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Biomedical subjects

K Ogino

Publications and source records attributed to K Ogino.

296 records · Page 17Linked to original sources

Heat produces uteroplacental circulatory disturbance in pregnant rats through action of corticotropin releasing hormone (CRH).

There is some evidence showing an existence of corticotropin releasing hormone (CRH) and opioid peptides, including beta-endorphin (betaEP), in human placenta, whereas physiological roles of the placental peptides in response to stress remain to be elucidated. To clarify the involvement of CRH and opioid system in the uteroplacental circulation in the pregnant rats exposed to heat, we examined the effects of heat and intravenous administration of CRH receptor antagonist alpha-helical CRH (9-41) on the uteroplacental blood flow, as well as blood CRH, and blood and placental betaEP in pregnant rats. Heat did not change uterine blood flow in virgin rats, but reduced uteroplacental blood flow in pregnant rats. The reduced uteroplacental blood flow induced by heat in pregnant rats was reversed by the administration of alpha-helical CRH. Independent of the status of pregnancy, heat increased blood CRH, which was not reversed by alpha-helical CRH. Although heat did not change placental betaEP, alpha-helical CRH reduced blood and placenta betaEP in pregnant rats. These results suggest that the uteroplacental circulatory disturbance caused by heat is mediated by CRH, possibly through the involvement of CRH receptor in rat placenta. The placental opioid system seems unlikely to be involved in the mediation of uteroplacental circulation.

Animals↗

Effects of diethyldithiocarbamate on activating mechanisms of neutrophils.

The effects of diethyldithiocarbamate on superoxide release by rat neutrophils were investigated in a chemiluminescence study. Diethyldithiocarbamate augmented lucigenin-dependent chemiluminescence in a concentration-dependent manner and inhibited luminol-dependent chemiluminescence at concentrations of 0.1-1 microM. In contrast, after the addition of 0.1 mM diethyldithiocarbamate, the chemiluminescence was markedly enhanced. Diethyldithiocarbamate inhibited both the myeloperoxidase activity of neutrophils and the chemiluminescence generated in a cell-free horseradish peroxidase/H2O2 and H2O2/HOCl system. The increase in lucigenin-dependent chemiluminescence brought about by diethyldithiocarbamate was inhibited by H-7, ML-7, W-7, EGTA and pertussis toxin. These results suggest that diethyldithiocarbamate may stimulate O2- production by a guanosine 5'-triphosphate protein-mediated and Ca(2+)-dependent process and that the increase in O2- release by neutrophils may be dependent not only on the direct stimulation of the signal transduction pathway but also on the increase in O2- by reducing the effect of the hydroperoxide (H2O2)-myeloperoxidase system.

Acridines↗

Effects of enalapril on the exercise capacity and neurohumoral factors during exercise in patients with chronic heart failure.

The effects of enalapril on exercise capacity and neurohumoral factors during exercise were evaluated in 10 patients with heart failure. Echocardiograms and exercise testing with expired gas analysis were performed before and after enalapril. Blood samples were obtained before and after exercise. Both ejection fraction and percent fractional shortening increased with enalapril (p < 0.05). The anaerobic threshold and peak VO2 did not change with enalapril. Epinephrine and norepinephrine levels at peak exercise decreased with enalapril (p < 0.1). Plasma renin both at rest and at peak exercise increased with enalapril (p < 0.1). Angiotensin II was lower after enalapril both at rest and at peak exercise (p < 0.1 and p < 0.05, respectively). Aldosterone was lower after enalapril both at rest and at peak exercise (p < 0.05). Atrial natriuretic peptide (ANP) was lower after enalapril both at rest and at peak exercise. There was no significant correlations between peak VO2 and changes in neurohumoral factors before and after enalapril during exercise. In conclusion, neurohumoral changes with enalapril occurred during exercise even if exercise capacity did not improve. Moreover, the improvement of cardiac function at rest and neurohumoral factors with enalapril did not lead to a change of exercise capacity.

Aged↗

Responses of plasma catecholamines, renin-angiotensin-aldosterone system, and atrial natriuretic peptide to exercise in patients with essential hypertension.

Neurohormonal responses to exercise have not been studied fully in patients with essential hypertension (HT). This study determined if neurohormonal responses to exercise are altered between three subgroups of HT categorized by basal plasma renin activity (PRA). Plasma norepinephrine, epinephrine, atrial natriuretic peptide (ANP), PRA, angiotensin II (AII), and aldosterone were measured at rest and after submaximal treadmill exercise in 39 patients with essential HT (WHO classes I-II) and 13 controls. Patients with HT were divided into three subgroups based on the PRA level [low-renin (< 0.5) HT (n = 14), normal-renin (0.5-2.0) HT (n = 13), and high-renin (> 2.0) HT (n = 12)]. Patients with HT had higher blood pressure during exercise compared to controls, but blood pressure responses were similar among low-, normal-, and high-renin HT. Neurohormonal factors were comparable between all hypertensives and controls, except for higher plasma AII at rest in patients with HT. When neurohormones were compared among three subgroups of HT, plasma norepinephrine and epinephrine responses were similar. Patients with high-renin HT had higher PRA and AII, and lower ANP levels at rest and after exercise. In all hypertensives, negative correlations were observed between resting PRA and resting ANP (r = -0.41, p < 0.01), as well as peak PRA and peak ANP (r = -0.33, p < 0.05). Thus, neurohormonal responses to exercise varied with similar cardiac responses among subgroups of essential HT stratified according to renin levels. Patients with high-renin HT had augmented renin-angiotensin system activity with a decrease in ANP levels both at rest and after exercise. A reciprocal relationship between renin-angiotensin system activity and ANP was observed both at rest and after exercise in HT.

Adult↗

The storage form of human renal renin.

We isolated renin granules from cadaver kidneys using discontinuous sucrose density gradient centrifugation, and investigated the storage form of the renin from these granules. Approximately 23% of the total renin activity in the original homogenate was obtained from the surface phase between 1.6 and 1.7 M sucrose (Fraction 6). Granule renin extracted from the granules in Fraction 6 was separated into active and inactive renin using pepstatin affinity chromatography. Only the active renin had an affinity for pepstatin. The inactive renin, albeit activated by trypsin, was little activated by acidification. The proportion of inactive renin was about 25% of the total granule renin (active renin + inactive renin). Trypsin concentrations over 10 micrograms/ml resulted in a decrease in the renin activity of the trypsin-activated renin, but the enzymatic activity of active renin was decreased by trypsin. With gel filtration, the inactive renin revealed a single peak, and the molecular weight (MW) was 48,000. The active renin had a MW of 44,000. The inactive renin could be activated by trypsin without an apparent change in molecular weight.

Aged↗

Circulatory pressure-volume relationship and cardiac output in DOCA-salt rats.

We studied the total vascular pressure-volume relationship and cardiac output (CO) in conscious rats receiving DOCA-salt or sham treatment. The mean circulatory filling pressure (MCFP) was measured by briefly inflation an indwelling balloon in the right atrium, and the MCFP-blood volume (BV) relationship over +/- 10% of BV was determined by rapid blood infusion or withdrawal. CO was measured in separate experiments using Fick's principle. Arterial pressure-volume relationship was also determined in additional experiments on anesthetized rats. Compared with sham rats, the mean arterial pressure was unchanged at 1 week, increased at 2 weeks, and increased further thereafter in the DOCA-salt rats. The BV was unchanged at 1 week, expanded at 2 weeks, unchanged at 5 weeks, and contracted at 8 weeks. There were no significant changes in MCFP, total vascular compliance (the inverse of the slope), nor unstressed volume (extrapolated volume axis intercept) at 2, 5, and 8 weeks. Total vascular capacity, assessed as BV at MCFP of 7.6 mm Hg, increased at 2 weeks, was unchanged at 5 weeks, and decreased at 8 weeks. Arterial compliance decreased at 5 and 8 weeks. CO remained unaltered at 1, 2, 5, and 8 weeks. These results suggest that the altered total vascular capacity may serve to maintain a normal CO against a rising afterload in the conscious DOCA-salt hypertensive rats, and that the decreased total vascular capacity may be a secondary hemodynamic feature with progression of hypertension.

Animals↗

Hemodynamic changes during dynamic exercise in patients after mitral valve replacement for chronic mitral regurgitation.

To evaluate hemodynamic changes during dynamic exercise, we investigated 13 patients after mitral valve replacement (MVR) for chronic mitral regurgitation (MR) and 5 control subjects by right heart catheterisation during supine bicycle exercise. According to the sizes of the St. Jude Medical (SJM) prosthesis during MVR, patients were divided into group A (n = 8) with SJM 31mm and group B (n = 5) with SJM 29mm. Significant rise in cardiac index (CI) was noted during exercise in both groups A and B (from 3.3 +/- 0.8 to 5.5 +/- 0.9 l/min/m2, p < 0.01 and from 3.0 +/- 0.6 to 5.6 +/- 0.6 l/min/m2, p < 0.01 respectively) and also in control subjects (from 3.4 +/- 0.7 to 6.2 +/- 0.6 l/min/m2, p < 0.01). Mean pulmonary artery and pulmonary capillary wedge pressure were significantly higher during exercise in patients of both groups A and B than control subjects (p < 0.05 and p < 0.01 respectively). Total pulmonary vascular resistance was significantly higher during exercise in both groups A and B than control subjects (p < 0.05 and p < 0.01 respectively). No difference in hemodynamics were noted between the patients of group A and B during exercise. It is concluded that response of CI to exercise in patients after MVR for chronic MR was adequate in comparison to control subjects irrespective of two different valve sizes.

Adult↗