Effects of angiotensin, bradykinin and oxytocin on electrical and mechanical activities in the taenia coli of the guinea pig.
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Biomedical subjects
Publications and source records attributed to H Ohashi.
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Tetrodotoxin, at concentrations up to 5 x 10(-6) gram per milliliter, has no effect on the spontaneous discharge in the smooth muscle of taenia coli. However, the spontaneous discharge is abolished by Mn(++) at a concentration of 0.5 millimole per liter. The contraction induced by immersing the muscle in isotonic KCl solution is also suppressed in the presence of Mn(++). Because Mn(++) is a specific suppressor of the spike induced by Ca(++) and tetrodotoxin is an inhibitor of the spike induced by Na(+), we suggest that Ca(++) is a charge carrier in the production of spike potential in the smooth muscle and that the entry of intervening Ca(++) through the membrane acts as a trigger for the contraction of smooth muscle.
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Cardiac diseases are well known among patients on maintenance hemodialysis (HD), and carnitine deficiency may be an important factor in cardiac morbidity. We studied the effects of low-dose L-carnitine treatment (500 mg/day) on chest symptoms (dyspnea on exertion, chest pain, palpitation), cardiac function, and left ventricular (LV) mass in 9 HD patients with reduced ejection fraction (EF). After 6 months of L-carnitine treatment, most patients had at least some improvement in chest symptoms, while LVEF was increased and LV mass was decreased. Carnitine fractions increased and reached plateaus at 2-3 times the baseline levels. These results suggest that prolonged low-dose L-carnitine treatment can improve the cardiac morbidity by restoring decreased carnitine tissue levels and impaired oxidation of FFA.
The effects of endogenous epinephrine (E), released by glucagon injection, and exogenously infused E on plasma norepinephrine (NE) and cardiovascular responses before and after beta-blockade were studied in patients with essential hypertension and in age-matched normotensive controls. The resting plasma NE and E levels were significantly higher in the borderline hypertensive subjects (NE: 251 +/- 21 pg/ml [SEM], p less than 0.005; E: 57 +/- 5, p less than 0.05, n = 18) than in controls (NE: 129 +/- 12; E: 39 +/- 5, n = 18). An intravenous injection of glucagon (1.0 mg) induced a transient rise of both plasma catecholamine levels and blood pressure in every subject studied. Plasma E levels rose transiently and returned to the basal levels by 20 minutes after the injection, whereas plasma NE levels showed a more prolonged rise over 20 minutes. beta-Blockade with propranolol did not affect the plasma E response to glucagon, but inhibited the prolonged rise of plasma NE levels. An intravenous infusion of exogenous E (1.25-1.50 micrograms/min) for 30 minutes caused an apparent rise of both plasma NE levels and blood pressure, which lasted more than 60 minutes after stopping the E infusion. Propranolol did not affect the time course of plasma E but again inhibited the prolonged rise of both plasma NE levels and blood pressure. No significant differences could be observed in the cardiovascular or plasma NE responses to glucagon or to E infusion between normal and hypertensive subjects. These findings lend support to the view that plasma E can act physiologically as a sustained stimulator of presynaptic beta-adrenergic receptors, which leads to an enhanced NE release from peripheral sympathetic nerve terminals and a rise of blood pressure in humans.
Tissue type (type 2) transglutaminase (TGase, EC 2.3.2.13) has been implicated in various cellular processes including cell death. In order to better understand the role of this enzyme in cell death, human melanocytic A375-S2 cells were treated with sphingosine, a cell-signaling mediator. During the rapid onset of cytotoxicity caused by this lipidic agent, tissue TGase was translocated from the cytoplasm to the cell nuclei. This observation was further remarked in relevance to its previously undescribed activity for DNA degradation. The DNA hydrolytic activity associated with tissue TGase was dependent on Mg2+ in contrast to the Ca2+ requirement for the classical cross-linking activity of TGase, and was inhibited by Zn2+. Based on the results shown here, we propose a novel aspect of tissue TGase in cell death.
A case of congenital mitral regurgitation associated with total anomalous pulmonary venous drainage, successfully treated surgically, is reported. To our knowledge, this combination has not been reported in the literature.
Renovascular hypertension due to iatrogenic thoracoabdominal aortic dissection in an 8-year-old girl with aortic valvular stenosis is presented. A splenorenal arterial anastomosis without splenectomy was successfully performed. This procedure is considered best suited for children with thoracoabdominal aortic dissection as the autogenous graft is expected to grow and provide long-term patency. The spleen left in situ was expected to be advantageous, from the immunological aspect, at the time of open heart surgery for aortic valvular stenosis, which was anticipated in the near future in this child.
Forty infants under 3 months of age underwent repair of coarctation of the aorta (CoA) during an 8-year period. Preoperatively, 55% of the patients received intensive circulatory and/or respiratory care, and surgical relief of CoA was effected within 24 hours of diagnosis. The last 38 patients were managed by simple repair of the CoA in patients with significant VSD (Group II), with the addition of pulmonary artery banding in patients with complex cardiac lesions with VSD, or patients with incremental risk factors in Group II. There were no intraoperative deaths, one (2.6%) postoperative, and four (11%) late deaths in the last 38 patients. Only one (2.9%) showed signs of recurrence in 34 patients followed for 10 to 104 (mean 46) months. Improvement in the survival rate in this study can be attributed to: (1) aggressive preoperative care, (2) early noninvasive diagnosis and operation, (3) refinement in the surgical technique, and (4) appropriate use of pulmonary artery banding.
Fifty-eight consecutive patients underwent percutaneous transvenous mitral commissurotomy (PTMC) for mitral stenosis from August 1987 to June 1990. Patients were divided by echocardiographic characteristics of the mitral valve according to the Sellors classification into three groups: group 1 (mobile cusps, 20 patients), group 2 (thickened cusps, 34 patients), group 3 (rigid cusps, 4 patients). Immediately after PTMC, the mitral valve area increased significantly from 1.41 +/- 0.37 to 2.07 +/- 0.38 cm2 (p < 0.01) in group 1 and from 1.09 +/- 0.21 to 1.64 +/- 0.25 cm2 (p < 0.01) in group 2. The mitral valve area did not increase significantly in group 3 (from 0.82 +/- 0.27 to 1.10 +/- 0.22 cm2). Mitral regurgitation developed or increased in severity in four patients (100%) in group 3 (p < 0.01 vs group 1, 20% and group 2, 21%). The symptomatic improvement was 0% for group 3 (p < 0.01 vs group 1, 90% and group 2, 91%). At follow-up period (mean 24.6 months), symptomatic improvement was maintained in 44 patients (76%) of the total patient population. The mitral valve area was maintained well in group 1 and group 2, but three patients in group 2 showed recurrence of symptoms due to valvular restenosis. PTMC is an effective nonsurgical treatment for patients with mobile or with thickened cusps. Surgical method is preferable for patients with rigid cusps.