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Biomedical subjects

R Katori

Publications and source records attributed to R Katori.

At least 19 recordsLinked to original sources
PubMed1995

What is the most appropriate variable for estimation of mean pulmonary capillary wedge pressure by transesophageal pulsed Doppler echocardiography?

UNLABELLED: Although left ventricular (LV) inflow and pulmonary venous (PV) flow variables estimated by transesophageal Doppler echocardiography (TEE) reflect pulmonary capillary wedge pressure (PCWP), they are also affected by changes in cardiac function. The purpose of the present study was to detect the most appropriate variable for the estimation of PCWP by TEE in patients (pts) with ischemic heart disease. Several variables of LV inflow and left upper PV flow were compared with PCWP in 36 pts (six with angina pectoris and 30 with old myocardial infarction). Early diastolic flow (E) and atrial contraction flow (A) were used as LV inflow, while systolic forward flow (X), diastolic forward flow (Y) and atrial contractile reversal flow (z) were used as PV flow. The peak velocity of each flow wave (Ep, Ap, Xp, Yp, and Zp) and the time-velocity integral (Ei, Ai, Xi, Yi, and Zi) were measured. The ratio of Ep to Ap (Ep/Ap), Ei to Ai (Ei/Ai), Xp to Yp (Xp/Yp), Xi to Yi (Xi/Yi), Zp to Ap (Zp/Ap), Zi to Ai (Zi/Ai) and the systolic fraction of PV forward flow were calculated. Among these variables, the Zi/Ai ratio was most strongly correlated with PCWP (R = 0.80). The Zi/Ai ratio may not be influenced by atrial function because the augmentation of atrial pump function increases Zi as well as Ai, and this may be one reason why the ratio correlated well with PCWP. CONCLUSION: The Zi/Ai ratio is a new useful variable for estimating PCWP by TEE.

Aged↗
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

[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↗
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↗
PubMed1991

Efficacy and safety of clentiazem in patients with essential hypertension: results of an early pilot test.

The purpose of this study was to evaluate the antihypertensive effect of a new calcium antagonist, clentiazem, on inpatients or outpatients with essential hypertension. After blood pressure was stable and greater than 160/95 mmHg with placebo for at least a 2-week observation period, oral clentiazem was administered once daily and dosage was increased stepwise from 10 to 40 mg over 10 weeks. Blood pressure significantly decreased by the second week of the study, and this hypotensive effect was maintained until the eighth week. Cumulative effective rate (percent of patients whose blood pressure decreased in 20/10 mmHg) in 62 outpatients were as follows; 10.3% at 10 mg, 39.6% at 20 mg, 70.2% at 30 mg, 76.6% at 40 mg. There was no significant postural change observed in the blood pressure from supine to standing position. Side effects such as dizziness, general malaise and gait disturbances were observed in 3 (3.9%) of 76 patients. No abnormal changes in clinical laboratory examinations or electrocardiograms were caused by clentiazem. Thus these data demonstrated that clentiazem produces certain antihypertensive effects with sufficient safety.

Adult↗
PubMed1991

Aprindine blocks the sodium current in guinea-pig ventricular myocytes.

Aprindine is a class Ib antiarrhythmic agent. We studied effects of aprindine (3 mumol/l) on the Na+ current using whole cell voltage clamp (tip resistance = 0.5 M omega, [Na]i ando = 10 mmol/l at 18 degrees C). Aprindine revealed tonic block (Kdrest = 37.7 mumol/l, Kdi = 0.74 mumol/l; n = 4). Aprindine, shifted inactivation curve to hyperpolarizing direction by 11.4 +/- 3.5 mV (n = 4) without changes in slope factor. In the presence of 3 mumol/l aprindine, aprindine showed phasic block, i.e., duration-dependent block at 2 Hz (64% +/- 3% at 1.5 ms, 82% +/- 6% at 20 ms, 93% +/- 7% at 200 ms; n = 4). Short single prepulse also produced aprindine-induced phasic block (12% at 1.5 ms, 22% at 100 ms; n = 2). After removal of fast inactivation of Na+ current by 3 mmol/l tosylchloramide sodium, aprindine revealed phasic block, independent of holding potential. The recovery time constant from aprindine-induced phasic block was 4.8 s at holding potential = -100 mV and 5.0 s at holding potential = -140 mV. This use-dependent block of aprindine had pH dependency. Under acidic condition (pH 6.0), 3 mumol/l aprindine showed smaller use-dependent block (14% +/- 7% at 2 Hz; n = 4) comparing with either at pH 7.4 (68% +/- 13%; n = 4) or at pH 8.0 (90% +/- 12%; n = 4). The results suggest that aprindine could bind to the receptor via activation process through channel pore, resulting in decrease of Na+ current, and egress from the receptor through the lipid bilayer. These effects might be attenuated under acidic condition due to changes in intracellular ratio of charged to neutralized form of drug molecule.

Action Potentials↗