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Biomedical subjects

J Tamai

Publications and source records attributed to J Tamai.

49 records · Page 3Linked to original sources
PubMed1988

Visualization of isolated conus artery as a major collateral pathway in patients with total left anterior descending artery occlusion.

To examine the existence of isolated conus artery (ICA) as a source of collateral circulation, we selectively visualized the ICA in patients with left anterior descending coronary artery (LAD) occlusion using a no. 5 French catheter. One hundred and fifty patients with a total LAD occlusion were selected from 639 consecutive patients who had diagnostic coronary angiography during an 18-month period; the ICA was found in 45 patients. Among these patients, 30 showed the ICA as a collateral vessel supplying the distal LAD. In nine of these patients, conventional left and right coronary angiography did not reveal any other significant collateral vessels, and the distal LAD was perfused mainly by the collaterals from the ICA. No serious complications such as ventricular fibrillation or myocardial infarction occurred during these procedures. These results indicate that the selective ICA visualization is clinically important when conventional left and right angiography does not demonstrate collaterals to the obstructed LAD.

Angiocardiography↗
PubMed1988

Alpha 2-adrenoceptor activity exerts dual control of coronary blood flow in canine coronary artery.

To test the hypothesis that alpha 2-adrenoceptor activity exerts a dual control of coronary blood flow, i.e., vasoconstriction and augmentation of the vasodilatory effect of adenosine, four doses of adenosine were infused into left anterior descending coronary artery before and during alpha 2-adrenoceptor stimulation or attenuation in anesthetized open-chest dogs. During a moderate alpha 2-adrenoceptor attenuation (yohimbine or rauwolscine, ic), which did not alter coronary blood flow (CBF) at the base-line condition, the hyperemic response of CBF to infused adenosine was markedly reduced, whereas during the potent attenuation both base-line CBF and adenosine-induced hyperemic CBF were significantly increased. Inversely, the moderate alpha 2-stimulation (0.03 microgram.kg-1.min-1 norepinephrine with prazosin, ic, or 0.04 microgram.kg-1.min-1 clonidine ic, under propranolol pretreatment) augmented the adenosine-induced coronary vasodilation, but the potent alpha 2-stimulation (0.3 microgram.kg-1.min-1 norepinephrine with prazosin ic, or 0.3 microgram.kg-1.min-1 clonidine ic) reduced both base-line CBF hyperemic CBF. In contrast, alpha 2-adrenoceptor activity did not affect papaverine-induced coronary vasodilation. Moreover, the reactive hyperemic flow after a brief coronary occlusion was reduced significantly during the moderate alpha 2-adrenergic attenuation, but it was augmented during the potent one. These results indicate that the moderate activation of the alpha 2-adrenoceptor augments the hyperemic response of CBF to both exogenous and endogenous adenosine, whereas the potent alpha 2-activation may mask this vasodilatory effect through the coronary vasoconstrictive effect.

Adenosine↗
PubMed1987

A possible model of the anginal syndrome with normal coronary arteriograms: microembolization of canine coronary arteries.

To investigate whether disseminative coronary embolization with microspheres brings about a pathophysiological mimicking of the syndrome of exertional angina with a normal coronary arteriogram, 25 dogs were studied immediately and 2 weeks after the coronary embolization with microspheres 15 micron [2.5 X 10(5) or 5.0 X 10(5)/regional flow (ml/min)] and 25 micron [2.0 X 10(5)/regional flow (ml/min)] in diameter. Two weeks after embolization with the 15-micron microspheres, the resting coronary blood flow recovered to the control (preembolization) level with the absence of myocardial necrosis, but the coronary flow reserve was significantly lower. In ten dogs receiving the larger dose embolization (5 X 10(5)/regional flow (ml/min], lactate production or a marked decrease in lactate extraction was observed during rapid atrial pacing. In five dogs subject to 25-micron microsphere embolization, however, disseminative patchy myocardial necrosis was observed and the coronary flow reserve remained normal. These results indicate that the chronic state after microembolization with a large dose of 15-micron microspheres mimics the syndrome of exertional angina with a normal coronary arteriogram, whereas 25-micron microsphere embolization does not. Thus, the condition of some patients with a normal coronary arteriogram but with reduced coronary flow reserve may be attributable to microcirculatory disturbances in the coronary arterioles or smaller vessels. Moreover, we observed that the coronary flow at the induction of myocardial ischemia by pacing was much less than the reactive hyperemic flow. This discrepancy may be a characteristic feature in this syndrome.

Angina Pectoris↗
PubMed1987

Alpha 1-adrenoceptor activity regulates release of adenosine from the ischemic myocardium in dogs.

The goal of this study was to test the hypothesis that alpha 1-adrenoceptor activity plays a key role in the release of adenosine from the ischemic myocardium. In 51 open-chest dogs, the left anterior descending coronary artery was perfused through an extracorporeal bypass tube from the carotid artery, and adenosine release into the local coronary vein was measured by the radioimmunoassay technique following the reduction of perfusion pressure for 20 minutes under alpha 1-, alpha 2-, and beta-adrenoceptor attenuations. Adenosine and lactate concentrations in the coronary arterial and venous blood sampled from the perfused area were determined, as well as fractional shortening. In the untreated condition, adenosine release was significantly (p less than 0.01) increased from 1.7 +/- 0.8 (SEM) to 8.8 +/- 1.3 nmol/100 g/min, 20 minutes after the onset of hypoperfusion (coronary blood flow: 28 +/- 2 ml/100 g/min) following the initial overshoot release. Neither beta- nor alpha 2-adrenoceptor attenuation affected the increase in adenosine release during hypoperfusion except for the slight attenuation of the overshoot release by beta-attenuation. In contrast, intracoronary infusions of prazosin and phentolamine during coronary hypoperfusion markedly attenuated (p less than 0.01) release of adenosine (1.8 +/- 0.7 nmol/100 g/min at 20 minutes). The extents of decreases in fractional shortening and lactate production were comparable between the untreated and alpha 1-adrenoceptor attenuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1986

Role of adenosine in hyperemic response of coronary blood flow in microembolization.

To investigate the pathophysiology of acute embolization of small coronary vessels and the role of adenosine in this abnormality, regional coronary blood flow (CBF), coronary vascular resistance, arteriovenous O2 difference, lactate extraction ratio, and adenosine release were studied in 39 anesthetized open-chest dogs after acute coronary embolization with microspheres of three different diameters (15 +/- 1, 94 +/- 8, and 293 +/- 23 microns). In 16 dogs, the left anterior descending coronary artery was embolized by repetitive injections of 15-microns microspheres, up to 4.4 +/- 0.4 X 10(5)/g myocardium; at this point CBF, determined by the electromagnetic flowmeter at the proximal site of the artery, was reduced toward zero. Up to 37% of total embolization, resting CBF increased to 175 +/- 36% of control; thereafter it decreased almost linearly as the extent of embolization was increased. After embolization, coronary arteriovenous O2 difference was significantly (P less than 0.01) decreased with a marked release of adenosine in the coronary vein. Despite a hyperemic flow response of CBF in the embolized area, myocardial ischemia was not prevented; maximal increase in CBF after 100-microns microsphere embolization (141 +/- 11% of control CBF, n = 6) was significantly (P less than 0.05) less than that in 15-micron microsphere embolization, whereas 300-microns microsphere embolization minimally increased CBF (123 +/- 13%, P greater than 0.1; n = 5). Hyperemic flow remained unchanged for at least 3 h when adenosine was persistently released. Theophylline significantly attenuated this response. These results indicate that in embolization with microspheres less than 300 microns in diameter, hyperemic response of coronary blood flow occurs, probably due to the hyperemia of nonoccluded vessels in the adjacent area of ischemic foci to adenosine released from the ischemic myocardium.

Adenosine↗
PubMed1986

Cardiotonic activity of a new inotropic agent, 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)- quinolinone (OPC-8212), in the dog with and without beta-blocker and Ca++-antagonist pretreatment.

Hemodynamic effects of a new inotropic agent, OPC-8212 (2(1H)-quinolinone derivative) were studied in anesthetized open chest dogs pretreated with propranolol and diltiazem. Three doses (1, 3 and 10 mg/kg) of OPC-8212 were administered intravenously and the net hemodynamic effect (% change) was obtained by subtraction of the effect of the solvent from the gross effect, since the vehicle has a transient, but significant hemodynamic effect. The maximal inotropic effect occurred 3 minutes after administration: LV dP/dt max and cardiac output (CO) increased by 19 +/- 2.5% and 28 +/- 8.5%, respectively, at 3 mg/kg. These cardiotonic effects were dose-dependent, whereas heart rate, peak LV pressure (PLVP) and mean aortic pressure were minimally changed at any dose. Accordingly, systemic vascular resistance (SVR) decreased in a dose-dependent manner although the decrease was much less than that in administration of isoproterenol. The inotropic effect was not blocked by beta-adrenoceptor blockade (propranolol 1 mg/kg), indicating that the cardiotonic action of this agent is not due to beta-adrenergic stimulation. Thus, this agent could reverse beta-blocker-induced heart failure. During infusion of diltiazem (0.1 mg/kg/min following bolus intravenous administration of 0.5 mg/kg), the increases in LV dP/dt max and CO due to OPC-8212 were similar to those in the control study. In contrast to the effects under beta-adrenoceptor blockade, however, decreased PLVP was restored by OPC-8212. Neither chronotropic nor rrhythmogenic effects were observed in the control or with either pharmacological intervention. These results indicate that OPC-8212 has a potent inotropic action with modest vasodilatory effect even with propranolol or diltiazem pretreatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Beneficial effect of OPC-8212 (3,4-dihydro-6-(4-(3,4-dimethoxy benzoyl)-1-piperazinyl)-2(1H)-quinolinone on myocardial oxygen consumption in dogs with ischemic heart failure.

The effect of a new inotropic agent, OPC-8212 (2(1H)-quinolinone derivative), on myocardial oxygen consumption (MVO2) following intravenous administration (1 and 3 mg/kg/min) was studied in normal and ischemic failing hearts in open chest dogs. Ischemic failing heart was obtained by intracoronary injection of 15-micron microspheres and volume loading. OPC-8212 significantly increased LV max dP/dt and decreased mean aortic pressure, whereas heart rate was not altered in both normal and failing hearts. Despite the remarkable positive inotropic effect, this agent did not increase MVO2 in the normal hearts and even decreased MCO2 in the ischemic failing hearts associated with a decrease in LV end-diastolic pressure and hence, LV chamber size. These results indicate that OPC-8212 does not increase myocardial oxygen demand, probably because the increase in MVO2 by positive inotropic effect is offset by a decrease in MVO2 due to a decrease in chamber size. Thus, OPC-8212 may be promising for the treatment of congestive heart failure with reduced coronary flow reserve.

Animals↗
PubMed1986

[Coronary thrombolytic therapy in acute myocardial infarction: time dependence of beneficial effects assessed by two-dimensional echocardiography].

To elucidate the effects of coronary thrombolytic therapy in acute myocardial infarction, we observed serially the degree of left ventricular (LV) wall motion immediately after on day 1, and on days 7, 14, 21 and 28 after thrombolytic therapy, in 22 patients with acute anteroseptal myocardial infarction. Base-line coronary arteriography revealed significant lesions in the proximal portions of the left anterior descending artery of all the patients. The patients were categorized according to results of thrombolytic therapy as Group I-a: seven patients with spontaneous or successful recanalization within three hours of onset of chest pain; Group I-b: nine patients with successful recanalization between three and seven hours, with a mean of 4.8 hours from onset; and Group II: six patients in whom thrombolytic therapy was unsuccessful and infarct-related vessels remained totally occluded. The LV wall motion index (WMI) was defined as the sum of point scores for the degrees of regional wall motion at nine segments on serial two-dimensional echocardiograms, and used for quantitative assessments of LV function. Results were as follows: On day 1, immediately after thrombolytic therapy, the WMI of Group I-a was smaller than that of Group II. However, there was no significant difference between Groups I-a and I-b and between Groups I-b and II. These findings suggest that LV function cannot be recovered immediately after recanalization of occluded arteries unless recanalization occurs exceptionally early. Percent improvement of the WMI from days 1 to 28 in Group I-a, 65 +/- 14%, was significantly greater than that in Group I-b, 31 +/- 18%. However, Group II did not show significant improvement in the WMI. The WMI in Group I-a decreased significantly from days 1 to 7 (9.0 +/- 1.6 vs 7.1 +/- 1.8, p less than 0.05); whereas, the WMI in Group I-b showed no significant decrease until day 21. On day 1, the regional wall motion of the antero-apical wall was akinetic or dyskinetic in all patients studied. On day 28, it improved in six of seven patients in Group I-a, while it remained akinetic or dyskinetic in all patients in Groups I-b and II.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1985

Comparison of coronary hemodynamic and cardiac metabolic alterations during coronary artery spasm associated with ST segment elevation or depression.

Coronary vasospasms are usually indicated by ST elevation or depression in the electrocardiogram (ECG). To test the hypothesis that ST elevation represents more severe myocardial ischemia than does ST depression, we determined the coronary sinus blood flow (CSBF) and the transcardiac lactate extraction ratio (LER) in 19 selected patients who had focal vasospasms in the left anterior descending artery. In 10 patients, ergonovine (0.11 +/- 0.02 mg, mean +/- SEM) provoked severe (total or subtotal) coronary vasospasm with ST elevation. Under these conditions, CSBF significantly decreased (from 97 +/- 8 ml/min to 79 +/- 5 ml/min, p less than 0.01) with a marked reduction in LER (from 29 +/- 5% to -14 +/- 6%, p less than 0.01). In contrast, 10 vasospastic events with ST depression after ergonovine (0.15 +/- 0.04 mg, NS) were recognized as mild spastic narrowing or severe spasms with well developed collateral circulation. Alteration of CSBF was significant in only a few patients and the overall CSBF response was non-significant (from 106 +/- 12 ml/min to 103 +/- 13 ml/min). The reduction in LER in this group was less pronounced than those in patients with ST elevation (p less than 0.05). These results indicate that coronary vasospasm with ST elevation may be related to the more pronounced reduction in coronary blood flow accompanied by more severe myocardial ischemia. Such observations may support the contention that some ischemic events associated with ST elevation or depression can be interpreted as a continuous spectrum of vasospastic disorders.

Adult↗