies indicating the close evolutionary relationship of the two retroviruses. However, a surface glycoprotein portion of the env gene shows no appreciable homology, which probably reflects a difference in their host ranges. The 3' end portion of the BLV genome (designated as pXBL) contains an unidentified long open reading frame that has a typical protein-coding property. The potential product of this open reading frame may be a glycoprotein of approximately 40 000 daltons. We note that its amino acid sequence shows low but appreciable homology, especially in its N-terminal quarter, to that of the HTLV-I counterpart (pX product), and we thus suggest that BLV pXBL and HTLV-I pX have diverged from a common ancestral gene. It is tentatively concluded that both the putative pXBL and pX products are respectively produced from a spliced mRNA.
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The study concerned the effects of lidocaine and mepivacaine on rat mast cell histamine release. At low concentrations these drugs inhibited the histamine release induced by concanavalin A and compound 48/80 although, at high concentrations, they caused cell lysis. The mechanism of their inhibition of histamine release was studied by examining the pH dependence of the inhibitory action. In the absence of drugs, the release of histamine was not affected by the pH of the medium, but the inhibitory effects of the drugs increased with increase in pH. The percent inhibition of histamine release by these drugs at each pH was plotted against the calculated concentration of the nonionized form of the drug, according to the Henderson-Hasselbalch equation. The inhibitory action was correlated with the concentration of nonionized molecules, which readily penetrate the cell membrane. From the interaction of lidocaine with the phospholipid bilayer, it was concluded that this drug penetrates the lipid bilayer and that this effect increases with increasing pH of the medium. Thus, it seems that it is the nonionized form of local anesthetics that inhibits histamine release and that it is nonionized molecules that penetrate the mast cell membrane.
A case of double-outlet left ventricle [I,D,D] with a subaortic ventricular septal defect and pulmonary stenosis is reported. The diagnosis was made at operation and was reconfirmed postoperatively by two-dimensional echocardiography. Repair was achieved by patch closure of the ventricular septal defect and enlargement of the functional right ventricular outflow tract using a valved patch. The postoperative course was uneventful except for a transient complete heart block. To our knowledge, this represents the second instance of surgical treatment of double-outlet left ventricle [I,D,D] reported in the literature.
We have studied the long-term results of valve replacement operations in 591 patients, one year or more after surgery, and also analyzed rates of social return in 523 patients (response rate, 86.1 per cent) by questionnaire. Of the 591 patients, 81 patients suffered early death (mortality rate, 13.7 per cent) and 41 patients late death (mortality rate, 6.9 per cent). The causes of the latter were left atrial thrombus (18 cases), heart failure (10 cases), artificial valve failure (five cases), renal failure (two cases) and hepatic insufficiency, infection and accident (one case each). Second replacement was performed in 18 patients (3.0 per cent), 49 months on average from the first operation. The survival rate at the 12th postoperative year was 68.7 per cent. The overall rate of social return after valve replacement was 64.8 per cent, including 74.8 per cent for mitral valve replacement, 54.3 per cent for aortic and 51.5 for multivalvular. The rate of social return has been improved to 76.4 per cent in the last five years.
Ultrasound-guided renal cyst puncture was performed on 22 cysts which were then 95% ethanol instilled to prevent recurrence of cystic fluid. Cystic lesions disappeared on the ultrasonogram in the follow-up period of 3 to 28 months. On CT, cystic lesions became smaller size but did not disappear. Average CT numbers of the cyst were 8.75 +/- 3.83 before and 12.96 +/- 3.27 after ethanol instillation. The cystic wall became thicker. Caliceal distortion and/or pelvis compression by cystic lesions improved on IVP 2 to 3 days after ethanol instillation. The renal image on Tc-99m-DMSA scintigram showed morphological improvement and DMSA renal uptake rate increased slightly but significantly 2 to 4 weeks after ethanol instillation. There were no major complications with this procedure except for one case in which the tip of the catheter became stuck in the cyst and broke off when the catheter was removed. A slight local irritable pain was noticed in all cases. Half of the patients had hot flushes and/or somewhat drunken sense but these symptoms were only temporary. Antabuse phenomenon appeared in one case with concomitant use of a cephem antibiotics after ethanol instillation. This method of therapy is a safe non-surgical approach to treat renal cysts. 95% ethanol instillation in the cyst seems to prevent recurrence of cystic fluid.
Valvuloplasty is first applied as the surgical treatment for congenital mitral regurgitation (MR). Follow up study after the operation around the valvuloplasty was performed in the patients with congenital MR. In the patient under 12 years old, there were isolated MR in 3; MR associated with VSD in 14; MR and ASD in 3; MR with PDA in 10; and MR with ECD in 36. Operative methods were suturing of mitral cleft in 27; mitral annuloplasty in 17; mitral valve a, advancement in 7; cusp plasty in 4; no treatment for the MR in 14. Early death was noted in 6 cases (9.0% of mortality) and late death was noted in 3 cases (mortality rate of 9.0%). Conclusions were as follows: Surgical treatment was required in the patients with MR more severe than Sellers' Grade-II. Single suturing was recommended for the suturing of mitral cleft because shortening of the valve occurred in a few degree and the residual regurgitation reduced. Mitral valve advancement by elongation of the valvular apex was useful for the impediment of the regurgitation caused by incompetence of mitral coaptation. Mitral annuloplasty increased the effect for the impediment of the regurgitation. Ultrasonic cardiogram was useful for the follow up after the operation of the mitral valvuloplasty.
Surgical result of atrial septal defect (ASD) in patients of over 30 years of age was unexpectedly good, but complications associated with ASD or aging made the postoperative management difficult and complicated. Our surgical results suggest that the surgical correction should be considered in patients of over 30 years of age before the deterioration of symptoms or the complications become manifest.
Abnormal ventricular septal motion is usually observed after open heart surgery, but its mechanism is not fully understood. Our previous study suggested that a sudden reduction of left ventricular (LV) volume overload after corrective surgery would be one mechanism, showing that postoperative abnormal septal motion is more frequent in patients who have preoperative LV volume overload. The purpose of this study was to investigate further the direct effect of LV volume alone on the ventricular septal motion in 22 patients who underwent non-surgical closure of a patent ductus arteriosus (PDA) by the Porstmann's method. The non-surgical closure of a PDA reduced LV diastolic diameter (LVDd) from 55.7 +/- 7.3 mm to 48.1 +/- 5.2 mm (P less than 0.001), and LV systolic diameter (LVDs) from 36.3 +/- 7.0 mm to 34.1 +/- 7.0 mm (p less than 0.01). Septal motion decreased in amplitude from 8.5 +/- 2.4 mm to 3.8 +/- 3.4 mm (p less than 0.01) and eight (36%) patients developed abnormal septal motion, while LV posterior wall excursions remained unchanged. When compared these eight patients with 14 without abnormal septal motion, the magnitude of postoperative LVDd reduction (delta LVDd) and its ratio to preoperative volume (delta LVDd/pre op LVDd) were significantly greater in patients with abnormal septal motion. Thus sudden reduction in LV volume overload alone could induce abnormal septal motion without altering other factors such as adhesion of the pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)