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Biomedical subjects

F Deguchi

Publications and source records attributed to F Deguchi.

At least 37 records · Page 2Linked to original sources

Plasma von Willebrand factor and thrombomodulin as markers of vascular disorders in patients undergoing regular hemodialysis therapy.

Increased plasma levels of von Willebrand factor antigen (vWF:Ag) are regarded as reflecting the release reaction by vascular endothelial cells and/or endothelial cell injury, and increased levels of thrombomodulin (TM) antigen as reflecting damage to endothelial cells. We investigated changes in plasma vWF:Ag and TM antigen levels during the course of regular hemodialysis treatment (RDT) in 14 patients undergoing RDT in order to evaluate the effect of hemodialysis (HD) on endothelial cells. vWF:Ag and TM were both measured by the sandwich EIA method. Predialysis levels of vWF:Ag and TM in RDT patients were both significantly higher than normal control values. Neither patient age nor blood pressure was not correlated with predialysis vWF:Ag and TM levels. Both vWF:Ag and TM levels significantly increased during a single HD session. There was a positive correlation between predialysis TM levels and duration of HD and an inverse correlation between the amount of vWF:Ag released during HD and duration of HD. It appears that HD procedures induce stimulation and damage of endothelial cells and that long-term, recurrent HD treatment may predispose to vascular disorders.

Adult↗

[Role of systemic and pulmonary hemodynamics in genesis pleural effusion in congestive heart failure].

We tried to make an estimate of how pleural effusion occur in congestive heart failure, using right atrial pressure (RA) and pulmonary arterial wedge pressure (PAW) as variables. We calculated the following equation by quoting the data in the past. RA greater than -0.02 x PAW + 13.3. We speculated that when this relationship is satisfied, pleural effusion will appear. We also studied the patients with severe congestive heart failure, dividing them into 2 groups, ie the pleural effusion group (EF) and pulmonary edema group (ED). Compared with ED, EF has a significantly higher RA (RA = 6.1 +/- 1.33 mmHg in EF and 13.3 +/- 2.21 mmHg in ED, mean +/- SE, p less than 0.02) and a significantly lower cardiac index (3.17 +/- 0.26 l/min/m2 vs 2.23 +/- 0.16 l/min/m2, mean +/- SE, p less than 0.01). Therefore, we thought that it was adequate to treat RA and PAW as independent variables. These equations appear to be useful in predicting the development of pleural effusion that's based in the plots of our patients on RA-PAW plane and their relationship to our equations.

Aged↗

Intraglomerular deposition of coagulation-fibrinolysis factors and a platelet membrane antigen in various glomerular diseases.

The intraglomerular location of coagulation-fibrinolysis factors (CFF) and a platelet membrane antigen (glycoprotein IIb-IIIa; GPIIb-IIIa) was determined in 101 patients with various glomerular diseases. Renal biopsy specimens were examined by immunofluorescence microscopy, using antisera against fibrinogen/fibrin reactive antigen (FRA), cross-linked fibrin degradation products (XL-FDP), fibronectin (FN), factor XIII-subunit a (F-XIIIa), plasminogen (Plg), alpha 2-plasmin inhibitor (alpha 2-PI) and GPIIb-IIIa. Intraglomerular deposits of the CFF were found at high rates in patients with IgA glomerulonephritis (GN), membranous nephropathy (MN) and lupus GN. The coexistence of deposits of these factors was ascertained by the double-staining method. The deposition rates of XL-FDP and GPIIb-IIIa were very low in patients with minimal-change nephrotic syndrome and focal glomerulosclerosis. Some cases of diabetic glomerulosclerosis (DGS) showed CFF deposition. FRA deposits associated with F-XIIIa and FN may indicate the presence of the cross-linked fibrin. Furthermore, the presence of Plg deposits together with alpha 2-PI and XL-FDP suggests the deposition of fibrin followed by fibrinolysis, but not of fibrinogen, and the coexistence of GPIIb-IIIa suggests the involvement of platelets in the reactions. These studies provide evidence that stabilized fibrin deposition with subsequent fibrinolysis and platelet activation take place in glomeruli in a fairly large proportion of patients with IgA GN, MN and lupus GN and in some cases of DGS.

Adolescent↗

[Study on the genesis of posturally induced crackles from hemodynamic data--in patients with ischemic heart disease having normal respiratory function].

The presence of fine crackles is suggestive of heart failure in patients without pulmonary disease. We have been interested in the clinical observation that fine crackles are frequently detected when posture was changed from sitting to supine positions or in patients going from sitting position to supine position with passive legs elevation in patients without obvious evidence of heart failure. We named these crackles, "the posturally induced crackles (PIC)". We have already reported that PIC was frequently detected in patients with ischemic heart disease. The present study was performed to estimate the mechanism of the genesis of PIC and to clarify its significance. Seventy-three patients with ischemia heart disease were included in this study. Pulmonary sounds were auscultated in sitting and supine positions and during passive elevation of both legs in a supine position. Patients were divided into 3 groups according to the presence or absence of fine crackles, i.e., those in whom fine crackles were not detected in either position (PIC (-)), those in whom fine crackles were detected in a supine position or during passive elevation of both legs, but not in a sitting position (PIC (+)), and those in whom fine crackles were detected even in a sitting position (Persistent crackles). We measured various hemodynamic parameters (cardiac index, RA pressure, PA pressure and PAW) and parameters of pulmonary circulation (pulmonary blood volume, pulmonary "venous" compliance) in these 3 groups and comparisons were made between them.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Volume↗

[Response of cardiac patients to dynamic exercise: analysis with "systolic" pressure-volume area].

In the present study, we constructed a left ventricular pressure-volume loop from catheterization data and RN-angiocardiography. By connecting the point of origin of the plane, not the point of Vd, with the end-systolic point of the loop, we calculated a "systolic" pressure-volume area (PVA), elastic potential energy (EPE), and stroke work (SW). A cardiac output (CO)-pulmonary artery wedge (PAW) pressure plot was constructed at rest and during exercise, using a bicycle ergometer, to evaluate cardiac pump function. End-systolic volume (ESV) was obtained from the left ventricular P-V loop, and the response of ESV to exercise was investigated. Thirty-five patients with various cardiac diseases were categorized in two groups according to the delta CO/delta PAW obtained from the shift of the CO-PAW plot during exercise; group I (n = 28) with the properly functioning hearts having the ratio greater than 0.12 l/min/mmHg and group II (n = 7) with the poorly functioning hearts having the ratio less than or equal to 0.12 l/min/mmHg. Group I was subdivided further into two subsets according to the changing pattern of ESV during exercise; group I-A with decreased or unchanged ESV (n = 20) and group I-B with increased ESV in which end-diastolic volume (EDV) was increased during exercise (n = 8). During exercise, PVA and SW were unchanged but SW/PVA increased in group I-A, suggesting improvement of external mechanical efficiency. SW/PVA was unchanged in group I-B, despite the increase in PVA and SW. This suggested that external mechanical work increased as a result of increased cardiac oxygen consumption. In group II, PVA increased, SW was unchanged and SW/PVA decreased, which could be explained by the mechanism that external mechanical work during exercise decreased as compared with that at rest. It was suggested that a different mechanism may have been responsible for the production of external mechanical work among patients in group I-A and in group I-B with properly functioning hearts judged from the CO-PAW plot. Therefore, it seems useful to calculate PVA, SW and SW/PVA during exercise using the left ventricular pressure-volume loop for evaluating cardiac function.

Adult↗

Measurement of left atrial systolic time intervals in hypertensive patients using Doppler echocardiography: relation to fourth heart sound and left ventricular wall thickness.

The concept of left atrial systolic time intervals and Doppler echocardiography were used in a quantitative assessment of left atrial function in relation to the presence or absence of a fourth heart sound and to left ventricular hypertrophy in 47 patients with hypertension. Left atrial systolic time interval indexes included atrial pre-ejection period (the time between the onset of an electrocardiographic P wave and the onset of left ventricular inflow during atrial systole [A wave]), corrected atrial pre-ejection period (the atrial pre-ejection period divided by the duration of the P wave), and atrial ejection time (the time between the onset and cessation of the A wave). Twenty-one patients with a fourth heart sound on the phonocardiogram had a shorter atrial pre-ejection period (81 +/- 10 versus 89 +/- 14 ms p less than 0.05) and a corrected atrial pre-ejection period (66 +/- 17 versus 83 +/- 18 ms, p less than 0.01), as well as a longer atrial ejection time (147 +/- 15 versus 126 +/- 13 ms, p less than 0.001) than did 26 patients without a fourth heart sound. The ratio of atrial pre-ejection period to atrial ejection time and that of corrected atrial pre-ejection period to atrial ejection time was smaller in patients with than in patients without a fourth heart sound (0.56 +/- 0.08 versus 0.71 +/- 0.11, p less than 0.001; 0.46 +/- 0.16 ms-1 versus 0.67 +/- 0.17 ms-1, p less than 0.001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Antihypertensive drugs and sodium restriction. Analysis of their interaction based on pressure-natriuresis relationship.

The hypotensive effects of some antihypertensive drugs are augmented under sodium restriction, while those of others are not. The mechanisms of these interactions were theoretically analyzed based on the arterial pressure-natriuresis relationship. Four-week studies were performed in 24 patients with essential hypertension who were given a regular sodium diet (12-15 g of NaCl/d) in the first and third weeks and a sodium-restricted diet (1-3 g/d) in the second and fourth weeks. One of three antihypertensive drugs, 60 mg/d of nicardipine (Ca-antagonist), 120 mg/d of propranolol (beta-blocker) or 150 mg/d of captopril (converting-enzyme inhibitor) was administered in the third and fourth weeks. The mean arterial pressure and urinary sodium excretion were measured on the last three days of each week. The degree of interaction between the antihypertensive drugs and sodium restriction was statistically compared. The hypotensive effect of nicardipine and propranolol did not differ with the change in sodium intake, whereas that of captopril was greater under sodium restriction than under the regular sodium diet. Urinary sodium excretion was plotted on the ordinate as a function of arterial pressure before and after administration of the antihypertensive drugs. The pressure-natriuresis curve was shifted left, without a change in the slope, by nicardipine and propranolol and also left, but with a decrease in the slope, by captopril. The hypotensive effect of nicardipine and propranolol, being independent of the amount of sodium intake, was based on the leftward shift of the pressure-natriuresis curve that was probably due to the decrease in renal vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Antihypertensive Agents↗

Effects of changes in dietary sodium intake and saline infusion on plasma atrial natriuretic peptide in hypertensive patients.

Plasma concentrations of immunoreactive (IR)-atrial natriuretic polypeptide (hANP) were measured by radioimmunoassay in 9 essential hypertensive patients after alteration of salt intake and acute saline infusion. Daily salt intake was altered every one week in the order of 15g/day, 3g/day, and 7g/day. On the last day of the first week, 1500 ml of 0.9% saline was infused intravenously over one hour. Plasma concentrations of IR-hANP tended to decrease, although not significant, by salt restriction. Further, there were significant positive correlations between changes in plasma concentrations of IR-hANP and those of several variables such as body weight, systolic blood pressure, and creatinine clearance. Plasma concentrations of IR-hANP rose significantly (p less than 0.05) from 50.7 +/- 20.1 (Mean +/- SEM) pg/ml to 119.0 +/- 48.8 after acute saline infusion. Although there was significant correlation between mean blood pressure and the increase in sodium excretion by saline infusion, this increase was unrelated to the rise in plasma concentrations of IR-hANP. These results suggest that the release of ANP is stimulated mainly by expansion of extracellular fluid volume in hypertensive patients. However, natriuretic and hypotensive effects attributable to the changes of ANP release could not be elucidated.

Adult↗

Hypertensive complications and home blood pressure: comparison with blood pressure measured in the doctor's office.

We have compared hypertensive target organ damage with home blood pressure readings (HBPs) and with office blood pressure readings (OBPs) in 100 patients with mild to moderate essential hypertension. The correlation between blood pressure levels and hypertensive target organ damage in HBPs and OBPs were similar (r = .42, p less than 0.001 for systolic HBPs; r = .33, p less than 0.001 for diastolic HBPs; r = .42, p less than 0.001 for systolic OBPs; r = .34, p less than 0.001 for diastolic OBPs). In most instances, HBPs were lower than corresponding OBPs. Among individual patients whose OBPs were identical, HBPs in some instances differed strikingly. Optic fundi abnormalities were significantly more severe in patients whose systolic HBPs were 150 mmHg or greater, than in those whose systolic HBPs were less than 150 mmHg (p less than 0.05). Hypertensive complications did not differ among office hypertensive patients who were normotensive or borderline hypertensive at home, from the differences of OBPs. We concluded that overall hypertensive complications were equally related to HBPs and OBPs, but patients with discrepancies between HBPs and OBPs had fewer hypertensive complications. Thus, both OBPs and HBPs should be considered in deciding therapy.

Adult↗

Alterations in renal Na+K+ATPase activity and [3H]ouabain binding in Goldblatt hypertensive rabbits.

To evaluate the role of renal Na+K+ATPase in the presence of Goldblatt hypertension, the enzyme activity and [3H]ouabain binding were examined in cortical and medullary homogenates from two-kidney, one clip (2K1C), one-kidney, one clip (1K1C), unilaterally nephrectomized and normal rabbits. Four weeks after the surgery, systolic blood pressures (SBPs) of 2K1C and 1K1C rabbits were increased significantly to 128 +/- 3 and 129 +/- 2 mmHg, respectively. In contrast, SBPs in the normal controls and unilateral nephrectomized (1K) animals were 83 +/- 2 and 86 +/- 3 mmHg, respectively. In the 2K1C rabbits, atrophy (91%) occurred in the kidney on the ischaemic side and hypertrophy (110%) occurred in the contralateral kidney. Na+K+ATPase activity and number of [3H]ouabain binding sites were reduced in the homogenates of the ischaemic kidney of 2K1C rabbits. In the 1K1C rabbits, marked hypertrophy of the kidney (155%) occurred, and the activity of Na+K+ATPase and the number of [3H]ouabain binding sites increased slightly in the cortex and medulla, compared with the normal controls. 5'-Nucleotidase, a plasma membrane marker enzyme, remained unchanged in both groups of hypertensive rabbits. Dissociation constant (KD) values for [3H]ouabain binding did not differ significantly in the renal homogenates of of 2K1C and 1K1C, compared with findings in the normal controls. The inhibitory activity of plasma was measured by studying [3H]ouabain binding to Na+K+ATPase of renal tubular basolateral membrane vesicles purified by Percoll gradient. The inhibition was more pronounced with plasma from 2K1C, 1K1C and 1K rabbits than from the control animals. Our findings suggest that in the Goldblatt hypertensive model, changes in Na+K+ATPase activity were due to alterations in glomerular filtration rate (GFR).

Animals↗

Normalizing effects of plasma on altered cation transport of red blood cells from essential hypertensive patients.

Net Na+ and K+ fluxes were measured in Na+-loaded red cells from 19 normotensive control subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive control subjects. However, by the addition of the patients' own plasma, the net Na+ efflux rate was significantly increased in essential hypertensive patients, which caused the increment in the ratio of Na+/K+ net fluxes. This resulted in disappearance of the difference between normotensive and hypertensive subjects in the ratio of cation fluxes. It was possible that the abnormalities of cation transport in red cells from essential hypertensive patients might be compensated for by humoral factors in the plasma.

Adolescent↗

Cation transport of red blood cells from hypertensive patients in Japan.

This study was performed to determine whether there is any difference in cation transport of red blood cells from normotensive subjects and hypertensive patients in Japan. Net Na+ efflux and net K+ influx rates were measured in sodium-loaded red cells from 19 normotensive subjects, 22 essential hypertensive patients, and 8 secondary hypertensive patients. The ratio of Na+/K+ net fluxes and the net cation flux rate were compared between these groups. The ratio of Na+/K+ net fluxes was significantly lower in essential hypertensive patients than in normotensive subjects. Parameters such as age, sex, blood pressure, plasma renin activity, and plasma aldosterone concentration were also examined in 2 groups of essential hypertensive patients, divided on the basis of their Na+/K+ net fluxes. However, there is no significant difference between the groups. These results suggest that the ratio of cation flux is related to hypertension independently of these parameters.

Adolescent↗