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Biomedical subjects

H Ijichi

Publications and source records attributed to H Ijichi.

At least 127 records · Page 7Linked to original sources
PubMed1983

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats.

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

Animals↗
PubMed1983

Characteristics of auto-antibodies to bovine TSH in the serum of two patients with Graves' disease.

In this report we describe the characteristics of auto-antibodies to bovine TSH (bTSH) detected in the serum of 2 females among 102 patients with Graves' disease. These patients had never been injected with bTSH. One patient had high LATS activity and high bTSH binding activity after isotope therapy. The other patient showed no detectable LATS activity. Interestingly, the antibody showed a specifically high binding activity for the labelled TSH preparation purified by receptor. The auto-antibody could be demonstrated by the double antibody method, polyethylene glycol method, and by gel-filtration. The antibody was polyclonal immunoglobulin G (IgG). Because the binding of [125I]bTSH with the patient's antibody was inhibited by pituitary extracts from mammalian species other than human, this antibody may cross-react with bovine, rat, dog, rabbit and whale TSH. Although the incidence of the antibody in Graves' disease is low and the pathological significance remains obscure, the existence of this antibody in the serum of patients may suggest that autoimmune mechanisms may involve not only the thyroid but also the pituitary in Graves' disease.

Adult↗
PubMed1983

Left ventricular size and performance during graded supine exercise in normal subjects.

To investigate left ventricular size and performance during graded submaximal exercise, 14 normal subjects with a mean age of 21 years exercised in a supine position to achieve the target heart rate. Using two-dimensional echocardiography, we recorded and analysed the left ventricular (LV) cross-sectional area and internal dimension at the level of the tips of the mitral valve at rest and during mild, moderate and severe exercise. The heart rate and systolic blood pressure increased substantially from rest to peak exercise (71 +/- 11 to 162 +/- 10 beats/min, 122 +/- 10 to 204 +/- 22 mmHg). The end-diastolic cross-sectional area and internal dimension (EDA & EDD) increased by 1.1-2.2 cm2 (7-13%) and 0.2-0.3 cm (4-7%), respectively, from mild to moderate exercise, (p less than 0.05-0.001). At peak exercise, however, these decreased and showed no statistically significant difference from the values at rest. The end-systolic cross-sectional area and internal dimension (ESA & ESD) decreased by 1.1 to 1.6 cm2 (14-20%) and 0.2-0.3 cm (7-10%), respectively, from moderate to severe exercise (p less than 0.01-0.001). However, the end-systolic values during mild exercise were not significantly different from those at rest. The stroke area (EDA-ESA) and dimension (EDD-ESD) increased by 1.6-2.6 cm2 (19-31%) and 0.2-0.6 cm (25-38%), respectively, during all levels of graded exercise (p less than 0.05-0.001). The percent change of LV cross-sectional area and internal dimension during systole increased gradually from rest to moderate exercise (51.0 +/- 7.1 to 61.9 +/- 4.4%, 35.4 +/- 3.9 to 45.0 +/- 3.7%), respectively, and showed no further increase during peak exercise. The mean circumferential fiber shortening velocity increased sharply from rest to peak exercise (1.27 +/- 0.14 to 2.25 +/- 0.21 circ/sec). These results suggest that the Frank-Starling mechanism operates during mild to moderate exercise, and contractility increases markedly at moderate to severe exercise levels as cardiac performance is augmented during graded submaximal exercise.

Adolescent↗
PubMed1983

[Analysis of coronary hemodynamics in exercise by T1-201 scintigraphy: examination of rates of change of cardiac output, myocardial blood flow distribution, coronary blood flow and coronary vascular resistance].

From our observation that initial distribution of 201T1 in tissue is mainly dependent on blood flow distribution, we designed the method to obtain the rates of change of coronary blood flow and coronary vascular resistance and applied it to the analysis of coronary hemodynamics in patients with ischemic heart disease during submaximal exercise. We measured the rates of change of cardiac output (delta CO) and myocardial blood flow distribution (delta Fract ) in two occasions by the sequential two injections of T1, and obtained the rate of change of coronary blood flow (delta Flow) from delta CO and delta Fract . Using the rate of change of mean blood pressure, we calculated also the rate of change of coronary vascular resistance (delta CVR). The initial components of histograms of the right ventricle by the first and second injections of T1 were fitted into gamma function curve. S1 and S2 were the areas bounded by the curve and baseline of the first and second injections, and then the cardiac output ratio was estimated by R X S1/S2, where R was the dose ratio measured by another camera system. The five min count rates on the myocardium by the first (H1) and second (H2) injections of T1 were calculated five min after the injection. H2 was approximately H1 X R in the same condition of T1 injection but H2 was not equal to H1 X R, when the T1 injection was done in the different loading condition. Therefore the rate of change of myocardial blood flow distribution was calculated as delta Fract = (H1 X R-H2)/H2.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Output↗
PubMed1983

Antihypertensive effect of nifedipine and its relationship to severity of hypertension.

The antihypertensive effect of nifedipine (Adalat), a Ca2+-antagonistic drug, was studied in patients with mild or severe hypertension. In both short- and long-term trials, nifedipine exerted a strong hypotensive effect, more pronounced in patients with severe than in cases with mild hypertension. The results of our short-term study showed a positive correlation between the maximum fall in blood pressure induced by nifedipine and pretreatment systolic blood pressure values or the total severity index score of hypertension. In our long-term trial, we also observed a positive correlation between maximum reduction of blood pressure--induced by nifedipine--and pretreatment values. However, no correlation between reduction of blood pressure and total severity index score of hypertension could be established. Our results indicate that nifedipine could be effective in the management of severe hypertension. The hypotensive action of nifedipine, at least partly due to its Ca2+ influx blocking action, suggests that etiologically hypertension may be connected with an abnormal calcium metabolism of the cardiovascular muscle cells.

Adult↗
PubMed1983

A possible mechanism of adriamycin cardiotoxicity. Inhibition of NADP-linked isocitrate dehydrogenase.

In heart muscle, NADP-linked isocitrate dehydrogenase activity is particularly high when compared with that of the other representative NADPH-generating enzyme, glucose-6-phosphate dehydrogenase. Approximately 80% of cardiac NADP-linked isocitrate dehydrogenase activity originates in the mitochondria. Adriamycin inhibited the activity of both mitochondrial and cytoplasmic NADP-linked isocitrate dehydrogenase dose dependently but had no effect on glucose-6-phosphate dehydrogenase. The inhibition was kinetically distinguished as noncompetitive. Preincubation of crude cardiac enzyme preparations with adriamycin enhanced the inhibition time dependently for 45 min. However, there was no evidence to suggest that the metabolites of adriamycin produced in this system were active as inhibitors. Adriamycin-binding protein was fractionated by affinity chromatography, but NADP-linked isocitrate dehydrogenase activity was not detected in this fraction.

Animals↗
PubMed1982

IgE-mediated 14C-serotonin release from rat mast cells modulated by morphine and endorphins.

The formaldehyde method was used to examine the interaction of PGE1 with morphine, beta-endorphin and Met-enkephalin on rat mast cells by their effects on IgE-mediated 14C-serotonin release. PGE1 (2x10(-8) -2x10(-5) M) caused a dose-related inhibition of the mediator release 1 min after an antigen challenge, and morphine (3x10(-7) -3x10(-5) M) reversed this PGE1 effect dose-dependently and stereospecifically; naloxone (2x10(-4) M) antagonized this action of morphine. Beta-Endorphin (3x10(-7) -10(-5) M) and Met-enkephalin (3x10(-6) -10(-4) M) mimicked this morphine action dose-dependently and were antagonized by naloxone (2x10(-4) M). These results suggest that morphine and endorphins modulate immunological mediator release from rat mast cells through opioid receptors.

Alprostadil↗
PubMed1982

IgE-mediated 14C-serotonin release from passively sensitized rat mast cells: comparative kinetic study with formaldehyde and ice-cold methods.

The kinetics of IgE-mediated release of serotonin from passively sensitized rat mast cells in vitro was studied by stopping 14C-serotonin release with the application of formaldehyde fixative or ice-cold mast cell medium (MCM). Antigen dose-release curves of 14C-serotonin and/or histamine were comparable when mediator release was terminated with either formaldehyde at a final concentration of 1% or ice-cold MCM 15 min after antigen challenge. However, the kinetic study of immunological mediator release stopped by formaldehyde showed that the addition of antigen resulted in a progressive increase of released 14C-serotonin for 7 min, the release curve being sigmoidal, whereas the application of ice-cold MCM artificially enhanced 14C-serotonin and histamine release in the first 2 min. The results suggest that stopping IgE-mediated release of 14C-serotonin with formaldehyde is a simple, rapid and accurate method of studying the kinetics of mediator release from mast cells.

Animals↗
PubMed1982

Endogenous brain angiotensin II-mediated sympathetic nerve responses are not augmented in mature spontaneously hypertensive rats.

Conjugated estrogens injected into the lateral brain ventricle in awake rats elicited behavioral excitation and vasopressor responses. Magnitude of pressor responses was greater in spontaneously hypertensive rats (SHR) than in normotensive Kyoto Wistar rats (WKY). Pressor responses in SHR were abolished by central pretreatments of either captopril or angiotensin II analog. Under urethane anesthesia, conjugated estrogens still produced greater pressor responses in SHR, but accompanying increases in sympathetic nerve firings were the same in both WKY and SHR. These results suggest that while centrally-administered estrogens may activate the brain renin-angiotensin system to increase sympathetic nerve firing and thereby elevated blood pressure, SHR have larger pressor responses only because peripheral vascular reactivity has been increased.

Angiotensin II↗
PubMed1982

The role of brain angiotensin II in the mechanism of the pressor responses to intracisternal injection of hypertonic NaCl in urethane anesthetized rats.

Intracisternal injections of hypertonic NaCl elicited the pressor responses in urethane anesthetized spontaneously hypertensive and normotensive Wistar rats. The intracisternal pretreatment of 1-Sar-8-Ile-angiotensin II, angiotensin II analog, could abolish the pressor responses to intracisternal injections of 5% NaCl in urethane anesthetized spontaneously hypertensive rats, while basal blood pressure was not affected by these pretreatment. Both intracisternal and intravenous administration of captopril, an angiotensin I converting enzyme inhibitor, did not alter the pressor effect of hypertonic NaCl in normotensive rats. Basal blood pressure was lowered by intravenous injection of captopril. The involvement of angiotensin II in the pressor mechanism of hypertonic NaCl was confirmed by the enhanced pressor responses to intracisternal injections of 5% NaCl in urethane anesthetized rats pretreated intracisternally with angiotensin II. These findings suggest that angiotensin II itself could play an important role in the pressor responses to intracisternal injections of hypertonic NaCl without involving a converting enzyme system.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1982

An assay for antibodies to thyroid plasma membrane using the isotope-labeled protein A.

An assay for detection of serum IgG binding to thyroid membrane using 125I-Protein A was examined. The test serum is incubated with purified thyroid membranes, and the IgG bound to the membrane is detected by its interaction with 125I-Protein A. Most of the bound IgG is not bound to the TSH receptor, because TSH does not induce any appreciable decrease in the binding of the IgG to thyroid membranes. Increased serum IgG binding to thyroid membrane is found in most patients with Graves' disease and Hashimoto's thyroiditis, but not in patients with thyroid cancer or simple goiter. Many sera with positive binding activity showed positive microsomal antibody. Serum IgG binding to thyroid membrane in Graves' disease correlates neither with LATS activity nor thyroglobulin antibody. This finding suggests that TSH receptor is not involved in the reaction. The assay method is useful for measuring the binding immunoglobulin for thyroid membrane that is frequently increased in autoimmune thyroid disease, and the present data provide further support to the concept that thyroid autoimmune disorders are associated with antibodies to thyroid cell surface components.

Cell Membrane↗