Search PubMed⌕ Search

Biomedical subjects

S Morimoto

Publications and source records attributed to S Morimoto.

At least 649 records · Page 36Linked to original sources

Histopathologic and ultrastructural observations of acute and convalescent myocarditis: a serial endomyocardial biopsy study.

Serial endomyocardial biopsy findings were analyzed in ten cases with acute myocarditis of possible viral origin. The histopathologic findings were analyzed at the acute (0-10 days after the onset), subacute (11-21 days), and convalescent stages (22-167 days). The incidence and severity of various cardiac myocyte and interstitial changes were compared at each stage of the disease. The time-course changes of the histopathologic findings in acute myocarditis were as follows. At the acute stage, we observed: interstitial cell infiltration composed of fibroblasts, macrophages, and lymphocytes, fragmentation of the muscle bundles, myocytolytic changes, swelling and scarcity of the cytoplasm and swelling of nuclei, variation in size of the myocytes, disarrangement of the muscle bundles, interstitial edema, increased glycogen deposition in the myocytes, abnormal branching of the myocytes, and interstitial fibrosis. At the convalescent stage, most of the above findings could still be seen except for myocytolytic changes, swelling of myocytes, and interstitial edema. At the subacute and convalescent stages, an increase in abnormal branching and in double nuclei in the myocytes and nuclear degeneration became observable. A further control study comparing the changes at the convalescent stage of myocarditis and the myocardial changes in cases with chronic right ventricular overload in 58 cases revealed that in the former fragmentation of the muscle bundles, abnormal branching, size variation, glycogen deposition, and large mononuclear cell infiltrations were significantly more frequent. Ultrastructural observation of the myocytes revealed that they have a great potentiality for regeneration; myocytes showing severe myocytolytic changes may recover to regain an architecture of almost normal appearance.

Acute Disease↗

Hemodynamic studies and response to a combined therapy of nitroglycerin ointment and dopamine in patients with acute myocarditis.

Left ventricular performance was assessed in ten patients with acute myocarditis during the acute stage (within the first 3 days after the onset of cardiac symptoms) and during the convalescent phase (3-5 weeks later). In nine, the diagnosis was confirmed by endomyocardial biopsy during the acute stage, when left ventricular function was markedly reduced, i.e., cardiac index 1.53 +/- 0.33 l/min/m2 (mean +/- SD), left ventricular stroke work index 14.1 +/- 3.9 g/beat/m2, pulmonary capillary pressure 25.9 +/- 4.3 mm Hg, and systemic vascular resistance 27.9 +/- 9.4 R units. During convalescence, seven patients improved clinically with normal cardiac function and in three it remained impaired. Cardiovascular response to nitroglycerin ointment in three patients and a combination of dopamine and nitroglycerin ointment in five were compared. Nitroglycerin ointment reduced pulmonary capillary pressure by an average of 28.5% (P less than 0.05) and systemic vascular resistance by 26.8%, while the cardiac index increased by 34.1% (P less than 0.05) and left ventricular stroke work index by 30.3% (P less than 0.01). The combined therapy was more effective, with a reduction of pulmonary capillary pressure by 30.4% (P less than 0.05) and systemic vascular resistance by 27.5% (P less than 0.05), accompanying an increase in cardiac index by 53.5% (P less than 0.005) and left ventricular stroke work index by 63.5% (P less than 0.01), with little change in the double products. This study suggests that serial hemodynamic monitoring accurately evaluates cardiac function, selection of appropriate therapy, and the hemodynamic effects of treatment in patients with acute myocarditis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Comparison of renal responses to synthetic human PTH(1-34) administration in normal young and elderly male subjects.

A parathyroid hormone (PTH) loading test with synthetic human PTH(1-34) was performed in 7 young and 6 elderly normal males. The elderly subjects had significantly higher mean basal levels of serum PTH than the young subjects (0.262 +/- 0.035(SE) vs 0.097 +/- 0.012 ng Eq/ml, P less than 0.001). When human PTH(1-34) at a dose of 100 U was administered to these subjects, the mean increases in urinary excretions of adenosine cyclic 3',5'-monophosphate(cAMP) and inorganic phosphorus (Pi), expressed as increases in absolute amounts per unit time, were significantly lower in the elderly subjects. (3.65 +/- 1.02 vs 7.41 +/- 1.05 mumol/h, P less than 0.05 for cAMP and 14.7 +/- 6.3 vs 41.8 +/- 8.6 mg/2h, P less than 0.05 for Pi) and an inverse correlation was found between the serum PTH levels and the increases in urinary cAMP excretion (mumol/hr; r = -0.63, P less than 0.05). However, when corrected for the glomerular filtration rate (GFR) and the units of PTH administered per kg body weight, the increases were not significantly different in the two groups (elderly 52.1 +/- 7.5 vs young 60.0 +/- 19.2 nmol . kg/100 ml GFR . U . h for cAMP and 0.315 +/- 0.061 vs 0.186 +/- 0.044 mg . kg/100 ml GFR . U . 2 h respectively for Pi).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Serum phosphate, parathyroid hormone and vitamin D metabolites in patients with chronic renal failure: effect of aluminum hydroxide administration.

Patients with chronic renal failure showed the existence of phosphate retention, secondary hyperparathyroidism, and reduced production of 1,25-(OH)2D. In order to determine the effect of correction of hyperphosphatemia on secondary hyperparathyroidism and vitamin D metabolism in those patients, 7 nondialyzed patients with chronic renal failure were treated with large doses of A1(OH)3 (15-18 g/day) to correct their high levels of serum phosphate. After treatment with A1(OH)3, serum phosphate fell significantly (p less than 0.005) from 6.3 +/- 1.3 (mean +/- SD) to 3.7 +/- 0.5 mg/dl. Serum parathyroid hormone decreased significantly (p less than 0.02) from 2.87 +/- 1.64 to 1.85 +/- 1.26 ngEq/ml. Serum 1,25-(OH)2D was low compared to the normal mean level before A1(OH)3 administration and decreased significantly (p greater than 0.02) from 19.4 +/- 6.1 to 11.4 +/- 4.3 pg/ml after the treatment. Aluminum levels increased significantly (p greater than 0.02) from 1.7 +/- 1.0 to 3.6 +/- 1.5 micrograms/dl. Serum calcium, calcitonin, and 25-(OH)D showed no significant change. Our data suggested that the suppression of secondary hyperparathyroidism by A1(OH)3 treatment results in a decrease of the 1,25-(OH)2D level in patients with chronic renal failure, even though their hyperphosphatemia has been corrected. We speculate that aluminum loading might play a role in diminishing the secretion of parathyroid hormone and the production of 1,25-(OH)2D in humans.

Adult↗

Changes in calcium homeostasis in acromegaly treated by pituitary adenomectomy.

Patients with acromegaly have alterations in mineral metabolism. To determine the effect of correction of excess GH secretion on calcium metabolism, we studied 12 acromegalic patients before and 3-4 weeks after pituitary adenomectomy. Treatment of acromegaly resulted in significant decreases in both serum calcium [from 9.3 +/- 0.2 to 8.7 +/- 0.1 mg/dl (mean +/- SEM); P less than 0.01] and urinary calcium excretion (from 200 +/- 24 to 88 +/- 12 mg/24 h; P less than 0.0002). Serum phosphate also decreased significantly (P less than 0.01) from 4.8 +/- 0.2 to 4.3 +/- 0.2 mg/dl. Both serum immunoreactive PTH and calcitonin levels were normal initially and did not change after surgery. The mean serum 25-hydroxyvitamin D (25OHD) level was significantly (P less than 0.01) lower and the 1,25-dihydroxyvitamin D [1,25-(OH)2D] level was significantly (P less than 0.0001) higher in acromegaly compared with measurements in 25 normal subjects. After surgery, the serum 25OHD level did not change; however, the serum 1,25-(OH)2D concentration fell significantly (P less than 0.0001) from 60 +/- 4 to 43 +/- 2 pg/ml. A positive correlation was found between the decrements in urinary calcium excretion and the serum 1,25-(OH)2D level when the comparison was made between the decrements as percentages of pretreatment values (r = 0.64; P less than 0.05). The accumulated data suggest that the hypercalciuria in acromegaly might be due to intestinal calcium hyperabsorption, which could be attributed to the elevated circulating 1,25-(OH)2D level. Excessive GH secretion might stimulate the production of 1,25-(OH)2D and might also directly stimulate calcium absorption.

Acromegaly↗

Renal inactive kallikrein as the possible origin of urinary inactive kallikrein in the rat.

An inactive kallikrein, which could be activated with trypsin was isolated from the rat kidney cortex using diethylaminoethyl (DEAE)-cellulose chromatography. The inactive kallikrein had no vasodilator action, whereas the injection of trypsin-activated form of this enzyme into the femoral artery of dogs resulted in a marked increase in the arterial blood flow. Apparent molecular weight of the inactive kallikrein was estimated to be 4.4 X 10(4) by gel filtration, and this enzyme was converted to the renal active kallikrein (M.W. 3.8 X 10(4] by trypsin. The inactive kallikrein is immunologically identical with the trypsin-activated form of inactive kallikrein and active kallikrein. There were no significant differences in the chromatographic behavior on a DEAE-cellulose column, Km value for prolyl-phenylalanylarginine-4-methylcoumaryl-7-amide hydrolysis and profile of inhibition by trypsin inhibitors between the active kallikrein and the trypsin-activated form of inactive kallikrein. The above properties of the renal inactive kallikrein were similar to those of inactive kallikrein found in the urine. These results suggest that the inactive kallikrein in the rat kidney would be proteolytically converted to its active enzyme and that a part of the inactive kallikrein would be excreted into urine in a form itself.

Animals↗

Effects of tinoridine on lipid peroxidation and renin release in the rat renin granule fraction.

This study was carried out to investigate the effect of tinoridine (2-amino-3-ethoxycarbonyl-6-benzyl-4,5,6,7-tetrahydrothieno[2,3-c] pyridine), a non-steroidal anti-inflammatory drug, on the lipid peroxidation and renin release in the renin granule fraction. The renin granule fraction was prepared from the kidney cortex homogenate by a discontinuous sucrose density gradient centrifugation. Incubation of this fraction at 37 degrees C resulted in an increase in lipid peroxide formation, accompanied by increased release of renin from the granules. When the renin granule fraction was incubated with 50 microM tinoridine at 37 degrees C, lipid peroxide formation in this fraction was completely inhibited. Simultaneously, the rate of renin release from the granules was significantly suppressed. Tinoridine, at concentrations from 5 microM up to 100 microM, produced a concentration-dependent inhibition on the simultaneous increases in lipid peroxide formation and renin release induced by 50 microM ascorbic acid in the renin granule fraction. On the other hand, indomethacin, hydrocortisone and prednisolone, which had no ability to inhibit the lipid peroxidation in the renin granule fraction, did not influence the release of renin from the granules. These results suggest that tinoridine suppresses renin release by inhibiting the oxidative disintegration of membranes of renin granules.

Animals↗

On the interstitial fibrotic changes in acute and convalescent myocarditis obtained by serial endomyocardial biopsy.

In order to determine the characteristics of the interstitial fibrotic change of the myocardium in cases with viral or idiopathic myocarditis, right ventricular endomyocardial biopsy findings in 9 cases where serial endomyocardial biopsy had been performed at the acute (5-10 days after the onset of the disease), subacute (11-21 days) and convalescent stages (22-167 days) and in 1 case at the acute stage were analyzed. They were then compared with right ventricular endomyocardial biopsy findings from 58 cases with chronic right ventricular overloading and which were of various kinds of congenital and valvular heart diseases. The following results were obtained: Interstitial fibrosis was seen at the acute stage along with an increase in fibroblasts, macrophages and lymphocytes. An analysis of the interstitial changes revealed that, at the acute stage, thin collagenous fibers were prominent as well as interstitial edema and at the convalescent stage, the edema became less prominent and instead, thick collagenous fibers increased. Comparison with the 58 cases with chronic right ventricular overloading revealed that diffuse and/or subendocardial fibrosis and endocardial thickening were more frequent and statistically more significant in cases with myocarditis.

Acute Disease↗

Right and left ventricular volume characteristics in children with transposition of the great arteries after Mustard's procedure.

With use of biplane cine-angiocardiograms, the measurements of right and left ventricular volume were determined in 11 children with transposition of the great arteries following Mustard's procedure. Right ventricular end-diastolic volume (RVEDV) ranged from 124 to 264 percent of the normal right ventricular volume with an average of 188 +/- 40 (SDM) percent, and left ventricular end-diastolic volume (LVEDV) ranged from 57 to 181 (122 +/- 43) percent of the normal (p less than 0.01, vs. RVEDV). Right ventricular ejection fraction (RVEF) ranged from 0.26 to 0.66 (0.42 +/- 0.11), and left ventricular ejection fraction (LVEF) ranged from 0.51 to 0.79 (0.66 +/- 0.09) (p less than 0.001, vs RVEF). Left ventriculography showed a deviation of the interventricular septum toward the left ventricle in patients with simple transposition of the great arteries not associated with left ventricular hypertension. The left to right ventricular systolic pressure ratio ranged from 0.22 to 1.02 (0.48 +/- 0.28), and the left to right ventricular end-diastolic volume ratio ranged from 0.43 to 1.00 (0.63 +/- 0.18). There was a high correlation between the left to right ventricular systolic pressure ratio and the left to right ventricular end-diastolic volume ration (r = 0.94, p less than 0.001). The left to right ventricular systolic pressure ratio also correlated well with the right ventricular ejection fraction (r = 0.90, p less than 0.001). Deviation of the interventricular septum was considered to result in a diminished ejection fraction of the right ventricle, in patients with simple transposition of the great arteries not associated with left ventricular hypertension, after Mustard's procedure.

Cardiac Volume↗

An acromegalic patient with recurrent urolithiasis.

A 52-year-old man with an acromegalic appearance of prolonged duration suffered abdominal colic attacks and hematuria during the middle of the course of the disease. The patient was diagnosed as having urolithiasis caused by increased urinary calcium. The calcium metabolic disorder was not considered to be due to hyperparathyroidism because serum calcium and PTH levels were within the normal range and no abnormality was observed in a parathyroidal scintigraph. The serum 1,25-dihydroxyvitamin D (1,25-(OH)2D) levels (55.0 and 73.0 pg/ml) were higher than the normal range (27.2-53.8 pg/ml). A selective adenomectomy by the transsphenoidal route (Hardy's method) was performed, resulting in an improvement in the hypercalciuria and urolithiasis, and a decrease in the levels of serum 1,25-(OH)2D (23.0 and 23.0 pg/ml). These findings suggest that GH may promote the activation of vitamin D in the kidney in acromegaly, resulting in an acceleration of calcium absorption in the intestine through the action of activated vitamin D and the induction of increased urinary calcium excretion by the urinary excretion of excessive blood calcium.

Acromegaly↗

Right ventricular function after extracardiac conduit repair for tetralogy of Fallot. A comparison among surgical approaches.

Right ventricular volume measurements and hemodynamic studies were performed in 20 patients after total correction of tetralogy of Fallot. There were 6 patients with an extracardiac conduit and Hancock xenograft (G-1), 8 with an outflow tract patch (G-2) and 6 without or with a minimal right ventriculotomy and repair of pulmonary valve (G-3). The age at the time of operation was over 3 years in each patient and averaged 5 +/- 2 (mean +/- SD) years. Right ventricular systolic pressure averaged 81 +/- 22, 55 +/- 22 and 58 +/- 30 mmHg in G-1, G-2 and G-3, respectively. Right ventriculography showed no contraction of the right ventricular free wall at the anastomosis to the conduit and poor contraction around the anastomosis in G-1. The right ventricular enddiastolic volume index (RVEDVI) was 114 +/- 31, 155 +/- 57 and 115 +/- 28 ml/m2 in G-1, G-2 and G-3, respectively. The right ventricular ejection fraction (RVEF) was 0.42 +/- 0.11 in G-1, 0.53 +/- 0.04 in G-2 (p less than 0.05, vs G-1) and 0.57 +/- 0.04 in G-3 (p less than 0.02, vs G-1). Pulmonary regurgitation was evident in 17 patients, and RVEDVI correlated well with degrees of pulmonary incompetence. Fourteen patients in G-2 and G-3 were divided into G-A and G-B to evaluate right ventricular function with or without pressure overloading of the right ventricle. G-A consisted of 7 patients with a right ventricular systolic pressure of more than 50 mmHg (74 +/- 26) and G-B of 7 patients with a value less than 50 mmHg (39 +/- 4). There was no difference in RVEDVI and RVEF between G-A and G-B. RVEF was significantly lower in G-1 than G-A (p less than 0.02) and G-B (p less than 0.05). These results suggested that an extracardiac conduit with Hancock xenograft reduced the contraction of the right ventricular free wall and induced a depressed right ventricular pump function in patients with a high right ventricular pressure.

Bioprosthesis↗

Unresponsiveness of plasma mineralocorticoids to angiotensin II in diabetic patients with asymptomatic normoreninemic hypoaldosteronism.

offlated hypoaldosteronism with or without hyperkalemia in patients with diabetes mellitus has been shown to exist occasionally without hyporeninemia. To assess in detail the adrenal function in this disorder, the responses of plasma aldosterone (PA) and its precursor steroids to angiotensin II (AII) infusion and adrenocorticotropic hormone (ACTH) injection were studied in seven patients with asymptomatic normoreninemic hypoaldosteronism (ANH) and 11 age-matched normal subjects. The ANH diabetic patients had, by definition, a low PA level after furosemide (80 mg orally) plus upright posture (4 hours) stimulation, low PA and high plasma renin activity (PRA) increases after the stimulation (a low delta PA/delta PRA ratio), and normokalemia. Plasma inactive renin and the inactive renin/total renin ration were similar in the ANH diabetic patients and in the normal subjects. Under the pre-AII condition, plasma DOC and corticosterone levels tended to be low, and the plasma 18-OHB and PA levels were low in the ANH diabetic patients compared with the normal subjects. The ratio of plasma 18-OHB to PA was similar in the two groups. All infusion produced no increases in plasma 18-OHB and PA in the ANH diabetic patients, whereas the infusion caused dose-dependent increases in these steroids in the normal subjects. Plasma DOC and corticosterone levels remained unchanged during AII infusion in the two groups. ACTH injection produced appropriate PA increases relative to the basal PA in the two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

18-Hydroxycorticosterone↗

Inhibitory effects of norepinephrine, methoxamine and phenylephrine on renin release from rat kidney cortical slices.

We attempted to determine whether the inhibition of renin release from rat kidney cortical slices by alpha adrenoceptor agonists is mediated by activation of alpha-1 and/or alpha-2 adrenoceptors, and to investigate the role of calcium in the mechanisms of this inhibition. Norepinephrine (NE), methoxamine (ME) and phenylephrine (PE) produced a concentration-dependent inhibition of renin release from rat kidney cortical slices, whereas clonidine was without effect. NE-, ME- and PE-induced inhibition of renin release was blocked by prazosin, which was 2 or 3 orders of magnitude more potent than yohimbine. The inhibitory effects of NE, ME and PE on renin release from the slices were abolished by removal of calcium from the incubation medium. Calcium antagonists, verapamil and nifedipine, attenuated the responses of renin release to NE, ME and PE, in a concentration-dependent manner. The inhibitory effects of NE, ME and PE on renin release were blocked significantly by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, a calmodulin antagonist, but not by N-(6-aminohexyl)-1-naphthalenesulfonamide, which has virtually no calmodulin antagonistic activity. These findings suggest that alpha adrenoceptor agonists inhibit renin release from rat kidney cortical slices mainly via alpha-1 adrenoceptors and that calcium influx followed by the activation of the calcium-calmodulin system is involved in the above inhibition.

Animals↗