Biomedical subjects

Hidezo Mori

Publications and source records attributed to Hidezo Mori.

62 records · Page 4Linked to original sources

PubMed2003

Repeated inhalation of adrenomedullin ameliorates pulmonary hypertension and survival in monocrotaline rats.

Adrenomedullin (AM) is a potent vasodilator peptide. We investigated whether inhalation of aerosolized AM ameliorates monocrotaline (MCT)-induced pulmonary hypertension in rats. Male Wistar rats given MCT (MCT rats) were assigned to receive repeated inhalation of AM (n = 8) or 0.9% saline (n = 8). AM (5 mug/kg) or saline was inhaled as an aerosol using an ultrasonic nebulizer for 30 min four times a day. After 3 wk of inhalation therapy, mean pulmonary arterial pressure and total pulmonary resistance were markedly lower in rats treated with AM than in those given saline [mean pulmonary arterial pressure: 22 +/- 2 vs. 35 +/- 1 mmHg (-37%); total pulmonary resistance: 0.048 +/- 0.004 vs. 0.104 +/- 0.006 mmHg.ml(-1).min(-1).kg(-1) (-54%), both P < 0.01]. Neither systemic arterial pressure nor heart rate was altered. Inhalation of AM significantly attenuated the increase in medial wall thickness of peripheral pulmonary arteries in MCT rats. Kaplan-Meier survival curves demonstrated that MCT rats treated with aerosolized AM had a significantly higher survival rate than those given saline (70% vs. 10% 6-wk survival, log-rank test, P < 0.01). In conclusion, repeated inhalation of AM inhibited MCT-induced pulmonary hypertension without systemic hypotension and thereby improved survival in MCT rats.

Administration, Inhalation↗

PubMed2003

Effects of moderate hypothermia on norepinephrine release evoked by ouabain, tyramine and cyanide.

Using the dialysis technique, we examined the effect of moderate hypothermia on the norepinephrine efflux evoked by ouabain, tyramine and cyanide in anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and we measured the dialysate norepinephrine levels as an indicator of norepinephrine output at the cardiac sympathetic nerve endings. Through the dialysis probe, locally applied ouabain, tyramine and cyanide induced the norepinephrine efflux. The addition of desipramine (neuronal norepinephrine transport blocker, 100 microM) suppressed the norepinephrine efflux evoked by ouabain, tyramine and cyanide. This finding suggests that pharmacological agent-induced norepinephrine efflux was due to carrier-mediated outward norepinephrine transport. Moderate hypothermia (27.4 +/- 0.2 degrees C) caused suppression of the norepinephrine efflux evoked by ouabain, tyramine and cyanide. We conclude that moderate hypothermia suppresses the non-exocytotic norepinephrine release evoked by ouabain, tyramine and cyanide.

Animals↗

PubMed2003

Irradiation of intense characteristic x-rays from weakly ionized linear molybdenum plasma.

In the plasma flash x-ray generator, a high-voltage main condenser of approximately 200 nF is charged up to 55 kV by a power supply, and electric charges in the condenser are discharged to an x-ray tube after triggering the cathode electrode. The flash x-rays are then produced. The x-ray tube is a demountable triode that is connected to a turbo molecular pump with a pressure of approximately 1 mPa. As electron flows from the cathode electrode are roughly converged to a rod molybdenum target of 2.0 mm in diameter by the electric field in the x-ray tube, weakly ionized linear plasma, which consists of molybdenum ions and electrons, forms by target evaporation. At a charging voltage of 55 kV, the maximum tube voltage was almost equal to the charging voltage of the main condenser, and the peak current was about 20 kA. When the charging voltage was increased, the linear plasma formed, and the K-series characteristic x-ray intensities increased. The K lines were quite sharp and intense, and hardly any bremsstrahlung rays were detected. The x-ray pulse widths were approximately 700 ns, and the time-integrated x-ray intensity had a value of approximately 35 micro C/kg at 1.0 m from the x-ray source with a charging voltage of 50 kV.

Electrodes↗

PubMed2002

Amelioration of ischemia- and reperfusion-induced myocardial injury by the selective estrogen receptor modulator, raloxifene, in the canine heart.

OBJECTIVES: We sought to investigate whether raloxifene reduces ischemia-reperfusion injury and what mechanisms are involved in the cardioprotective effects. BACKGROUND: Estradiol-17-beta reduces myocardial infarct size in ischemia-reperfusion injury. Raloxifene, a selective estrogen receptor modulator, demonstrates immediate coronary artery vasorelaxing effects. METHODS: The myocardial ischemia-reperfusion model included anesthetized open-chest dogs after 90-min occlusion of the left anterior descending coronary artery (LAD) and subsequent 6-h reperfusion. Raloxifene and/or other drugs were infused into the LAD from 10 min before coronary occlusion to 1 h after reperfusion without an occlusion period. RESULTS: Infarct size was reduced in the raloxifene (5 microg/kg per min) group compared with the control group (7.2 +/- 2.5% vs. 40.9 +/- 3.9% of the area at risk, p < 0.01). Either N(G)-nitro-L-arginine methyl ester (L-NAME), the inhibitor of nitric oxide (NO) synthase, or charybdotoxin, the blocker of Ca(2+)-activated K+ (K(Ca)) channels, partially attenuated the infarct size-limiting effect, and both of them completely abolished the effect. The incidence of ventricular fibrillation was also less in the raloxifene group than in the control group (11% vs. 44%, p < 0.05). Activity of p38 mitogen-activated protein (MAP) kinase increased with 15-min ischemia, and raloxifene pretreatment inhibited the activity. Myeloperoxidase activity of the 6-h reperfused myocardium was also attenuated by raloxifene. CONCLUSIONS: These data demonstrate that raloxifene reduces myocardial ischemia-reperfusion injury by mechanisms dependent on NO and the opening of K(Ca) channels in canine hearts. Deactivation of p38 MAP kinase and myeloperoxidase by raloxifene may be involved in the cellular mechanisms of cardioprotection.

Animals↗

PubMed2002

Disruption of vagal efferent axon and nerve terminal function in the postischemic myocardium.

Despite the importance of vagal control over the ventricle, little is known regarding vagal efferent conduction and nerve terminal function in the postischemic myocardium. To elucidate postischemic changes in the cardiac vagal efferent neuronal function, we measured myocardial interstitial acetylcholine (ACh) levels by using in vivo cardiac microdialysis and examined the ACh responses to electrical stimulation of the vagi or local administration of ouabain in anesthetized cats. Sixty-minute occlusions of the left anterior descending coronary artery (LAD) followed by 60-min reperfusion abolished electrical stimulation-induced ACh release (20.4 +/- 3.9 vs. 0.9 +/- 0.4 nmol/l; means +/- SE, P < 0.01). In different groups of animals, 60-min LAD occlusion followed by 60-min reperfusion decreased but did not completely abolish ouabain-induced release of ACh (9.2 +/- 1.8 vs. 3.9 +/- 0.7 nmol/l; P < 0.05). These results indicate that function of the vagal efferent axon was completely interrupted, whereas the local ACh release was partially suppressed in the postischemic myocardium. The postischemic disruption of vagal efferent neuronal function might exert deleterious effects on cardiac regulation.

Acetylcholine↗

PubMed2002

Modulatory effects of ketamine on catecholamine efflux from in vivo cardiac sympathetic nerve endings in cats.

With the use of the microdialysis technique, we examined the modulatory effect of ketamine on catecholamine efflux from in vivo cardiac sympathetic nerve endings. A dialysis probe was implanted in the left ventricular myocardium, and dialysate norepinephrine (NE) levels in anesthetized cats were measured with liquid chromatogram-electrical detection. A 60-min occlusion of the left anterior descending coronary artery caused increases in dialysate NE levels. Through the dialysis probe, locally applied ketamine (10 mM) augmented the dialysate NE responses to coronary occlusion in the presence and absence of desipramine (membrane NE transport blocker). Thus, the ketamine-induced NE increment is not mediated through the neuronal NE transporter. The sympathomimetic action of ketamine may augment the NE efflux evoked by myocardial ischemia.

Adrenergic Uptake Inhibitors↗

PubMed2002

Effects of brief ischaemia on myocardial acetylcholine and noradrenaline levels in anaesthetized cats.

Although brief ischaemic events make the myocardium tolerant to subsequent prolonged ischaemia, known as ischaemic preconditioning, whether brief ischaemia also affects neural regulation at the in vivo heart remains unknown. We examined the effects of brief ischaemia on myocardial interstitial acetylcholine (ACh) and noradrenaline (NA) levels in anaesthetized cats (n = 6). Baseline ACh and NA levels were 0.65 +/- 0.13 and 0.66 +/- 0.17 nmol l(-1) (mean +/- SE), respectively. Two sets of 5-min brief occlusion followed by 20-min reperfusion of the left anterior descending coronary artery (LAD) significantly increased the myocardial interstitial ACh level to 4.6 +/- 0.7 nmol l(-1) (P < 0.01), while not affecting the myocardial interstitial NA level. Subsequent 60-min LAD occlusion significantly increased the ACh and NA levels to 34.9 +/- 6.0 and 96.5 +/- 17.0 nmol l(-1) (P < 0.01), respectively. Vagotomy abolished the myocardial interstitial ACh release during brief ischaemia and attenuated the ACh release during subsequent 60-min ischaemia (n = 6). In contrast, vagotomy did not affect the subsequent ischaemia-induced myocardial interstitial NA release. We conclude that the brief ischaemia affects myocardial interstitial ACh release but not NA release in the ischaemic myocardium in vivo.

Acetylcholine↗

PubMed2002

Inhomogeneous vasodilatory responses of rat tail arteries to heat stress: evaluation by synchrotron radiation microangiography.

Tail blood flow is crucial for dissipating body heat in rats. Angiographies are convenient tools to evaluate tail circulation. However, conventional angiographies do not have sufficient sensitivity or spatial resolution for small vessels. Recently, we developed a novel microangiographic system using monochromatic synchrotron radiation and a high-definition video camera system. Here, we report an evaluation of rat tail circulation under heat stress using the synchrotron radiation microangiographic system. We performed an experiment using the microangiography of the caudal artery before and after heating up WKAH/HkmSlc rats to rectal temperature of 39 degrees C. The images were digitized and temporal subtraction was performed, and the diameters of caudal arteries were evaluated. After heating, the medial caudal artery was markedly dilated (320 +/- 53 to 853 +/- 243 micro m in diameter, p<0.001), while no significant change was observed in the lateral caudal arteries (139 +/- 42 to 167 +/- 73 micro m) and segmental anastomosing vessels. The heat stress allowed for visualization of the superficial caudal arteries with a diameter of approximately 60 micro m, not visible prior to heating. Thus, synchrotron radiation microangiography demonstrated that the rat tail possessed dual sets of arteries; one set was highly sensitive to heat-induced vasodilation (medial caudal artery and superficial caudal arteries) and the other set was less sensitive (lateral caudal arteries and segmental anastomosing vessels).

Angiography↗