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Biomedical subjects

T Haneda

Publications and source records attributed to T Haneda.

At least 73 records · Page 4Linked to original sources
PubMed1989

Effects of nicorandil and nipradilol on ischemic myocardium in perfused rat heart.

We examined the effect of nicorandil and nipradilol on the ischemic myocardium in the isolated perfused rat heart. The heart was perfused by the working heart technique with an afterload pressure of 60 mm Hg and with a left atrial filling pressure of 9 mm Hg. Ischemia was induced for 20 min by lowering the afterload pressure. The afterload pressure was raised to 60 mm Hg again during reperfusion. Ischemia decreased the pressure-rate product, coronary flow, adenosine triphosphate level and creatine phosphate level, and increased the lactate level. Reperfusion could not restore the pressure-rate product nor the adenosine triphosphate level completely. Nicorandil (5 x 10(-5) and 1.5 x 10(-4) M) or nipradilol (10(-5), 5 x 10(-5) and 1.5 x 10(-4) M) was introduced 5 min before ischemia. Nipradilol preserved the levels of adenosine triphosphate and creatine phosphate after 20 min of ischemia and increased the extent of recovery of the pressure-rate product during reperfusion, whereas nicorandil did not. Nipradilol, but not nicorandil, can protect the myocardium against ischemic damage.

Adenosine Triphosphate↗
PubMed1989

Release of adenosine and lactate from human hearts during atrial pacing in patients with ischemic heart disease.

Thirty-eight patients treated by atrial pacing were divided into three groups (Group I, patients with neither coronary stenosis nor anginal pain during pacing; Group II, patients with no coronary stenosis but having anginal pain during pacing; Group III, patients with coronary stenosis). The concentrations of adenosine and lactate were measured in the coronary sinus blood and in the arterial blood before, during, and after atrial pacing. During atrial pacing, significant levels of adenosine were released from the heart of patients in Group III, whereas significant lactate release was observed in Groups II and III. In Group II, the concentration of adenosine in coronary sinus blood appeared to increase during pacing, but not significantly. There was no significant correlation between the release of adenosine and that of lactate. A significant release of adenosine due to atrial pacing may be observed only in patients with coronary artery disease.

Adenosine↗
PubMed1989

Elevated aortic pressure, calcium uptake, and protein synthesis in rat heart.

Elevation of aortic pressure from 60 to 120 mmHg increased the initial rate of 45Ca2+ uptake and the steady-state level that was achieved. The increase in uptake was as great after the first 10 min of pressure elevation as it was after aortic pressure had been at 120 mmHg for 1 h. When aortic pressure was returned to 60 mmHg for 30 min after 1 h at 120 mmHg, calcium uptake was restored to the control value. Elevation of perfusate Ca2+, from 0.5 mM to 2.9 and 5.0 mM increased oxygen consumption and decreased creatine phosphate/creatine ratios in hearts supplied glucose but had not effect on the rate of total protein synthesis. When hearts were supplied pyruvate to maintain high energy phosphates, an increase in perfusate Ca2+ from 0.5 to 2.9 mM did not accelerate total protein synthesis or ribosome formation. These studies provide no support for a role for extracellular Ca2+ availability in mediating the effects of elevated aortic pressure on total protein synthesis and ribosome formation.

Animals↗
PubMed1989

Effect of higher aortic pressure on ribosome formation and cAMP content in rat heart.

Elevation of aortic perfusion pressure from 60 to 120 mmHg in beating and arrested rat hearts raised cAMP content and increased rates of ribosome formation but had no effect on total protein synthesis during 1 h of perfusion. The activity of adenosine 3',5'-cyclic monophosphate (cAMP)-dependent protein kinase increased as perfusion pressure was elevated in arrested hearts. A regulatory link between increased cAMP content and accelerated ribosome formation was hypothesized to exist. When hearts were arrested with tetrodotoxin and exposed to 0.2 mM methacholine, a muscarinic-cholinergic agonist that blocked pressure-induced increases in cAMP content, elevation of aortic pressure to 120 mmHg failed to increase the rate of ribosome formation. When aortic pressure was maintained at 60 mmHg, exposure of beating hearts to glucagon increased cAMP content and mimicked the effect of elevated aortic pressure to accelerate rates of ribosome formation. These studies support the hypothesis that increased aortic pressure preferentially accelerates rates of ribosome formation by a cAMP-dependent mechanism.

Animals↗
PubMed1989

Increased cyclic AMP content accelerates protein synthesis in rat heart.

Elevation of cyclic AMP (cAMP) content in perfused rat hearts by exposure to glucagon, forskolin, and 1-methyl-3-isobutylxanthine (IBMX) increased rates of protein synthesis during the second hour of perfusion with buffer that contained glucose in the absence of added insulin. When tetrodotoxin was added to arrest contractile activity, glucagon, forskolin, and IBMX still elevated cAMP content and rates of protein synthesis. Perfusion of beating rat hearts at elevated aortic pressure (120 mm Hg vs. 60 mm Hg) also accelerated rates of protein synthesis and raised cAMP content and cAMP-dependent protein kinase activity during the second hour of perfusion. Insulin accelerated rates of protein synthesis in beating hearts during the first and second hour of perfusion but did not increase cAMP content. Elevation of aortic pressure in insulin-treated hearts raised cAMP content but had no further effect on rates of protein synthesis. Perfusion of arrested hearts for as little as 2 minutes at 120 mm Hg resulted in a rapid and sustained increase in cAMP content, cAMP-dependent protein kinase activity, and rate of protein synthesis after 60-120 minutes of additional perfusion at 60 mm Hg. Exposure of arrested hearts to 0.2 mM methacholine, a muscarinic-cholinergic agonist, for 5 minutes before elevation of perfusion pressure blocked the pressure-induced increases in cAMP content, cAMP-dependent protein kinase activity, and rates of protein synthesis. When hearts were removed from pertussis toxin-treated animals, methacholine did not block the effects of forskolin on these same three parameters. These studies indicated that elevation of tissue cAMP by hormone binding, direct activation of adenylate cyclase, or inhibition of phosphodiesterase resulted in acceleration of protein synthesis. Furthermore, the effects of increased aortic pressure to accelerate synthesis appeared to involve a cAMP-dependent mechanism that was independent of changes in contractile activity but could be blocked with a muscarinic-cholinergic agonist. Acceleration of protein synthesis by insulin was not associated with an elevation of cAMP.

1-Methyl-3-isobutylxanthine↗
PubMed1988

The effect of sustained stellate ganglion stimulation on left ventricular contractility in the dog.

Although a progressive reduction in left ventricular contractility during sustained left stellate ganglion stimulation has been well documented, there have been no reports on the contractile state after nerve stimulation. Left ventricular contractility after cessation of 60 min of electrical (10 V. 10 Hz. 1 msec) left stellate ganglion stimulation has been assessed in open chest dogs. Before and 15 min after stimulation, left ventricular contractility was evaluated by the end-systolic pressure-segment length relationship using ultrasonic crystals during a stepwise aortic constriction to increase left ventricular afterload. Restimulation of the left stellate ganglion was also performed 15 min after cessation of the first stimulation. After sustained left stellate ganglion stimulation, the end-systolic points shifted to the right from the control and the slope of multiple pressure-segment length coordinates significantly decreased (102.5 +/- 16.1 to 76.5 +/- 10.2 mmHg/mm, mean +/- S.E., p less than 0.05, n = 5), indicating a depression of left ventricular contractility. Increased left ventricular dP/dt max and norepinephrine level in the coronary sinus gradually returned to near base line during 60 min of stimulation. These reduced responses lasted for at least 15 min after cessation of stimulation. The myocardial norepinephrine content was reduced to 0.59 +/- 0.08 (mean +/- S.E.) ng/mg wet tissue from 0.90 +/- 0.15 of the control level (p less than 0.05). These data suggested that left ventricular contractility decreased after sustained cardiac sympathetic nerve stimulation, probably due to norepinephrine reduction in the myocardium.

Animals↗
PubMed1988

[Obstructive sleep apnea syndrome with reversible interventricular septal displacement during sleep: a case report].

A case of the obstructive sleep apnea syndrome revealed reversible leftward displacement of the interventricular septum by echocardiography during sleep. A 46-year-old housewife with congenital micrognathia was admitted to our hospital complaining of severe dyspnea and general edema. On admission, she had severe hypoxemia (PaO2 = 35.2 mmHg), pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) and right heart failure. Her echocardiograms revealed enlargement of the right ventricle with a flattened left ventricle. A sleep study performed after partial resolution of her right heart failure disclosed that severe hypoxemia and pulmonary hypertension (mean pulmonary artery pressure = 70 mmHg) occurred after relatively long periods of apnea. With vigorous inspiratory efforts during sleep apnea, transient enlargement of the right ventricle and leftward displacement of the septum causing the flattened left ventricle were observed echocardiographically. A concomitant decrease in left ventricular inflow velocities was also observed by the pulsed Doppler method. However, these findings immediately returned to normal with the resumption of ventilation. We concluded that these repetitive apneic events due to obstruction of the airway during sleep might accelerate complete eventual pulmonary hypertension and right heart failure.

Echocardiography↗
PubMed1987

The degree of increment in plasma catecholamines in patients with mitral stenosis by mild exercise.

Although sympathetic excitation during mild exercise may readily occur in patients with mitral stenosis (MS), the degree of increment in plasma catecholamines has not been fully investigated. We imposed mild ergometric exercise (50 watts, 300 kg/min for 5 minutes) on five patients with mild MS (mitral valve area greater than or equal to 1.0 cm2) and eight with severe MS (mitral valve area less than 1.0 cm2) while they were undergoing cardiac catheterization. In patients with severe MS, total plasma catecholamine levels during exercise were remarkably higher (2821 +/- 783 [SEM] pg/ml) than in those with mild MS (957 +/- 113 pg/ml, p less than 0.05) and in seven control subjects (612 +/- 75 pg/ml, p less than 0.05). This marked increment could not be predicted by heart rate response, which did not differ between severe and mild MS (166 +/- 5 vs 153 +/- 10 bpm). In contrast with catecholamine change, the cardiac index in severe MS showed a very small increment. Results suggest that mild daily exercise can remarkably increase plasma catecholamine levels in severe MS, and this may accelerate various complications of this disorder.

Adult↗
PubMed1987

Inhibition of ischemia-induced subcellular redistribution of lysosomal enzymes in the perfused rat heart by the calcium entry blocker, diltiazem.

Effect of diltiazem on subcellular distribution of lysosomal enzymes, high-energy phosphate metabolism and mechanical function in the ischemic heart was studied. Ischemia was induced by lowering the afterload pressure of the perfused working rat heart. The activities of cathepsin D, beta,N-acetylglucosaminidase and acid phosphatase were determined in the nonsedimentable and sedimentable fractions after centrifugation of the tissue extract to assess the subcellular distribution of lysosomal enzymes. After ischemia, decreases in the mechanical function and the tissue level of high-energy phosphates were observed. In addition, ischemia caused subcellular redistribution of lysosomal enzymes from the lysosomes to the cytoplasm. Reperfusion of the ischemic heart did not restore the mechanical function and the level of high-energy phosphates completely. Diltiazem (2.21 X 10(-6), 1.11 X 10(-5) and 2.21 X 10(-5) M) was provided for the heart 5 min before the onset of ischemia. Diltiazem preserved high-energy phosphates in the ischemic heart, and inhibited the subcellular redistribution of lysosomal enzymes being caused by ischemia, depending on its concentration. Reperfusion after ischemia with diltiazem recovered the mechanical function that had been decreased by ischemia. These results may indicate that diltiazem can protect the myocardium against ischemic damage.

Acetylglucosaminidase↗
PubMed1986

Time course of pulmonary vasoconstriction with repeated hypoxia and glucose depletion.

To examine the effect of hypoxia on pulmonary vascular smooth muscle, rabbit lobar pulmonary artery was suspended in a glucose free solution and both chronologic changes in tension and ATP content were determined together at 30 min intervals after repeated hypoxic challenge (PO2 = 11 +/- 2 mm Hg). The pulmonary artery contracted and its ATP content decreased with hypoxia. This contraction was not inhibited by nifedipine, Ca++ -free EGTA, procaine, phentolamine, isoproterenol, diphenhydramine, prostaglandin E1, atropine or nitroglycerin. Upon reoxygenation (PO2 = 104 +/- 3 mm Hg), the elevated resting tension decreased in a biphasic fashion and the ATP content of the lobar pulmonary artery increased. When hypoxic challenges were repeated, the rate of constriction on hypoxia increased, while the relaxation rate on reoxygenation, tension developed by 30 min of hypoxia and the total amount of ATP decreased. These results suggest that the ATP content in the lobar pulmonary artery is very sensitive to in vitro acute hypoxia and that the Ca++ transport process is more easily impaired by reduction in ATP levels than is the contractile machinery.

Adenosine Triphosphate↗
PubMed1986

Functional and metabolic responses to ischemia in the perfused heart isolated from normotensive and spontaneously hypertensive rats.

The difference between normotensive rats (WKY) and spontaneously hypertensive rats (SHR) in functional and metabolic responses to ischemia was studied. Systolic arterial blood pressure of SHR (171.2 +/- 2.9 mmHg) was significantly higher than that of WKY (135.3 +/- 1.2 mmHg), and the left ventricular mass of SHR was larger than that of WKY. Hearts isolated from either WKY or SHR were perfused by the working heart technique. Ischemia was induced by lowering the afterload pressure of the working heart. Ischemia produced cardiac arrest, and decreased the tissue levels of adenosine triphosphate and creatine phosphate in both WKY and SHR. Recovery of mechanical function of the heart during reperfusion following ischemia in SHR was better than that in WKY, while recovery of the high-energy phosphates level in SHR was less prominent than in WKY. It is postulated that hypertension has a deleterious effect on myocardial energy metabolism in ischemic heart, even when cardiac mechanical function is maintained.

Adenosine Triphosphate↗