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Biomedical subjects

K Tobise

Publications and source records attributed to K Tobise.

At least 37 records · Page 2Linked to original sources
PubMed1995

Transforming growth factor-beta 1 proliferated vascular smooth muscle cells from spontaneously hypertensive rats.

To clarify whether the growth inhibitors, transforming growth factor-beta 1 (TGF-beta 1), heparin, and interferon-gamma (IFN-gamma) contribute to the development of vascular hypertrophy in spontaneously hypertensive rats (SHR), the growth of vascular smooth muscle cells (VSMC) was evaluated both for cell numbers over a period of 4 days, and [3H]thymidine incorporation over 24 h. Heparin and IFN-gamma inhibited the proliferation of VSMC from SHR and Wistar-Kyoto (WKY) rats. TGF-beta 1 enhanced SHR-VSMC proliferation by 16.6 +/- 8.9%; in contrast TGF-beta 1 inhibited WKY-VSMC proliferation by 60.5 +/- 7.4%. There was no difference in affinity, number of binding sites, or subtype expression of TGF-beta 1 receptor between SHR-VSMC and WKY-VSMC. This evidence suggests that the signal transduction system of TGF-beta 1 either the receptor itself or downstream signaling molecules, may be altered in SHR-VSMC versus WKY-VSMC. This abnormal responsiveness to TGF-beta 1 is involved in the proliferative characteristics of SHR-VSMC. Therefore, TGF-beta 1 could contribute to the development of hypertension or vascular hypertrophy in SHR.

Animals↗
PubMed1995

Comparison of 5-hydroxytryptamine-induced contraction of rat pulmonary artery to that of aorta in vitro.

We investigated the nature of the contraction produced by 5-hydroxytryptamine (5-HT) in the rat pulmonary artery, and compared it with that produced in the rat aorta. Both ketanserin and ritanserin inhibited 5-HT-induced contraction in the pulmonary artery non-competitively. In contrast, ketanserin competitively antagonized the contraction in the aorta. Bunazosin, a selective alpha 1-blocker, partially inhibited 5-HT-induced contraction in the pulmonary artery, but not in the aorta. In both the pulmonary artery and aorta, 8-OH-DPAT, a 5-HT1A selective agonist, produced a concentration-dependent contraction. In the pulmonary artery, 5-HT and 8-OH-DPAT produced contractions with similar potencies. In contrast, 8-OH-DPAT was less potent than 5-HT in the aorta. Bunazosin inhibited 8-OH-DPAT-induced contraction in both vessels. However, pindolol, a 5-HT1A antagonist, did not inhibit 8-OH-DPAT-induced contraction in the pulmonary artery. These results suggest that 5-HT produces contraction via not only 5-HT2 receptor, but also non-5-HT2 receptor (probably alpha 1-adrenoceptor) in the rat pulmonary artery. Furthermore, 8-OH-DPAT does not activate the 5-HT1A receptor to produce a contraction, but does activate other receptors which interact with alpha 1-adrenoceptor.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1995

[A case of rhabdomyolysis complicated with myocardial injury].

A 22-year-old man developed transient unconsciousness during running. He developed fever, nausea, vomiting, diarrhea and general fatigue. Next day, he was admitted to National Hospital Nayoro because of high serum CK level of 13,610U/l. Biochemical analyses revealed elevated serum myoglobin, increased CK-MM isozyme, aldolase and lactate dehydrogenase, increased serum osmolality, increased uric acid, and decreased serum potassium levels. Therefore, he was diagnosed as having rhabdomyolysis. In addition, serum CK-MB isozyme, cardiac myosin light chain I and troponin T were increased, suggesting the damage of cardiac muscle. Electrocardiogram showed elevated ST segment and inverted T on V2-4, which were not observed previously. He had no preceding infectious disease, drug ingestion or an underlying metabolic disorder. The rhabdomyolysis may be precipitated by the superimposition of dehydration and loss of potassium due to diarrhea and vomiting. The myocardial injury, probably produced by transient myocardial ischemia, should be paid attention in case of rhabdomyolysis.

Adult↗
PubMed1994

Absence of antioxidant effects of nifedipine and diltiazem on myocardial membrane lipid peroxidation in contrast with those of nisoldipine and propranolol.

Both the production of active oxygen species and cellular damage due to concurrent lipid peroxidation are believed to be important factors in the pathogenesis of cardiovascular diseases and the ageing process. Since cardiovascular drugs are often administered over a long term, it might be advantageous if they reduced lipid peroxidation. There have been conflicting reports concerning the antiperoxidant effect of nifedipine. Therefore, we investigated whether nifedipine could inhibit lipid peroxidation in a nonenzymatic active oxygen-generating system, utilizing rat crude myocardial membranes, and compared its effect with those of propranolol, nisoldipine, and diltiazem. Nifedipine and diltiazem had no inhibitory effects on the lipid peroxidation of myocardial membranes. In contrast, nisoldipine and propranolol had a concentration-dependent antiperoxidant effect, with IC50 values of 28.2 and 50.1 microM, respectively. In addition, nisoldipine appeared to possess dual antiperoxidant mechanisms, involving both preventive and chain-breaking properties.

Animals↗
PubMed1994

Changes in type VI adenylyl cyclase isoform expression correlate with a decreased capacity for cAMP generation in the aging ventricle.

We investigated the developmental regulation of the beta-adrenergic receptor-Gs-adenylyl cyclase pathway in myocardial membranes from fetal, neonatal, adult, and mature adult rats by measuring the density of the beta-adrenergic receptor and the activities of the stimulatory guanine nucleotide-binding protein Gs and the adenylyl cyclase enzyme. Total beta-adrenergic receptor content (in femtomoles per milligram protein) was greatest in the fetal (124.4 +/- 20.5 fmol/mg) and neonatal (122.3 +/- 16.1 fmol/mg) stages and gradually decreased in the adult (90.9 +/- 8.0 fmol/mg) and mature adult (70.0 +/- 9.6 fmol/mg) stages. An equivalent pattern was seen for adenylyl cyclase activity: the basal activity of the effector enzyme or that measured in the presence of 0.1 mmol/L isoproterenol with 0.1 mmol/L Gpp(NH)p, 10 mmol/L NaF, or 0.05 mmol/L forskolin was greater in the fetus and the neonate than in the adult and the mature adult. These data suggested that decreased stimulation of the catalytic unit by Gs could be the underlying cause of diminished adenylyl cyclase activity with aging. However, quantification of Gs by reconstitution into S49 cyc- membranes (in picomoles cAMP per microgram for 10 minutes) demonstrated no significant decrease during development from fetus (1.55 +/- 0.1 pmol/microgram) to neonate (1.9 +/- 0.5 pmol/microgram) and subsequent aging to adult (2.6 +/- 0.2 pmol/micrograms) and mature adult (1.9 +/- 0.2 pmol/microgram). When Northern blot analysis was used to characterize the relative amounts of mRNA coding for Gs alpha, no significant differences were seen among the developmental stages studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1994

Intraventricular changes in the beta-adrenoceptor-adenylate cyclase system of the rat heart with the progress of monocrotaline-induced right ventricular hypertrophy.

We investigated the changes in the membranous beta-adrenoceptor-adenylate cyclase system in the right ventricle, left ventricle and interventricular septum during the progress of monocrotaline-induced right ventricular hypertrophy and failure. The beta-adrenoceptor density was decreased in hypertrophied right ventricle 2 to 4 weeks after treatment. When the rats showed symptoms of right ventricular failure 4 weeks after treatment, the beta-adrenoceptor density was decreased in the interventricular septum. Both basal and forskolin-stimulated adenylate cyclase activities were decreased in the right ventricle at 3 and 4 weeks, and in the interventricular septum at 4 weeks, after treatment, which indicates that the catalytic activity of adenylate cyclase is reduced. Changes in isoproterenol plus Gpp (NH) p- or sodium fluoride-stimulated adenylate cyclase activity were generally similar to those in basal activity. These data indicate that a chamber-specific decrease in beta-adrenoceptor density begins in the early stages of right ventricular hypertrophy, and that beta-adrenoceptor density and adenylate cyclase activity in the interventricular septum are decreased in the advanced stages of heart failure in monocrotaline-treated rats.

5'-Nucleotidase↗
PubMed1993

Role of endothelium in biphasic hypoxic response of the isolated pulmonary artery in the rat.

We investigated the roles of the endothelium in the hypoxic responses of the isolated main pulmonary artery (PA) in the rat. Hypoxia was induced by gassing an organ chamber with 95% N2 + 5% CO2 (PO2 = 34.6 +/- 3.1 Torr) instead of 16% O2 + 5% CO2 + balance N2 (PO2 = 92.8 +/- 3.0 Torr). Vascular rings were precontracted with 2 x 10(-8) M phenylephrine. A transient hypoxic contraction and a subsequent relaxation were observed in the endothelium-intact rings. The hypoxic contraction was reduced in the endothelium-denuded rings. In contrast, there were no significant differences between the hypoxic relaxation in the endothelium-intact and endothelium-denuded rings. Inhibitors of endothelium-derived relaxing factor (EDRF) activity, 2 x 10(-6) M NG-monomethyl-L-arginine (L-NMMA) and 10(-6) M methylene blue, produced 53% and 66% reductions in hypoxic contraction, respectively, Furthermore, the amount of cyclic GMP in the endothelium-intact PA rings which had been precontracted with phenylephrine decreased from 2.10 +/- 0.45 pmol/mg protein during normoxia to 0.90 +/- 0.18 pmol/mg protein during hypoxia. Indomethacin and OKY-046 did not influence hypoxic contraction or relaxation. These results suggest that hypoxic contraction of the isolated pulmonary artery in the rat is partially induced by inhibition of the release of EDRF.

Animals↗
PubMed1993

A case report of isolated levocardia without intracardiac anomalies associated with sick sinus syndrome.

A 42-year-old female with cardiomegaly showed bradycardia without syncope. Clinical data showed that she had an isolated levocardia with interruption of the inferior vena cava. Isolated levocardia was defined as a normally placed heart associated with situs ambiguus of other viscera. She did not have intracardiac anomalies. Isolated levocardia without intracardiac anomalies, as in this case, has only been reported in 13 other cases. Isolated levocardia is often accompanied by severe complex intracardiac anomalies and, therefore, most of the patients have a short life span. Situs ambiguus, especially left isomerism, is frequently associated with deteriorated sinus node function, and an interruption of the inferior vena cava may also be an indication of this phenomenon. Therefore, the patient's sinus node function was examined using an electrophysiological study and a 24-hour ambulatory electrocardiogram. Sick sinus syndrome was finally confirmed.

Adult↗
PubMed1992

Time course of pulmonary vascular response to an acutely repetitive pulmonary microembolism in dogs--an analysis using pulmonary vascular impedance.

To understand the mechanism leading to progressive pulmonary hypertension, we investigated the time course of vascular response to an acutely repetitive pulmonary microembolism in dogs by using pulmonary vascular impedance. In a normal state, the mean pulmonary arterial pressure (mPAP) was transiently increased by emboli, and the impedance moduli of 0 Hz (= Rin), 1.5 Hz and 3 Hz were slightly increased. A four-element electrical vascular model showed the transient increase in peripheral pulmonary vascular resistance (R2) and inertia, and reduction in compliance (C). In contrast, in a state of a slight pulmonary hypertension, mPAP was continuously increased by the same amount of emboli, and the impedance moduli of both 0 Hz and 3 Hz were significantly increased. By a four-element model, a severe increase in R2 and reduction in C were observed, and these changes continued. Therefore, although the vascular response to pulmonary microembolism basically depends on the degree of mechanical obstruction, this response is thought to be modulated by the responsiveness of pulmonary vessels at that time, which is involved in the alteration in the local characteristics of pulmonary vessels, and/or the recruitment of a new blood flow.

Acute Disease↗
PubMed1992

Site of hypoxic pulmonary vasoconstriction in pulsatile perfused canine lung lobes.

To elucidate the site of hypoxic pulmonary vasoconstriction (HPV) in the dynamic lung, we studied the effect of alveolar hypoxia (0 approximately 4% O2) on excised canine lung lobes with pulsatile perfusion from artery to vein (antegrade perfusion: AP) or vein to artery (retrograde perfusion: RP), and compared responses to hypoxia with those to serotonin and histamine. In our preparation, increases in the pulmonary vascular resistance (R) resulted in a wide range of decreases in the flow wave amplitude at the lobar inflow site (FA). These decreases in FA reflected reductions in the compliance of the vasculature proximal to the main site of resistance. The FA/R ratios of serotonin were 2.29 in AP and 0.24 in RP indicating the predominant arterial constriction, those of histamine were 0.07 in AP and 1.24 in RP indicating the selective venous constriction. In contrast, the responses to hypoxia were 0.38 in AP and 0.42 in RP. These results suggest that HPV occurs not only on the arterial side but on the venous side in the dynamic lung, and the main site of HPV is located in the peripheral pulmonary vasculature, between muscular arteries and veins which are constricted by serotonin and histamine.

Animals↗
PubMed1992

The effect of acute hypoxia on left ventricular function with special reference to diastolic function--an analysis using ultrasonic method.

In order to evaluate the effect of acute hypoxia on left ventricular (LV) contractility and diastolic function, hemodynamics and LV wall motion were investigated in anesthetized open-chest paced dogs using M-mode or pulsed Doppler echocardiography. Animals were ventilated with 10% oxygen (Hypo 1) and 6.3% oxygen (Hypo 2). LV contractility and diastolic functions were enhanced under "Hypo 1" and at an early phase of "Hypo 2". However, LV functions, both systolic and diastolic, were simultaneously reduced in the presence of hypercapnic acidosis by "Hypo 2". Peak velocities of diastolic rapid filling flow (R) and atrial contraction flow (A) were increased under "Hypo 1", but showed a biphasic change (an increase and a subsequent decrease) under "Hypo 2". The ratio of A/R, known as an index of LV diastolic function, was not altered under hypoxia alone or even under hypercapnic acidosis. Even when hypoxia seems to enhance LV contractility, LV function has already begun to be depressed with a reduction of pH. This seems, however, to be compensated for by LV dilatation and increase in preload, or preservation of left atrial performance.

Acidosis↗
PubMed1992

[Effect of potassium channel openers on hypoxic pulmonary vasoconstriction].

The ATP-sensitive potassium channel (K+ATP) has been suggested as an important mechanism for the reactivity of vascular smooth muscle. We investigated the effects of K+ channel openers (lemakalim, pinacidil) on hypoxic pulmonary vasoconstriction (HPV) and angiotensin II (Ag II) induced vasoconstriction in isolated rat lungs (Sprague-Dawley rats: 300-450 g). Ventilation with hypoxic gas (2% O2, 5% CO2) was performed for 6 min after the injection of Ag II (0.1 microgram). Isolated lungs were perfused under constant flow (0.04 ml/g/min) using 20 ml of blood from donor rat. The perfusion pressure was used as the pulmonary artery pressure. Lemakalim or pinacidil was pre-administered through the reservoir. Pretreatment with pinacidil (10(-4) M) or lemakalim (10(-5) M) inhibited the pressor response to hypoxia, but did not inhibit the response to angiotensin II. Although the effect of lemakalim on HPV was reversed by administration of glibenclamide (10(-5) M) or tolbutamide (10(-3) M), the effect of pinacidil on HPV was not influenced by either drug. These results suggest that 1) K+ channel openers (lemakalim and pinacidil) inhibit the pressor response to hypoxia, and 2) lemakalim seems to act through K+ATP, whereas pinacidil may have other mechanisms of inhibition of vascular smooth muscle contraction. K+ATP may play an important role in the regulation of pulmonary vascular reactivity to hypoxia.

Angiotensin II↗
PubMed1991

Prolonged period of global ischemia causes no change in the GTP-binding proteins in the isolated perfused rat heart.

The response of the beta-adrenoceptor transduction system to global ischemia for 40 min was investigated in isolated working heart of rat. The enhancement of beta-adrenoceptors was not observed in the ischemic myocardium. A depression of forskolin-stimulated adenylate cyclase enzyme occurred with global ischemia, but no change in Gs or Gi2 was detected. Thus, the present in vitro ischemic heart model may not necessarily reflect the identical milieu induced by the in vivo myocardial ischemia.

Adenylyl Cyclases↗
PubMed1991

Transient pulsus alternans induced by isosorbide dinitrate: echocardiographic and hemodynamic evidence of reduced venous return--a case report.

Transient pulsus alternans was induced by isosorbide dinitrate (ISDN) in a patient with postmyocarditis congestive heart failure under diuretic therapy. The severity and duration of pulsus alternans depended on the dose of ISDN. According to the echocardiographic and hemodynamic examinations, the superimposed preload reduction caused by ISDN combined with decreased blood volume owing to diuretic therapy most likely contributed to the development of pulsus alternans.

Adult↗