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Biomedical subjects

F Marumo

Publications and source records attributed to F Marumo.

At least 505 records · Page 28Linked to original sources
PubMed1991

Regional sympathetic denervation in von Recklinghausen's disease with coronary spasm and myocarditis.

Two patients with von Recklinghausen's disease presented with coronary artery spasm, transient high concentrations of norepinephrine, catecholamine-induced myocarditis, and regional sympathetic denervation of the heart that was assessed by I-123 metaiodobenzylguanidine scintigram. It is postulated that regional sympathetic denervation of the heart may precipitate both coronary artery spasm and catecholamine-induced myocarditis in susceptible patients with von Recklinghausen's disease.

Autonomic Nervous System Diseases↗
PubMed1991

Characterization of the acetaminophen-glutathione conjugation reaction by liver microsomes: species difference in the effects of acetone.

NADPH-dependent production of acetaminophen-glutathione conjugate has been partly characterized in rat liver microsomes. The reaction showed the characteristics of mixed function oxidase when glutathione concentration was higher than 0.2 mM. It is suggested that hydroxy radical and superoxide are not involved in this reaction. When the reaction was compared among rat, mouse and rabbit microsomes, mouse microsomes showed the highest activity; this was almost 4 times higher than the others, which may, at least in part, explain the susceptibility of mouse to acetaminophen-induced hepatotoxicity. There was also a species difference in the effects of acetone; this was enhanced in the rat microsomes, inhibited in the mouse, and minimally affected in the rabbit.

Acetaminophen↗
PubMed1991

Effect of low-protein, very-low-phosphorus diet on diabetic renal insufficiency with proteinuria.

We describe the clinical outcome of 13 patients with non-insulin-dependent diabetes mellitus (NIDDM), renal insufficiency, and proteinuria, treated for 12.2 +/- 12.9 months (mean +/- SD) with a low-protein, very-low-phosphorus diet (LPVLP) containing 30 g protein and 11.3 mmol (350 mg) phosphorus. After a control period of 18.2 +/- 20.4 months, LPVLP therapy was initiated and serum urea nitrogen, uric acid, and phosphate, as well as urinary excretion of protein, creatinine, urea nitrogen, uric acid, and phosphate, decreased significantly. There was no change in mean blood pressure, hemoglobin, blood pH, and HCO3-, as well as in serum creatinine, protein, albumin, calcium, magnesium, cholesterol, triglyceride, beta-lipoprotein, and high-density lipoprotein (HDL)-cholesterol. Nitrogen balances were measured over 5 weeks in nine patients. Nitrogen balance increased significantly from a negative balance of -0.795 +/- 1.367 g/d in the first week, to almost neutral in the fourth week, and later, was neutral or positive. Neither uremic symptoms nor signs of malnutrition appeared during the LPVLP period. These results suggest that negative nitrogen balance during the initial few weeks does not predict future nutritional status of patients with diabetic renal failure.

Adult↗
PubMed1991

Urinary excretion of endothelin-1 in normal subjects and patients with renal disease.

To elucidate the pathophysiological significance of urinary endothelin-1 (ET-1), we measured urinary excretion of ET-1-like immunoreactivity (L1) in 17 patients with renal disease and 9 normal subjects. Twenty-four hour urinary ET-1-L1 excretion in patients with renal disease (358 +/- 68 ng, mean +/- SE) was significantly (P less than 0.005) greater than that of normal subjects (77 +/- 5 ng). In patients with renal disease. ET-1-L1 clearance (CET) exceeded creatinine clearance (CCR); CET/CCR (305 +/- 81%) was significantly (P less than 0.005) greater than that of normal subjects (43 +/- 13%). The 24-hour urinary excretion of ET-1-L1 in patients with renal disease showed significant correlation with that of N-acetyl-beta-D-glucosaminidase (r = 0.587, P less than 0.05), beta 2-microglobulin (r = 0.614, P less than 0.01) and albumin (r = 0.484, P less than 0.05). Intravenous infusion of saline (500 ml) in seven normal subjects did not affect urinary ET-1 excretion rate. These data suggest that urinary excretion of ET-1 derives mainly from renal tubular secretion at least in patients with renal disease, and that degradation and/or reabsorption of ET-1 at the tubular site may also contribute to the renal handling of ET-1. Therefore, urinary excretion of ET-1 should serve as a potential marker for renal injury.

Acetylglucosaminidase↗
PubMed1991

Response of plasma atrial natriuretic factor to experimentally induced aortic and mitral regurgitation in dogs.

STUDY OBJECTIVE: The correlations between the plasma concentration of atrial natriuretic factor and right atrial or left atrial pressure were studied in experimentally induced aortic regurgitation and mitral regurgitation in dogs. DESIGN: Aortic regurgitation was created by opening the tip of a basket wire catheter placed at the aortic annulus via the left ventricular wall, and terminated by pulling back the catheter. To create mitral regurgitation a basket catheter was inserted into the mitral annular position via a pulmonary vein. Regurgitation was induced by opening the tip of the catheter, and terminated promptly by closing it. EXPERIMENTAL MATERIAL: Seven beagle dogs were prepared for the aortic regurgitation model and six for the mitral regurgitation model (weights 11.5 to 14.5 kg). MEASUREMENTS AND MAIN RESULTS: The plasma concentration of atrial natriuretic factor was highly correlated with right atrial pressure (r = 0.78, SD = 0.07, n = 7) and left atrial pressure (r = 0.82, SD = 0.05, n = 7) in aortic regurgitation; and with right atrial pressure (r = 0.82, SD = 0.05, n = 6) and left atrial pressure (r = 0.84, SD = 0.05, n = 6) in mitral regurgitation. Further evaluation of the molecular forms of plasma atrial natriuretic factor revealed the alpha form in all 13 dogs and the gamma form in two (one with aortic and the other with mitral regurgitation); no evidence of the beta form was seen. CONCLUSIONS: Atrial natriuretic factor secretion responds rapidly to the circulatory changes caused by valvular incompetence.

Animals↗
PubMed1991

Endothelin-1 as an autocrine/paracrine factor for human tumor cell lines.

We determined whether endothelin-1 (ET-1) is produced and secreted by human tumor cell lines and whether ET-1 can affect cytosolic free Ca2+ concentrations ([Ca2+]i) in these cells. Dilution curves of extracts of cultured conditioned media from several human cancer cell lines (HeLa, HEp-2, DLD-1, and Ca9-22) were parallel to those of standard ET-1 in radioimmunoassay (RIA). Amounts of ET-1-like immunoreactivity released into conditioned media were reduced by omitting fetal bovine serum from culture media. Synthetic ET-1 dose-dependently induced gradual and sustained increases in [Ca2+]i in HeLa, HEp-2, GOTO, and Lovo cells, an effect completely abolished by a Ca2+ channel blocker or by chelating extracellular Ca2+. These data suggest an autocrine/paracrine role of ET-1 in human tumor cell lines.

Calcium↗
PubMed1991

Endothelin-3 stimulates prostacyclin production in cultured bovine endothelial cells.

Among three endothelin (ET) isopeptides, ET-3 shows the most potent initial depressor response through endothelium-dependent mechanism. We have recently reported that ET-3 induces receptor-mediated phosphoinositide breakdown, which increases the intracellular Ca2+ concentration [( Ca2+]i) and stimulates synthesis of endothelium-derived relaxing factor (EDRF), or nitric oxide (NO), in endothelial cells (ECs). We examined whether ET-3 has any effect on synthesis of prostacyclin, a potent vasodilator prostanoid in bovine ECs. ET-3 dose-dependently (10(-10) - 10(-8) M) stimulated the formation of 6-keto-prostaglandin F1 alpha, a stable metabolite of prostacyclin, in culture media of ECs, whose stimulatory effect was inhibited by indomethacin, a cyclooxygenase inhibitor. These data suggest that ET-3 stimulates, in addition to EDRF (NO), the synthesis and release of prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Endothelin-1- and endothelin-3-like immunoreactivity in human cerebrospinal fluid.

Using highly specific and sensitive radioimmunoassays (RIAs) for endothelin-1 (ET-1) and endothelin-3 (ET-3), we have determined the concentrations of ET-1- and ET-3-like immunoreactivities (LI) in human cerebrospinal fluid (CSF). The concentration of ET-3-LI (82.5 +/- 4.8 pg/ml) was about 1.5-fold greater than that of ET-1-LI (34.3 +/- 1.3 pg/ml). There was no significant correlation between ET-1-LI and ET-3-LI concentrations in human CSF (r = 0.44). Reverse-phase high-performance liquid chromatography (HPLC) revealed a single major component of ET-1-LI and ET-3-LI coeluting with authentic ET-1 and ET-3, respectively. It is suggested that ET-1 and ET-3 play a neuropeptide-like role in the central nervous system.

Chromatography, High Pressure Liquid↗
PubMed1991

Plasma endothelin-1 levels in patients with diabetes mellitus with or without vascular complication.

Plasma endothelin-1 (ET-1) concentrations were measured in 25 patients with non-insulin-dependent diabetes mellitus (11 with angiopathy and 14 without angiopathy) and 21 normal subjects using radioimmunoassay specific to ET-1. Basal plasma immunoreactive (ir) ET-1 levels in diabetic patients with and without angiopathy were 1.73 +/- 0.29 and 1.68 +/- 0.20 pg/ml, respectively. Although high glucose levels may stimulate ET-1 release from vascular endothelial cells in vitro, our data suggest that circulating ET-1 may not be elevated in most diabetic patients with or without angiopathy.

Adult↗
PubMed1991

Effects of pirmenol on electrical induction of sustained ventricular tachycardia in a seven-day-old canine myocardial infarction.

Effects of pirmenol on electrical induction of sustained ventricular tachycardia (VT) were examined in 14 dogs with 7-day-old myocardial infarctions. Before administration of the drug, sustained VT was induced in 8 of 14 dogs. After administration of 3 mg/kg pirmenol, induction of VT was suppressed in 2 dogs but remained inducible in 6 dogs. After cumulative administration of 5 mg/kg pirmenol, VT was no longer inducible in 3 dogs but in the other 3 dogs VTs were still inducible at increased cycle lengths. After 7 mg/kg pirmenol, VT was not inducible in the remaining three dogs. Arrhythmias could not be provoked in any postinfarction dogs after pirmenol administration. Plasma concentrations after sequential and cumulative administration of 3, 5, and 7 mg/kg pirmenol averaged 0.43, 0.65, and 1.15 micrograms/ml, respectively. Administration of pirmenol increased the effective refractory period (ERP) and paced QRS duration in both the normal and infarcted ventricular myocardium. In the infarcted myocardium, prolongation of the ERP for the second and third extrastimuli was greater than for the first one (p less than 0.05). Results indicate that pirmenol is effective for prevention of sustained VT owing to prolongation of both the ERP and conduction time in recent myocardial infarction.

Animals↗
PubMed1991

Prolongation of the kidney preservation period by simple cold storage up to 72 hours by human atrial natriuretic peptide.

To prolong the preservation period of donor kidneys, we tried to evaluate the effect of human atrial natriuretic peptide (hANP), which has vasodilator, natriuretic, and GFR-increasing effects. Autotransplantations were successful in 6 of 8 hANP-treated cases, but only one of 7 untreated cases (P less than 0.05) was successful. When removed kidneys were perfused prior to preservation, the gravity perfusion time was shorter in hANP-treated kidneys, resulting in rapid cooling. Renal biopsy 1 hr after transplantation revealed normal histology in the hANP-treated kidneys while a remarkable capillary collapse occurred in controls. A hANP-like immunoreactivity contents of biopsied tissue in the hANP-treated kidneys showed a higher value than in the controls, and cyclic GMP contents were also higher in the hANP-treated kidneys. Microangiography showed complete clarity, down to the peripheral vessels, in the hANP-treated kidneys, but not in the controls. Thus, the present study suggests that hANP is useful for prolonging the preservation time of donor kidneys.

Animals↗
PubMed1991

Action of nicorandil on ATP-sensitive K+ channel in guinea-pig ventricular myocytes.

1. Patch-clamp techniques were used to study the effects of nicorandil (2-nicotinamiodethyl nitrate) on the adenosine 5'-triphosphate (ATP)-sensitive K+ channel current (IK.ATP) in guinea-pig ventricular myocytes. 2. Nicorandil activated the time-independent outward current. This effect was dependent on intracellular ATP concentration ([ATP]i) showing a larger effect at 2 mM than at 10 mM [ATP]i. The nicorandil-induced outward current was inhibited by application of 0.3 microM glibenclamide. 3. In the inside-out patch configuration, 0.3-1.0 mM nicorandil increased the open-stage probability of IK.ATP without a change in its conductance value (about 90pS). This effect was inhibited by glibenclamide. Analysis of the open and closed time distributions showed that nicorandil had no effect on open and closed distributions shorter than 5 ms. On the other hand, nicorandil increased the life time of bursts and decreased the interburst intervals. 4 The inward rectifier K+ channel current was not influenced by internal application of nicorandil. 5 Therefore, we conclude that IK.ATP is the only K+ current activated by nicorandil, and the main effect of nicorandil is on the kinetics of the IK.ATP bursting behaviour. These actions are similar to that of pinacidil on this preparation.

Adenosine Triphosphate↗
PubMed1991

Comparative efficacy of subcutaneous mesh and plate electrodes for nonthoracotomy canine defibrillation.

To determine the optimal configuration for the subcutaneous placement of electrodes for the performance of ventricular defibrillation without thoracotomy, internal defibrillation using four different subcutaneous electrodes was performed in 13 anesthetized dogs (7-12 Kg, mean +/- SD: 9.2 +/- 1.5 Kg). An electrode (7 cm2) was positioned transvenously in the superior vena cava with the following electrodes randomly implanted subcutaneously on the left chest: small mesh electrode (14 cm2), large mesh electrode (28 cm2), small titanium plate electrode (14 cm2), and large plate electrode (28 cm2). Ventricular fibrillation was induced by applying alternating current; a monophasic defibrillation wave was administered between the superior vena cava and the subcutaneous electrodes 10 seconds later. The energy level associated with a 50% successful defibrillation, as predicted by logistic regression analysis, was defined as the ED50. After the completion of the defibrillation protocol using the four subcutaneous electrodes, the small mesh electrode was sutured to the epicardium and the ED50 measurements were repeated. Energy ED50s were lower when the superior vena cava electrode was used as the cathode rather than as the anode. Of the subcutaneous electrodes, the large plate electrode showed the lowest energy ED50 (3.3 +/- 0.9 joules). The plate electrodes had lower energy ED50s than the mesh electrodes, and the large electrode had a lower energy ED50 than the small electrodes. Using the epicardium electrode, transient arrhythmias and ST elevation were observed following successful defibrillation; however, no arrhythmias or ST-T changes were observed following defibrillation using the subcutaneous electrodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Appearance of alpha-smooth-muscle-actin-positive cells in hepatic fibrosis.

The appearance of alpha-smooth-muscle-actin (alpha-smA)-positive cells during hepatic fibrosis was studied immunohistochemically in rat and human livers. In the normal rat liver, alpha-smA was observed only in vascular smooth muscle cells. With the progression of fibrosis induced by CCl4 injection, alpha-smA-positive cells appeared in the perisinusoidal space and the fibrous septa, and ultimately surrounded regenerative nodules. An increase of desmin-positive cells was recognized in the fibrotic areas and the perisinusoidal area. In the human liver, alpha-smA-positive cells appeared in the fibrotic area, whereas no desmin-positive cells were observed, except in vascular walls of the central vein and the portal tract, alpha-smA is a good marker for the detection of myofibroblast-like cells, and the appearance of alpha-smA in liver mesenchymal cells seems closely related to the process of hepatic fibrosis in both rat and man.

Actins↗
PubMed1991

Cl-HCO3 exchange and Na-HCO3 symport in rabbit outer medullary collecting duct cells.

The mechanisms of basolateral HCO3- (or related base) transport were examined in the outer stripe of the outer medullary collecting duct (OMCDo). Rabbit OMCDo were perfused in vitro and cell pH (pHi) of principal cells (PC) and intercalated cells (IC) was monitored with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) using fluorescence ratio imaging microscopy. Basolateral HCO3- exit was stimulated either by bath HCO3- reduction or by NH3/NH4(+)-induced cell alkalinization. Rates of pHi decrease were twice as high in IC than in PC. In both cell types HCO3- exit was dependent on Cl(-)-coupled and Na(+)-coupled mechanisms; the former was dominant in IC, whereas the latter was dominant in PC. pHi of PC and IC significantly increased by bath Cl- removal in the absence of Na+ and decreased by bath Na+ removal in the absence of Cl- but with amiloride. 4,4'-Diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) inhibited these pHi responses to a reduction of bath HCO3-, Cl-, or Na+, and an alkali loading. Our results suggest that 1) the capacity for basolateral HCO3- transport is twice as high in IC than in PC, 2) both PC and IC possess basolateral Na(+)-independent Cl(-)-HCO3- exchange and Na(+)-HCO3- cotransport, and 3) basolateral HCO3- transport is mediated mainly by Na(+)-HCO3- cotransport in PC and by Na(+)-independent Cl(-)-HCO3- exchange in IC.

Alkalies↗
PubMed1991

Mechanisms of inhibition of proximal acidification by PTH.

The parathyroid hormone (PTH) effects on luminal Na-H exchange and basolateral Na-HCO3 cotransport were examined in isolated perfused rabbit proximal convoluted tubules. Lumen pH (pHi) and cell pH (pHi) were measured by a fluorescent technique using 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein (BCECF). The time course of the PTH effect on proximal acidification was first determined by continuous monitoring of pHi in a stop-flow condition. PTH 10(-8) M added to the bath promptly inhibited the acid pHl generation. Adenosine 3',5'-cyclic monophosphate (cAMP) (10(-4) M) added to the bath mimicked the PTH effect. Luminal Na-H exchange was assayed by monitoring changes in pHi (dpHi/dt) in response to luminal Na+ removal in HCO3- free condition. The addition of PTH or cAMP for 5 min decreased dpHi/dt by 30 and 37%, respectively. Basolateral Na-HCO3 cotransport was assayed by measuring dpHi/dt caused by bath Na+ removal. The addition of PTH or cAMP for 5 min did not change the dpHi/dt. PTH also did not alter the dpHi/dt induced by reducing the bath HCO3- from 25 to 5 mM. The addition of PTH or cAMP to the bath slightly reduced pHi by 0.05. These results suggest that 1) PTH inhibits proximal acidification very rapidly and the effect reached a maximum within 10 min, 2) PTH rapidly inhibits luminal Na-H exchange but not basolateral Na-HCO3 cotransport in a short period, and 3) this effect is at least partly mediated by cAMP-dependent mechanisms.

Animals↗
PubMed1991

Endothelin-1 inhibits AVP-stimulated osmotic water permeability in rat inner medullary collecting duct.

Endothelin causes diuresis despite an accompanying decrease in glomerular filtration rate and renal plasma flow. Binding sites for endothelin are located not only in glomeruli but also in the inner medulla, possibly in inner medullary collecting ducts (IMCD). To determine whether endothelin has a direct tubular effect, effects of endothelin on water and urea transport were investigated using isolated microperfusion of rat IMCD segments in vitro. Endothelin, at 10(-10) and 10(-8) M, reversibly inhibited 10(-11) M arginine vasopressin (AVP)-stimulated osmotic water permeability (Pf) by 18 and 24%, respectively. Endothelin (10(-8) M) also inhibited Pf by 23% in the presence of a much higher dose of AVP (10(-9) M), whereas endothelin had no effect on Pf in the absence of AVP. On the other hand, 10(-8) M endothelin did not inhibit Pf stimulated by 10(-3) M dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). Endothelin had no inhibitory effect on AVP-stimulated urea permeability. These data suggest that endothelin can cause diuresis by inhibiting AVP-stimulated Pf in IMCD and that the site of action is previous to cAMP generation.

Animals↗