Nihon Ika Daigaku zasshi最新文献

Stimulation of receptors for alpha 1-adrenergic agonist, endothelin (ET) and angiotensin II (AT) activates the cardiac sarcolemmal Na+/H+ exchanger (NHE), perhaps via protein kinase C(PKC)-mediated pathway(s). We tested for the ability of these extracellular stimuli to exacerbate reperfusion arrhythmias and for the possible role of NHE activation and PKC in such phenomena. Isolated rat hearts (n = 12/group) were subjected to dual coronary perfusion. After 15 min of aerobic perfusion, flow to the left coronary bed was reduced to 5% of basal values for 12 min, and the same bed was then reperfused for 5 min. An alpha 1-adrenergic agonist phenylephrine (PE) at 1 or 10 mumol/L, ET at 0.5 or 5nmol/L or AT at 1 or 10mumol/L was infused selectively into the left coronary bed during 12 min of regional low flow ischemia. The incidence of reperfusion-induced ventricular fibrillation (VF) was increased from 17% in control to 33% and 75%* with 1 and 10 mumol/L PE(*p < 0.05 vs control) from 8% in control to 8% and 12% with 0.5 and 5 nmol/L of ET. However, AT had no effect. The selective NHE inhibitor NOE642 at 1 mumol/L, infused concomitantly with 10 mumol/L PE, reversed the proarrhythmic effects of PE; VF incidence was reduced from 67% to 8%*. However, glibenclamide (a blocker for the ATP-sensitive K+ channel) at 1 mumol/L did not affect the proarrhythmic effects of PE. Infusion of a specific PKC inhibitor GF109203X(GF) at 30 or 300 nmol/L, starting from 5 min before ischemia and maintained throughout ischemia concomitantly with 10 mumol/L of PE, was partially effective in reducing VF incidence; which reduced from 75% in control to 42% with 300 nmol/L of GF. These results suggest that, in rat hearts subjected to regional low-flow ischemia and reperfusion, stimulation of alpha 1-adrenergic receptor can exacerbate reperfusion-induced VF, whose mechanism(s) may involve NHE activation. Moreover, PKC activation does not appear to be the sole signaling mechanism for this phenomenon.

Surgery for posterior skull base tumors may be associated with high morbidity and mortality because of the complex anatomy, irregular bony topography, and vital neurovascular structures in this region. We experienced three benign posterior skull base tumors. These were petroclival and foramen magnum meningiomas and a jugular formen neurinoma. Three dimensional computed tomography (3 D-CT) in addition to the conventional CT, magnetic resonance imaging (MRI), and cerebral angiography were performed preoperatively. Preoperative embolizations for the tumors were also done, and intraoperative neurophysiological monitorings were performed. The tumors could be subtotally removed with no damage to the brainstem, cranial nerves, and vessels. No newly developed postoperative neurological symptoms were observed. As to the remaining tumors, gamma knife (gamma-knife) therapy was planned. 3 D-CT was very useful in the preoperative evaluation of the surgical approach, and the intraoperative neurophysiological monitoring was considered to be necessary to prevent permanent damage. gamma-knife after direct approach was recommended for the benign posterior skull base tumors.

To investigate the role of cervical proprioceptive inputs in the process of vestibular compensation, we performed static posturography in patients with acute and compensated unilateral vestibular dysfunction, by applying vibratory stimulation to the dorsal neck muscles. Neck vibration induced disequilibrium in both groups of patients, but was more pronounced in the compensated patients. These results indicate that manipulation of the neck afferents causes discompensation in subjects whose vestibular dysfunction has already been compensated by multisensory inputs including neck afferents.

With the recent development of measurement in intact PTH, increases of hypoparathyroidism and adynamic bone disease have been reported in patients on chronic maintenance dialysis. To clarify the frequency of hypoparathyroidism in maintenance dialysis patients, the present study investigates the relationship between the occurrence of hypoparathyroidism and clinical background, several bone metabolic markers and the bone mineral density. We divided 298 maintenance dialysis patients (HD 270, CAPD 28) without parathyroidectomy into 4 groups based on intact PTH. Group A was absolutely hypo (intact PTH < 60 pg/ml), group B was relatively hypo (60 < or = intact PTH < 160), group C was normal (160 < or = intact PTH < 300), and group D was hyperparathyroidic (300 < or = intact PTH). Groups A and B together accounted for 71.8% of the patients. The mean age in groups A and B was higher than in group D (p < 0.05), and the dialysis duration was shorter (p < 0.01). The concentration of 1, 25 (OH)2D was significantly higher in groups A and B than in group D (p < 0.01), and remarkably higher in group A than in group C. The level of Ca, i-P did not differ among the groups. In our investigation of bone metabolic markers, group D was found to have significantly higher Al-p, intact-BGP, and P 1 PC compared with the other 3 groups (p < 0.01), and the concentration of intact BGP was lower in group A than in groups B and C (p < 0.01). The bone mineral density measured by DEXA did not differ among the groups. The results suggest that, due to multiple factors, the actual occurrence of hypoparathyroidism in maintenance dialysis patients is higher than the predicted occurrence.