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Biomedical subjects

O Iimura

Publications and source records attributed to O Iimura.

At least 271 records · Page 15Linked to original sources
PubMed1977

Studies on the role of sympathetic nervous system in the mechanism of essential hypertension.

In order to investigate a role of sympathetic nervous system in the mechanism of blood-pressure elevation in essential hypertension, urinary catecholamines, serum dopamine-beta-hydroxylase (DBH) activity and a pressor response to infused noradrenaline (noradrenaline response) were measured, in the patients with essential hypertension, before and 2 weeks-rest after hospitalization or following salt restriction. In addition, plasma renin activity (PRA) and water-sodium contents were determined and a correlation between these variables and noradrenaline excretion, serum DBH or noradrenaline response was observed. A blood pressure fall after hospitalization was associated with a decrease of urinary noradrenaline and serum DBH, and there was a significantly positive correlation between the changes in blood pressure and those in urinary noradrenaline or in serum DBH. A significantly adverse correlation was found between plasma volume and the amounts of urinary noradrenaline excretion. The changes in noradrenaline response was negatively correlated with those in urinary noradrenaline excretion. In addition, noradrenaline response was correlated positively with plasma volume, extracellular fluid volume and total exchangeable sodium and negatively with PRA. Following salt restriction, a fall of the blood pressure was associated with an elevation of urinary noradrenaline excretion. The patients with more marked blood pressure fall showed a higher increase of urinary noradrenaline, and a significant correlation was found between the changes in these two variables. Noradrenaline response was significantly reduced, although it was not correlated significantly with noradrenaline excretion. In these experiments, adrenaline, unlike noradrenaline, did not show any obvious changes. These findings suggested that an excessive sympathetic nerve activity caused an elevation of blood pressure in the labile type of essential hypertension. It was demonstrated that a sympathetic nervous function was dependent on sodium intake and that there exisited a close relationship between noradrenaline response and water-sodium contents or PRA.

Adolescent↗
PubMedDate not supplied

Effects of verapamil on myocardial stunning in xanthine-oxidase deficient hearts: pre-treatment vs. post-ischemic treatment.

The role of free radicals and the protective action of calcium antagonists have been established in myocardial stunning in canine hearts, which contain a considerable level of xanthine oxidase, a free radical producing enzyme. However, myocardial stunning in hearts which lack xanthine oxidase and its modification by calcium antagonists in vivo remain uncharacterized. The present study examined this issue using open-chest anesthetized rabbits. Myocardial stunning was induced by a 10-min coronary occlusion and reperfusion. Regional systolic thickening fraction (TF) was determined using an epicardial Doppler sensor, together with other hemodynamic parameters. In untreated control rabbits, recovery of TF from the 10 min transient ischemia was 43 +/- 3% of the baseline at 30 min after reperfusion. Administration of verapamil (200 micrograms/kg bolus plus 40 micrograms/kg/min), which was started before the onset of ischemia and continued until 20 min after reperfusion, significantly improved the recovery of TF to 74 +/- 6% (p < 0.05). A similar improvement in post-ischemic contractile function (TF = 77 +/- 10%) was observed when verapamil was injected at the same rate, but the infusion was discontinued 1 min after the coronary occlusion. Myocardial ATP depletion after the 10 min ischemia was significantly less in the verapamil-pretreated rabbits compared with untreated controls (10.1 +/- 1.0 vs. 6.2 +/- 0.7 mumol/g dry wt., p < 0.05). The difference in TF between the rabbit with and without verapamil treatment could not be explained by afterload reduction. When verapamil (100 micrograms/kg bolus plus 20 micrograms/kg/min) was given during the reperfusion period alone, TF recovery was poorer (TF = 22 +/- 8%) than the control value. Thus, it was concluded that verapamil attenuates myocardial stunning in the hearts with trace levels of xanthine oxidase, and that the beneficial effect is achieved only by pretreatment, not by post-ischemic treatment with verapamil.

Adenosine Triphosphate↗
PubMedDate not supplied

Suppression of the degradation of adenine nucleotides during ischemia may not be a sufficient mechanism for infarct size limitation by preconditioning.

Preconditioning is known to decelerate degradation of the tissue adenine nucleotides during ischemia and to delay ischemic myocardial necrosis. However, it is not known whether these two phenomena are related. To obtain an insight into this question, the present study examined whether adenosine and B2 receptor antagonists, which block the infarct size-limiting effect of preconditioning, modify the interstitial purine levels during preconditioning and subsequent sustained ischemia. In pentobarbital anesthetized open-chest rabbits, a microdialysis probe was placed in the territory of a branch of the left coronary artery, and perfused with Ringer solution. Preconditioning was performed with 5 min ischemia/5 min reperfusion. Dialysate adenosine and inosine were elevated from the baseline values of 0.064 +/- 0.011 and 0.329 +/- 0.044 microM to 0.189 +/- 0.069 and 4.106 +/- 1.451 microM, respectively during preconditioning, but their elevation during a subsequent 20 min of ischemia was significantly lower compared with that in the non-preconditioned myocardium. This suppression of the purine accumulation during ischemia by preconditioning was not abolished by 2 micrograms/kg of Hoe 140, a specific B2 receptor antagonist, or by 10 mg/kg of 8-phenyltheophylline, a non-selective adenosine receptor antagonist. Since the doses of Hoe 140 and 8-phenyltheophylline are sufficient to block the infarct size-limiting effect of preconditioning, the present results suggest that there is a dissociation between the suppression of adenine nucleotide degradation during ischemia by preconditioning and the enhancement of myocardial resistance against infarction. Thus, it is unlikely that a reduction of adenine nucleotide utilization by preconditioning is sufficient to protect the myocardium against ischemic necrosis.

Adenine Nucleotides↗
PubMedDate not supplied

Reduction of regional contractile function by preconditioning ischemia does not play a permissive role in the infarct size-limitation by the preconditioning.

Although previous studies have shown that preconditioning cannot be explained by concurrent myocardial stunning alone, it remains unclear whether reduction of contractile function by preconditioning ischemia is required for its cardioprotective effect. The present study examined whether preconditioning occurs in the absence of regional contractile dysfunction. In the first series of experiments, rabbits received two cycles of 2-min coronary occlusion separated by 5-min reperfusion, with or without dobutamine infusion (10 micrograms/kg/min, i.v.) commencing before the onset of ischemia. Regional thickening fraction measured by epicardial Doppler sensor was 72.8 +/- 4.7% of baseline (mean +/- SEM) in the untreated group and 102.9 +/- 3.1% in the dobutamine group at the end of the second cycle of ischemia/reperfusion. In the second series of the study, four groups of rabbits underwent 30-min coronary occlusion and reperfusion. The control group was untreated, and the PC group was preconditioned with two cycles of 2-min ischemia/5-min reperfusion before the 30-min ischemia. The PC-DOB group received both preconditioning and dobutamine infusion (10 micrograms/kg/min, i.v.), which was started 5 min before the preconditioning and continued for 19 min. The DOB group was given dobutamine infusion like the PC-DOB group, but was not preconditioned. After 72-h reperfusion, infarct size and area at risk were determined by histology and fluorescent particles, respectively. Infarct sizes in the PC and PC-DOB groups (25.0 +/- 3.4% and 22.7 +/- 3.3% of area at risk, respectively) were significantly smaller than that in the control group (48.2 +/- 2.6%). In the DOB groups, infarct size (43.5 +/- 4.0%) was similar to the control value. Infusion of dobutamine at a dose sufficient to abolish the contractile dysfunction which would have been induced by ischemic preconditioning did not attenuate the infarct size-limiting effect of preconditioning. Thus, it is unlikely that reduction of contractile function plays a permissive role in the appearance of the cardioprotective effect of preconditioning.

Animals↗
PubMedDate not supplied

Suppression of reperfusion arrhythmia by ischemic preconditioning in the rat: is it mediated by the adenosine receptor, prostaglandin, or bradykinin receptor?

The mechanism for the suppression of reperfusion arrhythmia by preconditioning (PC) remains unknown. This study aimed to examine the roles of the adenosine receptor, prostaglandin (PG), and bradykinin (BK) receptor in PC. Under pentobarbital anesthesia, the coronary artery of the rat was occluded for 5 min and then reperfused. In untreated controls, this protocol induced ventricular tachycardia (VT) in 100% of the rats and ventricular fibrillation (VF) in 60%. PC with 2 min ischemia/5 min reperfusion prior to the 5 min coronary occlusion significantly reduced the incidence of reperfusion VT and VF to 30% and 0%, respectively. This antiarrhythmic effect of the PC was not blocked when rats were pretreated with 8-phenyltheophylline (8-PT, 10 mg/kg), aspirin-DL-lysin (18 mg/kg), or a specific BK receptor antagonist, Hoe140 (20 nmol/kg). None of these agents alone significantly modified the incidence of reperfusion VT or VF. These results suggest that neither the adenosine receptor, endogenous PG, nor BK receptor play a major role in the mechanism of suppression of perfusion arrhythmias by PC in the rat heart.

Adrenergic beta-Antagonists↗