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Biomedical subjects

J Sakurai

Publications and source records attributed to J Sakurai.

At least 91 records · Page 5Linked to original sources
PubMed1989

Proline-dependent expression of aryl hydrocarbon hydroxylase in C57BL/6 mouse hepatocytes in primary culture.

Induction of aryl hydrocarbon hydroxylase (AHH) was studied in mouse hepatocytes in primary culture and compared with that in rat hepatocytes. Enzyme activity in hepatocytes from C57BL/6 mice was found to increase dose dependently after treatment with benz(a)anthracene. However, the induction was strictly dependent on culture medium. Although appreciable levels of AHH activity were inducible in Sprague-Dawley rat hepatocytes cultivated in either Dulbecco's minimal essential medium (DMEM) or Waymouth's medium, C57BL/6 mouse cells cultivated in DMEM responded to the inducer only very slightly, whereas those in Waymouth's or Ham's F-12 medium demonstrated a marked increase. Proline, but not glutamic acid or cysteine, all of which were lacking in DMEM but present in Waymouth's and Ham's F-12 medium, restored the potential for response to the cells in DMEM. While increased amounts of P450 mRNA in C57BL/6 cells cultivated in DMEM were transient and decreased after a peak observed at 24 h, levels of mRNA in Waymouth continued to demonstrate an increase at 48 h. Addition of proline to mouse hepatocytes in DMEM increased the generation of transcripts without, however, influencing the decrease observed from 24 h to 48 h. Timing of treatment with benz(a)anthracene and incubation in Waymouth greatly influenced the eventual AHH activity. Thus, while enzyme activities measured at 48 h were in the same range after treatment with benz(a)anthracene for either the whole period or only for the initial 24 h, and prominent induction was observed with cells in Waymouth for 24 to 48 h regardless of whether they were at first cultivated in DMEM or Waymouth, levels remained low if the cells were incubated in DMEM during the 24- to 48-h period. These observations suggest that induction of AHH in mouse hepatocytes is regulated by both transcriptional and posttranscriptional events and that proline-dependent events are required for expression of the enzyme activity.

Animals↗
PubMed1989

Dissociation of various biological activities of Clostridium perfringens alpha toxin by chemical modification.

The effect of N-acetylimidazole, tetranitromethane, maleic anhydride and N-ethylmaleimide on various biological activities of Clostridium perfringens alpha (alpha)-toxin was investigated. Treatment of the toxin with N-acetylimidazole, tetranitromethane or maleic anhydride resulted in significant reduction of lethal, hemolytic and platelet-aggregating activities and phospholipase C activity (EY activity), as measured by increased turbidity in egg yolk emulsions. However, EY activity was more resistant to these reagents than lethal, hemolytic or aggregating activities. Phospholipase C activity (PN activity) as measured by hydrolysis of p-nitrophenylphosphorylcholine was retained after treatment with N-acetylimidazole, tetranitromethane or maleic anhydride. The activities of the toxin were not inactivated by treatment with N-ethylmaleimide. These data suggest that alpha-toxin contains multiple sites for biological activities of the toxin.

Animals↗
PubMed1989

Contraction induced by Clostridium perfringens epsilon toxin in the isolated rat ileum.

Clostridium perfringens epsilon toxin caused contraction of the isolated ileum of the rat in a dose-dependent manner. The contraction caused by the toxin was inhibited by a low Na medium, tetrodotoxin (TTX), atropine, mecamylamine or tetraethylammonium (TEA). Furthermore, the contractile response induced by the toxin was abolished by incubation in Ca-free medium, and completely restored by and addition of Ca2+. In addition, verapamil inhibited contraction induced by the toxin in a dose-dependent manner. These data suggest that epsilon toxin induces contraction of the isolated ileum and that the toxin-elicited contraction is the result of an indirect action mediated through the nervous systems.

Animals↗
PubMed1989

Participation of the sympathetic nervous system in hypertension in rats with subtotal renal ablation.

To clarify the role of the sympathetic nervous system in the development of hypertension in chronic renal failure, plasma levels and urinary excretions of catecholamines were evaluated in male Sprague-Dawley rats. The renal mass of the rats was reduced by removing one kidney and two-thirds of the contralateral kidney (5/6 nephrectomy). Five-sixths nephrectomy was followed by significant increases in serum creatinine (to 0.55 +/- 0.03 mg/dl) and urea nitrogen (to 42.9 +/- 3.8 mg/dl). There was a concomitant increase in mean blood pressure, measured directly by an implanted aortic catheter, in comparison with control rats (155.3 +/- 8.3 versus 123.6 +/- 3.3 mmHg, P less than 0.01). Both plasma levels and urinary excretion of norepinephrine and epinephrine were elevated in the 5/6-nephrectomized rats compared with controls. Mean blood pressure correlated negatively with 24-h creatinine clearance (r = -0.66, P less than 0.05), and positively with plasma norepinephrine (r = 0.83, P less than 0.01) and urinary excretion of norepinephrine (r = 0.63, P less than 0.05). These results suggest that not only the decrease in renal function, but also hyperactivity of the sympathetic nervous system, may be involved in the pathogenesis of hypertension in rats with subtotal renal ablation.

Animals↗
PubMed1989

Contraction of the rat isolated aorta caused by Clostridium perfringens alpha toxin (phospholipase C): evidence for the involvement of arachidonic acid metabolism.

1. Alpha toxin produced by Clostridium perfringens contracted the rat isolated aorta and stimulated release of arachidonic acid in the tissue. 2. Quinacrine did not inhibit contraction caused by the toxin. 3. Indomethacin blocked contraction caused by the toxin in a dose-dependent manner and markedly increased levels of arachidonic acid released by the toxin. 4. The toxin-induced contraction was blocked by the thromboxane synthetase inhibitor OKY-046 and the thromboxane A2 (TXA2) antagonist ONO-3708. 5. The toxin stimulated production of TXB2 and this was blocked by pretreatment with either indomethacin or OKY-046. 6. Toxin-induced contraction was diminished by pretreating aorta with collagenase or by rubbing the intimal surface to remove the endothelium. 7. These data suggest that the contractile response to the toxin is associated with stimulation of TXA2 production from arachidonic acid released by the toxin in the endothelial cells of the aorta.

Animals↗
PubMed1989

Captopril, an angiotensin I-converting enzyme inhibitor, decreases proteinuria in hypertensive patients with renal diseases.

A crossover study was planned in order to compare the effects of captopril and slow channel calcium entry blocker (Ca antagonist) on urinary protein excretion in 7 hypertensive patients with renal diseases, including 4 with IgA nephropathy, 2 with lupus nephritis and 1 with benign nephrosclerosis. Captopril decreased urinary protein excretion by 52% without any change in creatinine clearance, while Ca antagonist was having a slight effect on proteinuria even though the drug showed an equivalent antihypertensive effect as captopril. These results suggest that the attenuation of proteinuria induced by captopril may be related to an inhibition of angiotensin II formation and/or a direct action of this drug on protein permeability of glomerular basement membrane.

Adult↗
PubMed1989

Effect of sodium restriction on platelet function in patients with essential hypertension.

The effects of sodium intake on blood pressure and platelet function were evaluated in 19 subjects with essential hypertension (10 men and 9 women; mean age 49.7 years). The study was conducted under 3 conditions: (1) normal sodium diet (12 g/day of salt was used in cooking), (2) after 5 days of mild sodium restriction diet (6 g/day of salt was used in cooking) and (3) after moderate sodium restriction (no salt was used in cooking). Blood pressure was significantly reduced following sodium restriction without any change in heart rate. The ratio of the plasma level of beta-thromboglobulin to platelet factor IV, regarded as the most reliable index for platelet activation in vivo, increased significantly after mild sodium restriction; this change was maintained after moderate sodium restriction. Plasma thromboxane B2, a stable metabolite of thromboxane A2, increased significantly after sodium restriction; the level of 6-ketoprostaglandin F1 alpha, a stable metabolite of prostacyclin, was unaffected. These results indicate that dietary sodium restriction induces both a reduction of blood pressure and an activation of platelet function in vivo. Thus, one must consider both antihypertensive effects and effects on platelet function as factors in adjusting the dietary sodium intake in the course of antihypertensive therapy.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

Effect of sodium intake on the hypotensive effect of calcium antagonists.

To clarify the influence of Na balance on the hypotensive effect of calcium antagonists, the changes of blood pressure and humoral factors after a single oral administration of 40 mg nicardipine were evaluated in 15 subjects with essential hypertension under high, normal, and low Na regimens (mean 24 hour urinary Na excretion: 320 +/- 24, 147 +/- 7, 27 +/- 6 mEq, respectively). Nicardipine induced a significant reduction of mean blood pressure and increase in heart rate. The change of mean blood pressure after nicardipine was negatively related to the pretreatment mean blood pressure under the three levels of Na intake (p less than 0.01). The slopes of the correlation lines for high, normal, and low Na regimens were -0.61, -0.69, and -0.52, respectively, without statistical significance. Nicardipine brought about significant increases in plasma renin activity and plasma norepinephrine, but no changes in plasma levels of epinephrine, 6-keto-prostaglandin F1 alpha, thromboxane B2 or serum aldosterone concentration. These results suggest that the magnitude of the untreated blood pressure and thereby the peripheral resistance are major determinants of the blood pressure fall caused by calcium antagonists, and that the failure to increase aldosterone and epinephrine in the face of peripheral vasodilation may be responsible in part for the hypotensive effect of this drug.

6-Ketoprostaglandin F1 alpha↗
PubMed1989

[A case report of thrombosed St. Jude Medical valve in aortic position].

We report a successful elective re-aortic valve replacement following thrombolysis therapy with Urokinase. Patient was a 56-year-old male with acute heart failure caused by thrombosed St. Jude Medical valve in aortic position. The thrombosed valve occurred 6 years after the implantation due to poor control of anticoagulation therapy. Surgical findings demonstrated the origin of thrombus at the hinge area. Prompt diagnosis and adequate therapy is essential for the thrombosed valve especially in case of mechanical valve. Thrombolysis therapy should be considered if possible, although emergency operation is always indicated.

Aortic Valve↗
PubMed1989

[Atypical coarctation of the thoracic aorta with fibromuscular dysplasia--report of a successful surgical repair and review of the literature].

We report a case of 14-year-old woman of fibromuscular dysplasia (FMD) with involvement of the thoracic aorta. Our case is characterized by a segmental stenosis of the thoracic aorta with multiple systemic arterial branch lesions. Atypical coarctation of the thoracic aorta was replaced with Dacron woven graft and the specimen of the lesion demonstrated medial fibroplasia. There have been reported only 9 cases of FMD of the aorta so far and all were female except one case. This report is the first case report of FMD of the thoracic aorta.

Adolescent↗
PubMed1989

[A case report of concomitant surgery of mitral regurgitation and lung cancer].

We report a case of 70-year-old woman who was simultaneously operated on mitral valve replacement for severe mitral regurgitation and the right middle lobectomy for adenocarcinoma through a median sternotomy. Concomitant cardiac and pulmonary operation can be safely performed through a median sternotomy excluding left lower lobectomy.

Adenocarcinoma↗
PubMed1989

[A successful surgical treatment of left coronary artery-pulmonary artery fistula with giant saccular aneurysm].

A surgical case of left coronary artery-pulmonary artery fistula with giant saccular aneurysm was reported. The aneurysm was successfully resected under total extra-corporeal circulation. The patient was 67-year-old female who was admitted for evaluation of chest pain and heart murmur. On coronary angiography, the diagnosis was made as a coronary artery fistula originating from the left anterior descending artery and draining into the pulmonary artery. The operation was indicated by the fact that the combination with giant saccular aneurysm and positive findings of ischemic changes on exercise electrocardiogram. Intraoperative flowmetry on the fistula revealed that estimated average flow was 200 ml/min and the coronary steal phenomenon was strongly suggested. We concluded that surgical treatment for coronary fistula with giant aneurysm can be done with minimal risk.

Aged↗
PubMed1988

Effects of guanfacine monotherapy on blood pressure, heart rate, plasma renin activity, aldosterone, and catecholamines in hypertensive patients with chronic glomerulonephritis.

Effects of guanfacine, a centrally acting antihypertensive, on blood pressure, heart rate, plasma renin activity, serum aldosterone, plasma norepinephrine, and renal function were evaluated in 16 patients with hypertension with biopsy-proved chronic glomerulonephritis. Guanfacine monotherapy with a daily dose of 1 to 2.5 mg at bedtime for 6 months brought about a significant reduction in blood pressure (171 +/- 2/110 +/- 2 to 144 +/- 2/89 +/- 1 mm Hg; P less than 0.01), with concurrent decreases in heart rate (78 +/- 2 to 70 +/- 2 bpm; P less than 0.01), plasma renin activity (1.96 +/- 0.12 to 1.21 +/- 0.19 ng/ml/hr; P less than 0.05), aldosterone (14.6 +/- 1.5 to 9.7 +/- 0.9 ng/dl; P less than 0.05), plasma norepinephrine (220.5 +/- 24.2 to 132.8 +/- 27.7 pg/ml; P less than 0.05). There was no change in serum creatinine, beta 2-microglobulin, or endogenous creatinine clearance during guanfacine monotherapy. Our data suggest that guanfacine exerts its antihypertensive effect via the inhibition of sympathetic outflow and in part the suppression of the reninangiotensin-aldosterone system and that guanfacine is suitable for the effective treatment of hypertension associated with chronic glomerulonephritis.

Adult↗
PubMed1988

Surgical treatment of coronary aneurysm developed after PTCA.

Two patients who developed coronary aneurysm at the site of Percutaneous Transluminal Coronary Angioplasty (PTCA) in proximal LAD accompanied by severe re-stenosis just proximal to the aneurysm are described. Both patients underwent Coronary Arterial Bypass Grafting (CABG) to distal LAD to stop anginal attacks refractory to any anti-anginal drugs and to prevent a rupture of a coronary aneurysm. After the operation the anginal attacks disappeared and no trace of coronary aneurysm was visible in the coronary angiogram.

Angioplasty, Balloon↗
PubMed1988

Plasma beta-thromboglobulin to platelet factor 4 ratios as indices of vascular complications in essential hypertension.

The ratio of the plasma level of beta-thromboglobulin (beta-TG) to platelet factor 4 (PF-4) which is regarded as a most reliable indicator of platelet activation in vivo, was followed in 52 subjects at various stages of essential hypertension according to the WHO classification. These comprised 30 cases at stage I, 19 cases at stage II and three cases at stage III, and 20 age-matched normotensive control subjects. The observed beta-TG:PF-4 ratio in the hypertensive patients was 4.59 +/- 0.20, which was significantly higher than the value of 3.13 +/- 0.19 recorded in the normotensive control subjects. According to the WHO classification, beta-TG:PF-4 ratios in hypertensive patients at stages I, II and III were 3.93 +/- 0.19, 5.31 +/- 0.35 and 6.56 +/- 0.12, respectively. The beta-TG:PF-4 ratio revealed a tendency of platelet activation to increase with advanced progress of hypertensive vascular lesions. These results suggest that the abnormal platelet function observed in patients with essential hypertension plays an important role in the development of hypertensive vascular complications.

Blood Platelets↗