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Biomedical subjects

R Katori

Publications and source records attributed to R Katori.

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

New collateral flow increasing early after coronary occlusion prevented myocardial necrosis in dogs.

Increases in regional myocardial blood flow (Qm) developing soon after myocardial infarction may minimize myocardial necrosis. To test this hypothesis, Qm in the area surrounding an acutely occluded coronary artery was determined successively over 4 weeks in 11 dogs. Non-radioactive colored microspheres were injected into the left atrium 5 s (Qm at this time is referred to as Q1), 3 h (Q2), 12 h (Q3), and 4 weeks (Q4) after occlusion of the coronary artery. After termination of the experiment, the heart was removed, and Qm and three indices of myocardial necrosis i.e., myocardial creatine kinase activity (CK), infarct size determined by triphenyl tetrazolium chloride stain (TTC), and myocardial fibrosis visualized by Azan-Mallory stain, were determined. Each Qm was expressed as a percentage of normal: Qm (% of normal) = [Q/Qc] ischemic area/[Q'/Qc']non-ischemic area x 100, where Qc indicates Qm determined before coronary occlusion. In the ischemic area of the left ventricle, Q1, Q2, Q3, and Q4 were 25 +/- 3%, 30 +/- 3%, 31 +/- 3%, and 42 +/- 3% of normal, respectively, in the inner layer, and 31 +/- 3%, 52 +/- 4%, 52 +/- 4%, and 77 +/- 6% of normal, respectively, in the outer layers. During the 4-week period, the increase of Qm in the outer layer was greater than that in the inner layer. The inner layer showed a small increase of flow from Q3 to Q4 (9 +/- 2%), but in the outer layer there were greater flow increases from Q1 to Q2 (21 +/- 3%) and from Q3 to Q4 (24 +/- 6%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The effect of AL0671, a novel potassium channel opener, on potassium current in rat aortic smooth muscle cells.

1. We evaluated the mechanism of activation by AL0671, a novel potassium channel opener, of potassium current in rat aortic smooth muscle cells. 2. Under conditions of whole cell recording, AL0671 (1-1000 microM) markedly increased potassium current with a Hill coefficient of 2 and dissociation constant of 1.5 x 10(-4) M. This activation was completely inhibited by intracellular ATP. 3. Under inside-out patch conditions, the ATP-sensitive K+ channels (KATP) treated with AL0671 (100 microM) showed prolongation of the slower open time component and shortening of the slower closed time component without modification of channel conductance.

Animals↗
PubMed1995

Atrial natriuretic peptide and antihypertensive action due to beta-blockade in essential hypertensive patients.

The effects of beta-blocker treatment on hemodynamics were studied in relation to plasma atrial natriuretic peptide (ANP) levels in 17 outpatients with essential hypertension. Administration of propranolol for twelve weeks to untreated subjects resulted in a significant (P < 0.001) rise in plasma ANP levels (from 37.9 +/- 21.2 to 66.7 +/- 46.2 pg/mL, mean +/- SD). Systolic and diastolic blood pressures were significantly decreased (P < 0.05 and P < 0.01, respectively). Heart rate was also significantly decreased (P < 0.001). On the other hand, a significant reduction of cardiac index was detected (from 4.12 +/- 1.34 to 2.96 +/- 0.75 L/min/m2, P < 0.01) with chronic administration of propranolol, suggesting a reflection of decreased cardiac function. A significant negative correlation was observed between %changes in systolic blood pressure and %changes in plasma ANP (r = -0.594, P < 0.05). These results suggest that the increased plasma ANP levels may contribute to the antihypertensive effect with propranolol.

Adrenergic beta-Antagonists↗
PubMed1995

Effect of methylprednisolone on metabolism and contractility in the stunned myocardium.

The effect of glucocorticoid on the metabolism and contractility in the stunned myocardium was examined by phosphorus 31 nuclear magnetic resonance (31P-NMR) in Langendorff rabbit hearts by use of an artificial blood substitute, perfluorochemical emulsion Flusol-43. After normothermic global ischemia of fifteen minutes, postischemic reperfusion of sixty-five minutes was carried out. Methylprednisolone sodium succinate (MPSS) was administered either prior to global ischemia or during postischemic reperfusion. Adenosine triphosphate (ATP), creatine phosphate (CrP), inorganic phosphate (Pi), pH, left ventricular systolic developed pressure (LV DevP) and coronary flow were continuously measured. Thirty-six hearts were divided into three experimental groups consisting of 12 hearts each; CONT consisted of controls, Pre-MPSS perfusion with MPSS-containing solution (10(-4)M) from forty-five minutes prior to global ischemia, and Post-MPSS with the same MPSS solution immediately after postischemic reperfusion. Pre-MPSS showed a significant inhibition of the increase in Pi and of the decrease in ATP and pH during global ischemia, in comparison with the other groups, and a suppression of the overshoot of CrP observed immediately after postischemic reperfusion. LV DevP of Pre-MPSS showed a marked improvement during the postischemic reperfusion as compared with CONT. In Post-MPSS, Pi was significantly increased and ATP decreased during the postischemic reperfusion as compared with the other two groups. There were no differences in coronary flow during postischemic reperfusion among the three groups. In conclusion MPSS has a beneficial effect on metabolism and contractility of the stunned myocardium when it is administered prior to ischemia.

Adenosine Triphosphate↗
PubMed1995

Beta-adrenergic stimulation induces ST-segment elevation in dogs with healing myocardial infarction.

There is controversy with regard to the mechanism of the exercise-induced ST-segment elevation in myocardial infarction. The purpose of the present study was to investigate the mechanism of ST-segment elevation through pharmacologic interventions. Transmural anterior myocardial infarction was produced by gelatin sponge embolization of the left anterior descending artery in seven closed-chest dogs. One and four weeks after myocardial infarction, the dogs underwent the following three interventions: right atrial pacing, norepinephrine infusion (3.75, 7.5, and 15 micrograms/min) with the pacing, and methoxamine injection (2.5 and 5.0 mg) with the pacing. All dogs had transmural infarction with a mean infarct size of 12.0 +/- 4.2% of the left ventricular weight. Right atrial pacing did not induce significant changes in ST-segment. Norepinephrine induced a marked elevation of ST-segment at leads V1 to V4, while methoxamine did not. Norepinephrine induced a significant increase in left ventricular ejection fraction, while methoxamine produced a marked decrease in the ejection fraction and an increase in ventricular volume. The mean percent radial shortening of the non-infarct ventricular wall showed a significant increase with norepinephrine, but a decrease with methoxamine. In conclusion, myocardial ischemia and wall motion abnormality may be excluded as possible mechanisms of ST-segment elevation and an enhanced beta-adrenergic mechanism in the non-infarct myocardium is suggested to be responsible for ST-segment elevation.

Adrenergic beta-Agonists↗
PubMed1995

[Isoproterenol induces ST-segment elevation without wall motion aggravation and myocardial ischemia in experimental myocardial infarction].

The mechanism of exercise-induced ST-segment elevation in previous myocardial infarction was investigated using isoproterenol infusion with atrial pacing to simulate exercise hemodynamics in seven closed chest dogs with myocardial infarction. The myocardial infarction was induced by cellulose embolization of the left anterior descending artery. One week after infarction, 1) isoproterenol 0.3 microgram/min infusion, 2) right atrial pacing alone, and 3) isoproterenol infusion after the injection of propranolol 0.5 mg/kg were performed. The heart rate was kept constant by atrial pacing during the examination. Precordial ST-segment deviation, left ventricular global and regional wall motions, lactate extraction ratio, and regional myocardial blood flow were measured. Isoproterenol induced a significant elevation of the ST-segment, i.e., the sum of ST-segment elevation at chest leads V2, V3 and V4, sigma STV234, increased from 0.32 +/- 0.11 (mean +/- SEM) to 0.82 +/- 0.22 mV (p < 0.01). However, pacing alone and isoproterenol with pretreated propranolol did not. During isoproterenol-induced ST-segment elevation, left ventricular ejection fraction increased (29.2 +/- 3.3 to 39.1 +/- 3.9%, p < 0.01), lactate extraction ratio decreased but within the normal range for lactate metabolism (30.2 +/- 7.0 to 16.7 +/- 4.2%, p < 0.01), and the inner/outer ratio of regional blood flow did not change significantly (0.81 +/- 0.18 to 0.97 +/- 0.13 in the non-infarct border area, NS; 0.37 +/- 0.04 to 0.42 +/- 0.07 in the infarct border area, NS). Isoproterenol enhanced ventricular wall motion in the border and non-infarct areas, but did not induce aggravation in the infarct area.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Adult left isomerism complicated with life threatening arrhythmias detected by the use of biplane transesophageal echocardiography: a case report.

Left isomerism with critical arrhythmia in a 34-year-old housewife is reported. Left isomerism is rare among adult congenital disorders. The prognosis in childhood depends on intractable heart failure, but is unclear in adulthood. We describe an adult patient with left isomerism who recovered from life-threatening arrhythmias. Transesophageal echocardiography was especially useful to identify the morphology of both atrial appendages.

Adult↗
PubMed1995

A new class III antiarrhythmic drug, MS-551, blocks the inward rectifier potassium channel in isolated guinea pig ventricular myocytes.

We have studied the effects of MS-551 on the inward rectifier potassium channel (IK1) in isolated guinea-pig ventricular myocytes by use of whole-cell and single-channel recording techniques. MS-551 (5 microM) blocked the IK1 current. The percent blockade of the peak and steady-state IK1 current by MS-551 was constant at each test potential. In contrast 50 microM MS-551 failed to block either the sodium or the calcium current. Under cell-attached patch conditions, MS-551 reduced the open probability of IK1 channel activity by prolonging the interburst interval without changing either the unitary amplitude or the equilibrium potential. The blockade of IK1 was concentration-dependent. MS-551 did not change either the mean open time or mean closed time within a burst. Extracellular acidification (pH 6.4) strongly attenuated the effect of MS-551 on the open probability of IK1 channel activity when compared with its effect at pH 7.4. In summary, our results demonstrated that MS-551 blocked the IK1 channel. The neutral form of this drug molecules may penetrate the cardiac cell membrane via a hydrophobic pathway to block the steady-state IK1 current by reduction of open probability.

Animals↗
PubMed1995

[Dobutamine stress echocardiography in the diagnosis of myocardial ischemia in patients with implanted pacemakers: report of two cases].

Dobutamine stress echocardiography was used in the diagnosis of myocardial ischemia in patients with implanted VVI pacemakers. A 69-year-old woman received a pacemaker for Mobitz II type AV block in October 1992. She had suffered from chest pain during effort since January 1993 and underwent dobutamine stress echocardiography in April 1993. Although the electrocardiogram failed to identify ischemia because of the pacemaker rhythm, ischemia of the anterior wall was revealed as a worsening of the wall motion on the echocardiogram. The coronary angiogram showed 99% stenosis of the left descending artery. A direct coronary atherectomy was performed on the lesion. A 68-year-old man received a pacemaker for sick sinus syndrome in August 1993. He had suffered from chest oppression during effort since May 1992 and underwent dobutamine stress echocardiography in October 1993. Spontaneous rhythm appeared with dobutamine infusion, but the electrocardiogram could not demonstrate ischemia because of incomparability with the rhythm at rest. Echocardiography detected a new wall motion abnormality of the inferior wall caused by dobutamine. The coronary angiogram showed 90% stenosis of the right coronary artery. PTCA was performed on the lesion. Dobutamine stress echocardiography is useful for the diagnosis of myocardial ischemia in patients with implanted pacemakers.

Adrenergic beta-Agonists↗
PubMed1994

Preservation of high regional blood flow at epicardial rim after coronary occlusion in dogs.

A thin myocardial layer adjacent to the epicardium (epicardial rim) often survives after transmural myocardial infarction. Regional myocardial blood flow (Qm) at this rim may be high enough to maintain myocardial viability during coronary occlusion. To test this hypothesis, we measured Qm in 12 anesthetized dogs during left anterior descending coronary artery occlusion using nonradioactive colored microspheres. Myocardium in the region supplied by the occluded artery was sliced into sections approximately 0.5 mm thick from the epicardial surface to the endocardium, and the Qm in each section was determined. During occlusion, the Qm of myocardium within 0.5 mm of the epicardial surface remained at 74.8 +/- 8.8% of the preocclusion level. Maintenance of this high Qm during occlusion was abolished when an epicardial incision approximately 1 mm deep was made around the occluded area. These findings suggest that Qm is maintained at a surprisingly high level at the epicardial rim after coronary occlusion through epicardial arterial communications, which may be sufficient to maintain myocardial viability.

Animals↗
PubMed1994

Exercise-induced ST-segment elevation and hemodynamic responses one month after myocardial infarction.

Changes in hemodynamics and plasma norepinephrine levels during supine bicycle exercise after myocardial infarction were measured to investigate the mechanism of exercise-induced ST-segment elevation. Seventy-eight patients were divided into groups which showed either ST elevation (STE), ST depression (STD), or no ST changes (STU). Most of the STE group had anterior myocardial infarction (90.6%) and single-vessel disease (76.7%). The STE group achieved a significantly higher workload (119.5 +/- 4.0 watts, mean +/- SEM) than the STD group (82.3 +/- 2.8, p < 0.01). Heart rate and cardiac output at maximal workload were significantly higher in the STE group (136.6 +/- 3.4 beats/min, 7.44 +/- 0.28 l/min/m2) than in the STD group (110.0 +/- 3.9, 4.83 +/- 0.36, p < 0.01). Pulmonary artery pressures were less elevated in STE than STD patients. Plasma norepinephrine levels increased significantly at maximal workload in STE patients, as compared to the other groups. In conclusion, the STE group achieved a higher exercise level associated with augmented sympathetic activity, which may be a possible mechanism of exercise-induced ST elevation after myocardial infarction.

Cardiac Output↗
PubMed1994

Effect of an angiotensin II receptor antagonist, TCV-116, on rat carotid artery neointimal formation after balloon injury.

Arterial injury by a balloon catheter produces marked smooth muscle cell proliferation and the participation of angiotensin II in this response has been suggested. In this study, we examined the effect of a novel angiotensin II type I receptor antagonist, TCV-116, on neointimal formation after rat carotid artery balloon injury. Oral administration of TCV-116 at doses of 1, 5 or 10 mg/kg/day significantly reduced the cross-sectional intimal area by 30%, 46% and 54%, respectively, and reduced the ratio of the intimal to medial cross-sectional areas by 23%, 41% and 50%. An angiotensin-converting enzyme inhibitor, lisinopril, had an effect similar to that of TCV-116. The effect of both drugs was significantly correlated with the reduction of both blood pressure and cardiac hypertrophy. We conclude that TCV-116 can prevent neointimal formation after balloon injury as well as reducing blood pressure and preventing cardiac hypertrophy.

Angiotensin Receptor Antagonists↗
PubMed1993

Characterization of renal aldosterone receptors in genetically hypertensive rats.

To investigate the aldosterone responsiveness of genetically hypertensive rats, we compared characteristics of renal cytosolic aldosterone receptors from the M strain of stroke-prone, spontaneously hypertensive rats (M-SHRSP) with normotensive Wistar-Kyoto rats (WKY). In M-SHRSP, blood pressure was elevated significantly at 6 wk of age, when their plasma aldosterone concentrations were similar to those in WKY. Decreases in urine volume and sodium excretion were also observed in M-SHRSP. At 10 wk of age, M-SHRSP plasma aldosterone concentrations became significantly higher than those in WKY. On the other hand, the concentration of renal cytosolic aldosterone receptors (type I, aldosterone specific) had already increased at 6 wk of age in M-SHRSP, with no difference in affinity, and levels remained increased thereafter. There were no significant differences in molecular weights or ionic charges of either "activated" or "non-activated" aldosterone-receptor complexes between M-SHRSP and WKY, indicating that the molecular properties were similar in both groups. These results suggest that the increased concentration of aldosterone receptors in the kidneys of M-SHRSP might increase their aldosterone responsiveness and contribute to the development of high blood pressure in these animals.

Animals↗
PubMed1992

Sodium channel states control binding and unbinding behaviour of antiarrhythmic drugs in cardiac myocytes from the guinea pig.

OBJECTIVE: The aim was to investigate whether cardiac sodium channel states (rested, activated, inactivated) regulate the binding and unbinding behaviour of antiarrhythmic drugs on the receptor sites. METHODS: Single ventricular myocytes of adult guinea pig heart were obtained by an enzymatic dissociation method in the Langendorff manner. The channel state dependent blocking effects on cardiac sodium current (INa) of quinidine and disopyramide were studied under the whole cell variation of the patch clamp technique. RESULTS: 10 microM quinidine and 20 microM disopyramide produced similar levels of tonic block and use dependent block. The steady state inactivation curve (h infinity curve) was shifted parallel in the negative potential direction by quinidine (10 microM) and disopyramide (20 microM) to the same extent (-10 mV). Removal of the fast inactivation process of INa by chloramine-T did not reduce tonic and use dependent block by these drugs. Onset block study using a double pulse protocol revealed that block developments by both drugs were fitted to the sum of double exponential functions. However, time constant of fast phase of block by disopyramide was faster than that by quinidine, while slow phase was not significantly different. Definition of time courses of unbinding (recovery) at -140 mV indicated that quinidine dissociated relatively slowly as compared to disopyramide. CONCLUSIONS: Quinidine produces more potent tonic and use dependent block of INa by binding to sodium channels at both rested and inactivated states, while disopyramide has a higher affinity for activated state. Therefore, sodium channel states regulate the binding and unbinding behaviour of antiarrhythmic drugs. Furthermore, the fast inactivation process is not essential in producing tonic and use dependent block by antiarrhythmic drugs.

Action Potentials↗
PubMed1992

ST-segment re-elevation and left ventricular expansion soon after acute anterior myocardial infarction.

The sum of ST-segment elevation (sigma ST on V2-4) was measured to evaluate ST-segment re-elevation during early convalescence in 57 patients with acute myocardial infarction. Following rapid ST-segment elevation resolution during the first 12 h, sigma ST again increased in many patients without signs of reinfarction or pericarditis, reaching a maximum approximately 5 days after onset. The magnitude of this re-elevation (delta sigma ST) was less than 0.3 mV in 30 patients (group A), and 0.3 mV or more in another 27 (group B). Based upon left ventriculography, the global ejection fraction in group B decreased significantly from 51 +/- 10% at the acute phase to 46 +/- 10% at the chronic phase. No such decreases were seen for group A. Regional ejection fraction in the infarcted portion improved significantly from 28 +/- 13% at the acute phase to 35 +/- 14% at the chronic phase in group A, but did not improve in group B. In addition, the non-infarcted portion in group B showed a significantly reduced regional ejection fraction. These results suggest that myocardial expansion of the infarcted portion may contribute to ST-segment re-elevation, an ominous sign of left ventricular dysfunction soon after acute myocardial infarction.

Cineangiography↗
PubMed1992

Residual critical coronary stenosis during myocardial reperfusion is deleterious to myocardial salvage in dogs.

Hyperemia, which occurs immediately after coronary reperfusion, injures the myocardium. Mild coronary stenosis may mitigate this hyperemia and thus may augment myocardial salvage. To test this hypothesis, left anterior descending coronary arteries of dogs were occluded for 3 h. Then, reperfusion was permitted without residual stenosis (group A, n = 17) or with 75% stenosis (group B, n = 10). Regional myocardial blood flow (RMBF) was determined using colored microspheres. Dogs were sacrificed 1 week later to measure myocardial creatine kinase activity (CK) and for staining with triphenyl tetrazolium chloride (TTC). The RMBF measured 5 min after reperfusion increased significantly (inner layer, 171 +/- 16; outer layer, 165 +/- 11% of control) in group A. This hyperemia disappeared in group B (inner, 106 +/- 8; outer, 117 +/- 10% of control). However, the myocardial CK was more preserved (group A: inner, 31 +/- 4; outer, 44 +/- 4%; and group B: inner, 21 +/- 6; outer, 29 +/- 5%), and the infarct size was smaller in group A than in group B (group A: inner, 44 +/- 6; outer, 33 +/- 5; and group B: inner, 53 +/- 10; outer, 58 +/- 7% of the area at risk). We concluded that a residual stenosis of 75% at reperfusion abolishes the hyperemia but does not improve myocardial salvage.

Animals↗
PubMed1992

Disopyramide block of cardiac sodium current after removal of the fast inactivation process in guinea pig ventricular myocytes.

To determine the necessity of sodium channel fast inactivation for the block of sodium current (INa) by disopyramide, we studied the effects of disopyramide on INa in guinea pig ventricular myocytes treated with chloramine-T, which removes the fast component of INa inactivation. After exposure to chloramine-T (2 mM), INa amplitude was reduced at all voltages and INa decay was irreversibly prevented. Disopyramide (20 microM) produced both tonic block and use-dependent block of INa in chloramine-T-treated myocytes. Before treatment with chloramine-T, the time course of both the onset of and recovery from use-dependent block by disopyramide were best fit by the sum of double exponential functions, and the time constant of the slow phase of recovery increased as the membrane was hyperpolarized. After removal of the fast component of INa inactivation by chloramine-T, the fast phase of the onset block and the fast phase of recovery from block were abolished. However, the voltage dependency of the time course of recovery from block was unchanged. Thus, although the fast sodium inactivation process is not required for tonic and use-dependent block of INa by disopyramide, it contributes to the fast phase of block development and unbinding from use-dependent block.

Animals↗