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Biomedical subjects

S Maie

Publications and source records attributed to S Maie.

8 recordsLinked to original sources
PubMed1994

[Case report: infective endocarditis caused by Streptococcus agalactiae].

A 42-year-old male was admitted to our hospital because of high grade fever on October 6, 1992. He had no history of cardiac and underlying disease. For the past 10 days, he had complained of high grade fever and noticed arthralgia on his left shoulder. Physical examination on admission revealed that there was a body temperature of 39.0 degrees C and tenderness in the left shoulder. There were no abnormal findings for the chest or abdomen. On the second hospital day, he developed a diastolic murmur which had not been present on admission. And blood culture was positive for Streptococcus agalactiae. Ultrasonic-cardiogram indicated the presence of vegetation. He was diagnosed as infective endocarditis and treated with PCG 20 million units/day, IPM/CS 2 g/day and ISP 400 mg/day. But he was not responding to the chemotherapy. Aortic valve replacement was done on 22nd, October. Valve surgery succeeded and he became well after that time. Endocarditis caused by S. agalactiae is extremely rare, and is an important condition which carries a high mortality. Only seven cases of S. agalactiae endocarditis have been reported in Japan. It is difficult to treat these cases with antibiotic therapy alone. Therefore, we suggest that early surgery should be considered in infective endocarditis caused by S. agalactiae.

Adult↗
PubMed1994

Reduction of beta-adrenergic receptors in atrial cell membranes of patients following mild to moderate heart failure.

The density of cardiac beta-adrenoceptors (Bmax) was measured in eighteen patients [2 with atrial septal defect (ostium secundum), 4 with aortic valve disease, 3 with mitral valve disease, 1 with aortic and mitral valve disease, 5 with a history of myocardial infarction, and 3 with angina pectoris] following mild to moderate cardiac failure. Measures were obtained by cardiac catheterization prior to cardiac surgery and also during the surgical procedures. On the basis of symptoms immediately preceding surgery, the severity of the condition in each patient was categorized as either Class I (n = 5) or Class II (n = 13) following the New York Heart Association (NYHA) functional classification system. The Bmax was measured using right atrial appendage tissue obtained during cardiac surgery. [125I]-iodocyanopindolol was used for the assay. The Bmax of atrial cell membranes in patients with NYHA class II was significantly lower than that of class I (34.1 +/- 2.5 vs 55.4 +/- 9.3 fmol/mg protein, M +/- SE, p < 0.05). Correlation coefficients between the Bmax and hemodynamic parameters measured just prior to cardiac surgery were examined, but only that between Bmax and the minimum value of the time derivative of left ventricular pressure (max negative dp/dt) was significant (r = -0.552, p < 0.05). Further study is needed to understand and clarify the relationship between Bmax and dp/dt min.

Adult↗
PubMed1994

Protective effects of verapamil and adenosine treatment on high energy phosphate metabolism in ischemic and reperfused myocardium.

Isolated rat hearts were subjected to retrograde perfusion to investigate the protective effects of adenosine and verapamil on the myocardium. In group 1, the perfusate was standard Krebs-Henseleit buffer solution. The perfusate was changed to Krebs-Henseleit buffer containing verapamil (100 nM) in group 2, adenosine (100 microM) in group 3 and both drugs in combination in group 4 for 30 min before ischemia and during 20 min of reperfusion. Group 2 displayed a recovery of creatine phosphate but not of ATP at the end of reperfusion. In group 4, the recovery of both ATP and creatine phosphate was significantly greater than in group 1. The coronary flow of group 4 was significantly higher than that of the other groups. Treatment with both verapamil and adenosine before and after global ischemia may protect the ischemic myocardium by improving high energy phosphate metabolism and coronary circulation.

Adenosine↗
PubMed1992

Enhanced myocardial adenylate cyclase activity in spontaneously hypertensive rats.

This study was designed to clarify the state of beta-adrenergic signal transduction and the disordered level of its transduction in hypertensive hearts, using myocardium from spontaneously hypertensive rats (SHR) as a generic model of essential hypertension. Beta-adrenergic receptor binding sites and dissociation constants in the extracted membranes of adult (70-100 days of age) SHR heart were not significantly different from those of Wistar-Kyoto (WKY) rats, the non-hypertensive control. The adenylate cyclase activities stimulated by isoproterenol with GTP, NaF and forskolin were significantly higher in SHR compared to those in WKY. To determine whether differences in signal transduction are natural or are a result of hypertension, we evaluated chronotropic responses in cultured cells of fetal hearts which had not been exposed to hypertension. Fetal cardiac muscle cells of SHR were more sensitive than WKY to isoproterenol stimulation over a wide concentration range. However, there were no statistically significant differences between these two strains with respect to the density of binding sites. These results suggest that in the transduction of adrenergic signals, alterations distal to the beta-receptors are present in the adult hearts of hypertensive rats, and, that the adrenergic signal transduction is already exaggerated in the pre-hypertensive fetal stage.

Adenylyl Cyclases↗
PubMed1991

Effects of human superoxide dismutase on ischemic and reperfused myocardium in isolated perfused rat heart.

The effect of human superoxide dismutase (h-SOD) on the ischemic heart was studied in the isolated perfused working rat heart. Myocardial mechanical function expressed as pressure-rate product decreased and completely stopped within 5 min after the onset of global ischemia, and never recovered after reperfusion following 20 min of ischemia. In the ischemic myocardium, the levels of ATP, ADP, and creatine phosphate decreased, and those of AMP and lactate increased. Reperfusion of the ischemic heart did not restore the level of ATP completely. When the heart was treated with h-SOD, the perfusion medium was switched from the buffer containing no h-SOD to that containing h-SOD at either 100, 300 or 1,000 units/ml 5 min before the onset of ischemia. The pressure-rate products of the heart treated with 100, 300, and 1,000 units/ml of h-SOD were restored by reperfusion to 22%, 59%, and 51% of the preischemic level, respectively. The levels of ATP and creatine phosphate in the reperfused heart with 300 and 1,000 units/ml of h-SOD were significantly higher than those without h-SOD. However, a dose-response relationship was not observed when h-SOD was used in concentrations greater than 300 units/ml. These results indicate that a certain amount of h-SOD has some beneficial effects on the ischemic myocardium.

Adenine Nucleotides↗
PubMed1989

Effect of flunarizine on ischemic myocardial metabolism in dogs.

The effect of flunarizine, a calcium entry-blocker, on the ischemic myocardial metabolism of the open-chest dog heart was examined and compared to that of diltiazem. During ischemia, initiated by ligating the left anterior descending coronary artery, the metabolism of the myocardium switched from aerobic to anaerobic; the levels of glycogen, fructose-1,6-diphosphate (FDP), adenosinetriphosphate and creatinephosphate decreased, and the levels of glucose-6-phosphate (G6P), fructose-6-phosphate (F6P), lactate, adenosine diphosphate and adenosine monophosphate increased during 3 min of ischemia. The calculated energy charge potential decreased, and the [( G6P] + [F6P]/[FDP] ratio and the lactate/pyruvate ratio were increased by ischemia. Flunarizine (0.3 or 1 mg/kg) or diltiazem (0.1 mg/kg) was injected i.v. 5 min before the start of ischemia. Pretreatment with either flunarizine or diltiazem reduced the decrease in the energy charge potential and the increase in the [( G6P] + [F6P]/[FDP] ratio during ischemia. Flunarizine (1 mg/kg) and diltiazem (0.1 mg/kg) reduced the accumulation of lactate due to ischemia, leading to a decrease in the lactate/pyruvate ratio. Flunarizine and diltiazem may lessen the influence of ischemia on the myocardial tissue.

Adenine Nucleotides↗