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Biomedical subjects

M Kohno

Publications and source records attributed to M Kohno.

At least 451 records · Page 25Linked to original sources
PubMed1988

[Management of hemoperitoneum due to rupture of visceral branches of the aorta with a cylinder-type balloon catheter].

We have designed a cylinder-type balloon catheter and devised a new procedure for the management of the aneurysm in a condition difficult for treatment. This balloon catheter consists of a balloon located at the tip of a catheter. The balloon has a central lumen for maintaining the distal aortic bloodflow and can be inflated at various intended sites. The catheter with a deflated balloon was inserted into the abdominal aorta upward through a vascular graft sutured at the side of the aorta. In the case of a ruptured visceral artery, e.g., celiac axis or superior mesenteric artery, controlling of hemorrhage is very difficult because the ruptured lesion is surrounded by an intricate anatomical structure and therefore it is necessary to do the highly invasive procedure of aortic cross-clamping. Therefore we attempted this time to use the device in the management of this disease. In experimental investigation in dogs, this balloon selectively blocked the blood flow to the visceral branches successfully while maintaining the distal aortic flow. With this method, the various hemostatic procedures can be performed satisfactorily without concern for complications, namely renal failure provided that hemorrhage is easy to control in a short time without the aortic clamp. As mentioned above, this instrument will be useful for the management of rupture of the visceral artery and so reduce its mortality rate.

Animals↗
PubMed1987

Induction of cytochrome P-450 and related drug-oxidizing activities in muscone (3-methylcyclopentadecanone)-treated rats.

In the present study, we investigated the effects of muscone on both in vitro and in vivo parameters of the hepatic microsomal drug-metabolizing enzyme system and other enzyme activities in rats. In the in vivo study, the serum dimethadione (DMO)/trimethadione (TMO) ratios at 2 hr after oral administration of TMO (100 mg/kg) were significantly increased in both male and female rats treated with 75 and 150 but not 40 mg muscone/kg. Antipyrine metabolite profile in 24 hr urine of rats pretreated with muscone (150 mg/kg) was examined. The results showed that the excretion of norantipyrine was significantly increased as compared to the control group. In the in vitro study, we found that the content of cytochrome P-450, and activities of aminopyrine, N-demethylase, aniline hydroxylase and delta-aminolevulinic acid (ALA) synthetase were significantly increased as compared to the controls in both male and female rats treated with muscone (75 and 150 mg/kg). This type of induction of the hepatic metabolizing enzymes was similar to that seen after treatment with a prototype drug, phenobarbital.

5-Aminolevulinate Synthetase↗
PubMed1987

Decreased intracellular free magnesium in erythrocytes of spontaneously hypertensive rats.

Using 31p-NMR (the phosphorus nuclear magnetic resonance) spectroscopy, we measured intracellular free Mg levels in the erythrocytes of untreated (n = 7) and diltiazem-treated spontaneously hypertensive rats (SHR) (n = 8), and compared them with age-matched Wistar-Kyoto rats (WKY) (n = 10). The intracellular free Mg levels were significantly (p less than 0.01) decreased in untreated SHR compared with those in control WKY. A successful antihypertensive treatment with diltiazem increased the intracellular free Mg levels compared with untreated SHR (p less than 0.05). Furthermore, an inverse correlation was observed between intracellular free Mg levels and blood pressure levels in all groups (r = -0.48, p less than 0.01, n = 25). These observations suggest that abnormalities of intracellular Mg metabolism may be, in part, related to the development or the maintenance of hypertension in SHR.

Animals↗
PubMed1987

Characterization of interleukin 2-stimulated phosphorylation of 67 and 63 kDa proteins in human T-cells.

We have investigated rapid and marked phosphorylation of cellular proteins induced by interleukin 2 (IL-2) in both phytohaemagglutinin-stimulated normal peripheral blood leucocytes, and IL-2-dependent or -independent human T-cell lines bearing human T-cell leukaemia (lymphotropic) virus type I. Two-dimensional electrophoretic analysis showed that the IL-2-induced phosphoprotein was of Mr 67,000 with a pI of 5.8 (pp67) and was distinct from the IL-2 receptor. IL-2 also stimulated phosphorylation of four other proteins, with an Mr of 63,000 and pI values 5.3-6.1 (pp63s). The stimulation of pp67 phosphorylation was observed within 5 min after addition of IL-2 and was maximal after 15 min. The maximal phosphorylation was more than 10-fold that observed initially. In IL-2-dependent cells, IL-2 dose responses of pp67 phosphorylation and cell proliferation were exactly correlated. Phosphoamino acid analysis showed that the phosphorylation site of pp67 and pp63s was a serine residue. Subcellular-fractionation studies indicated that pp67 was localized in cytosol, whereas pp63s phosphorylation was induced by IL-2 in nuclear and cytosol fractions. Similar phosphorylation of pp67 and pp63s was observed when the cells were treated with phorbol 12-myristate 13-acetate instead of IL-2. These results suggest that IL-2-IL-2-receptor interaction leads to activation of protein kinase(s), resulting in phosphorylation of certain cellular proteins such as pp67 and pp63s, and that this phosphorylation could be an early event in the transmission of intracellular growth signalling from the IL-2 receptors.

Cell Division↗
PubMed1987

Left ventricular wall motion at rest in patients with organic coronary artery disease vs coronary spasm.

Left ventricular ejection fractions and regional ejection changes obtained from left ventriculograms at rest were analyzed in 15 normal subjects, in 17 patients with isolated, organic left anterior descending coronary artery disease, and in 11 patients with isolated left anterior descending coronary artery spasm. Patients with coronary artery spasm did not have significant organic lesions at the site of spasm. All patients with organic coronary artery disease and coronary artery spasm had a history of angina pectoris without myocardial infarction. No significant differences in ejection fraction were observed among the three groups. The regional ejection change of the anterolateral and apical wall supplied by the left anterior descending coronary artery was significantly decreased in patients with organic coronary artery disease compared with those in normal subjects (anterolateral 39.5 +/- 10.3% vs 48.4 +/- 7.7%, p less than 0.05; apical 48.4 +/- 8.8% vs 55.6 +/- 7.8%, p less than 0.05). However, the anterolateral and apical wall motion was not impaired in patients with coronary artery spasm. Thus, patients with organic coronary artery disease had impairment of left ventricular wall motion, while those with coronary artery spasm did not, although both groups of patients had symptoms of angina. These results suggest that patients with organic coronary artery disease may have had coronary blood flow disturbances through stenosed vessels and chronic active ischemia that produced left ventricular impairment.

Coronary Disease↗
PubMed1987

Circulating atrial natriuretic polypeptide in essential hypertension.

To investigate the significance of atrial natriuretic polypeptide (ANP) in essential hypertension, we measured plasma ANP concentrations in 43 subjects with essential hypertension uncomplicated by cardiac or renal failure, in 16 subjects with borderline hypertension, and in 17 normotensive control subjects. Plasma ANP levels were significantly higher in hypertensive subjects compared to borderline hypertensive subjects (p less than 0.05) and normotensive control subjects (p less than 0.05). Hypertensive subjects with left ventricular hypertrophy (LVH) had higher plasma ANP levels than the hypertensive group as a whole (p less than 0.05). A significant positive correlation was observed between mean blood pressure and plasma ANP level in the hypertensive group (n = 43, gamma = 0.77, p less than 0.01). Furthermore, plasma ANP level was decreased significantly after 4 weeks of effective antihypertensive therapy compared with the initial value (p less than 0.05). These results suggest that plasma ANP is frequently elevated in hypertensive subjects with markedly high blood pressure or LVH, and it can be reduced by effective therapy with antihypertensive drugs.

Adult↗
PubMed1987

Circulating atrial natriuretic peptides in hyperthyroidism and hypothyroidism.

Plasma concentrations of atrial natriuretic peptides were measured in 32 normal control subjects, 25 patients with hyperthyroidism, and 18 patients with hypothyroidism. Atrial natriuretic peptide values were measured before and after successful therapy with methimazole or 1-thyroxine. Plasma atrial natriuretic peptide concentration was increased in patients with hyperthyroidism (48.0 +/- 19.5 pg/ml) but was decreased in patients with severe hypothyroidism (16.3 +/- 5.7 pg/ml) compared with values in normal control subjects (31.2 +/- 9.5 pg/ml). There was no significant difference between values in normal control subjects and mildly hypothyroid patients (35.0 +/- 12.2 pg/ml). The plasma atrial natriuretic peptide concentration was correlated with the serum thyroxine level and heart rate. The elevated atrial natriuretic peptide concentration in hyperthyroidism decreased, whereas the reduced atrial natriuretic peptide concentration in severe hypothyroidism increased, compared with the initial value after successful therapy. These results suggest that plasma atrial natriuretic peptide concentration is frequently increased in hyperthyroidism and is frequently decreased in severe hypothyroidism, and that thyroid hormone is one of the regulatory factors for circulating atrial natriuretic peptides.

Adult↗
PubMed1987

Evaluation of aortic wall distensibility by aortic pressure-dimension relation: effects of nifedipine on aortic wall.

The relation between aortic pressure and dimension was studied before and after nifedipine infusion in eight anaesthetised dogs. An electromagnetic flowmeter was positioned in the proximal ascending aorta and one pair of ultrasonic dimension gauges attached to the thoracic aorta. A Millar micromanometer was positioned just below the dimension gauges. A constrictor was placed around the thoracic aorta distal to the dimension gauges to produce an abrupt rise in aortic pressure for 15 s. After complete recovery nifedipine (0.75 micrograms.kg-1.min-1) was infused for 10 min and the same procedure repeated. The ratio (delta D:delta P) of the difference (delta D) between maximum and minimum dimensions (D) to the pulse pressure (delta P) and the percentage distensibility (delta D/delta P/minimum D) were decreased significantly after aortic constriction (0.037(0.013) to 0.019(0.004) mm.mmHg-1 and 0.247(0.075) to 0.121(0.033)%.mmHg-1, p less than 0.01, respectively), suggesting that these indices depend on afterload. Beat to beat mean pressure-dimension relations during the release of aortic constriction showed a convex upward curve and was fitted by an exponential function with a high correlation coefficient (r = 0.99). The slope of this relation was significantly reduced after nifedipine compared with before nifedipine (379(83) to 330(119) mmHg.cm-1, p less than 0.05), suggesting an increase in aortic distensibility by nifedipine. When mean aortic pressure or stroke volume before and after nifedipine was compared at the same mean dimension, which was reduced by 5% of the control mean dimension, stroke volume increased to 128%(p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1987

Involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in spontaneously hypertensive rats.

The hypotensive effect of bromocriptine in young (6 week old) spontaneously hypertensive rats (SHR) was studied. Blood pressure and plasma norepinephrine level in bromocriptine-treated SHR were significantly lower than those in vehicle-treated SHR after 3 weeks of treatment (5 mg/kg per day, i.p.), while no significant decrease of blood pressure or plasma norepinephrine level was observed after 2 weeks of treatment. These results suggest the involvement of sympathetic nervous system inhibition in the hypotensive effect of bromocriptine in SHR.

Aging↗
PubMed1987

Effects of volume change on circulating immunoreactive atrial natriuretic factor in rats.

The mammalian atrial hormone atrial natriuretic factor (ANF) has been shown to have potent natriuretic and diuretic actions as well as vasodilator effects when released into the circulation. To investigate how the levels of the circulating form of this peptide change with alteration of intravascular fluid volume, we measured immunoreactive ANF in the plasma of Wistar rats after acute saline load, acute furosemide treatment, and chronic water restriction. Circulating levels of immunoreactive ANF increased significantly (p less than 0.001) 1 minute after acute saline load and returned to normal levels within 5 minutes. Volume contraction induced by furosemide treatment of chronic water restriction significantly reduced the circulating immunoreactive ANF. These data indicate that acute volume expansion causes an immediate release of immunoreactive ANF into the general circulation and acute volume contraction results in a decline of circulating levels of immunoreactive ANF, which is maintained during chronic volume contraction. These results suggest that the atria detect alterations in intravascular fluid volume and respond by changing the levels of ANF acutely as well as chronically and thereby participate in the regulation of body fluids and, perhaps, of blood pressure.

Animals↗
PubMed1987

Central alpha 2-adrenergic stimulation increases neurointermediate lobe immunoreactive beta-endorphin in spontaneously hypertensive rats.

A possible influence of the central alpha 2-adrenergic system on beta-endorphin was examined in rat anterior pituitary, neurointermediate lobe, and plasma. The concentration of beta-endorphin in anterior pituitary, neurointermediate lobe, and plasma was determined by radioimmunoassay 15 minutes after subcutaneous injection of clonidine in 14-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Clonidine reduced the concentration of the plasma beta-endorphinlike immunoreactivity in SHR and to a lesser extent in WKY. No significant changes in the concentration of beta-endorphinlike immunoreactivity were observed in anterior pituitary. Clonidine increased the concentration of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR in a dose-related manner but did not affect the concentration in WKY. Administration of yohimbine (1 mg/kg) completely blocked the clonidine-induced increase of neurointermediate lobe beta-endorphinlike immunoreactivity in SHR, while prazosin (1 mg/kg) had no effect. These data suggest that the central alpha 2-adrenergic activation increases the neurointermediate lobe concentration of beta-endorphinlike immunoreactivity in SHR by suppressing beta-endorphin release from the neurointermediate lobe into the circulation.

Animals↗
PubMed1987

Studies on the monoexponential nature of the left ventricular pressure fall during isovolumic relaxation period in the diseased heart.

Our recent clinical studies on the negative dP/dt upstroke pattern suggested that the left ventricular pressure (LVP) deviated from the exponential curve during isovolumic relaxation period (IRP) in diseased hearts. To examine this further two types of monoexponential curve fitting were done in various heart diseases (normal (N): 8, angina pectoris (AP): 8, myocardial infarction (MI): 13, hypertrophic cardiomyopathy (HCM): 10, dilated cardiomyopathy (DCM): 8). LVP was measured by a Millar's catheter-tip transducer, and four types of time constant (T1-T4) were derived: T1 was calculated by an exponential curve fitting e-t/T1 + B (B is constant), T2 by the ratio Pm/peak (-) dP/dt (Pm is LVP at peak (-) dP/dt), T3 by the best exponential curve fit e-t/T3 + B + C (C is constant), and T4 by the ratio (Pm-C)/peak (-) dP/dt. If the exponential curve fitting was reasonable, the relation between T1 and T2, or T3 and T4, should be on the line of identity. The result was as follows: T2 = 1.4 T1 - 6.1 (r = 0.84) and T4 = 1.1 T3 - 10.7 (r = 0.94). Additionally, C (mmHg) in MI (-26 +/- 15), HCM (-36 +/- 19) and DCM (-32 +/- 20) were lower (p less than 0.05) than in N (-13 +/- 7). These findings suggest that the LVP during IRP could deviate from the monoexponential curve and that careful attention should be given to calculate the time constant in diseased hearts.

Adult↗