PubMed Health⌕ Search

Biomedical subjects

R Katori

Publications and source records attributed to R Katori.

At least 19 recordsLinked to original sources
PubMed1999

Alpha1-adrenergic stimulation induced hypertrophy in protein kinase C down-regulated cultured cardiac myocytes.

To examine whether protein kinase C (PKC) activation is essential for the induction of cardiac myocyte hypertrophy caused by alpha1-adrenergic stimulation, we investigated the hypertrophic effect of phenylephrine in PKC down-regulated and non-treated cultured cardiac myocytes obtained from neonatal Sprague-Dawley rat ventricles. The treatment with 10 nmol/L 12-tetra decanoylphorbol-13-acetate (TPA) for more than 2 hours decreased PKC activity by approximately 80% without marked hypertrophy. Phenylephrine increased [14C] phenylalanine (Phe) incorporation in both TPA non-treated and treated cells, 1.54- and 1.71-fold as large as control, respectively. The cell surface area also enlarged in both groups, 1.67- and 1.74-fold, respectively. Thus, phenylephrine induced the similar grade hypertrophy in cultured cardiac myocytes even when PKC was down-regulated. These results suggest that conventional PKC activation may not be essential for mediating myocyte hypertrophy by alpha1-adrenergic stimulation.

Adrenergic alpha-Agonists↗
PubMed1998

Basic fibroblast growth factor increased regional myocardial blood flow and limited infarct size of acutely infarcted myocardium in dogs.

Basic fibroblast growth factor (bFGF), a growth factor potent in promoting angiogenesis, has been shown to reduce infarct size in experimentally induced acute myocardial infarction. However, the effect of bFGF on regional myocardial blood flow (Qm) in the acutely infarcted myocardium has not been well clarified. In 20 open-chest dogs, the left anterior descending (LAD) coronary artery was occluded and animals were maintained in this condition for 4 weeks. In eight of these dogs, bFGF (300 microg) was injected into the myocardium supplied by the LAD and the artery was ligated (bFGF group), and in the other 12 dogs, saline was injected (control group). Nonradioactive colored microspheres were used to measure Qm. The amount of viable myocardium as percent of visual field in the microscope and the extent of fibrosis scored histologically from 0 to 5 in the infarcted area 4 weeks after occlusion were measured. In the outer layer, the Qm values immediately after and 4 weeks after occlusion were 26 +/- 2% and 70 +/- 6%, respectively, in the control group, and 46 +/- 5% and 121 +/- 13%, respectively, in the bFGF group. The Qm at both times in the bFGF group was significantly higher than the corresponding control group values (p < 0.01). The Qm at 4 weeks in the inner and the middle layers also significantly increased in the bFGF group. There was more viable myocardium (control vs bFGF group; 41 +/- 5 vs 61 +/- 7%, p < 0.05) and less fibrosis (3.1 +/- 0.2 vs 2.0 +/- 0.4, p < 0.01) at the outer layer in the bFGF group. It was found that bFGF caused a marked increase in Qm, an increase of viable myocardium, and a decrease of fibrosis in the infarcted myocardium in dogs.

Animals↗
PubMed1998

Significant role of the increase in renin-angiotensin system in cardiac hypertrophy and renal glomerular sclerosis in double transgenic tsukuba hypertensive mice carrying both human renin and angiotensinogen genes.

Tsukuba hypertensive mice (THM) are a hypertensive model prepared by mating a transgenic mice with human renin gene and a transgenic mice with human angiotensinogen gene. In the present study, we examined effects of renin-angiotensin system (RAS) on cardiac hypertrophy and renal disorders using Tsukuba hypertensive mice. While THM showed an increase of about 30 mmHg in systolic pressure compared to C57BL/6 mice employed as normal control animals, the increase in blood pressure was not observed in the mice to which either gene was transferred. Urinary volume, water intake volume, urinary albumin excretion, heart to body weight ratio and renal glomerular sclerosis index increased significantly in THM, but none of these parameters showed a significant difference from the C57 mice when they were examined in mice to which either of the genes was transferred. In contrast, when lisinopril was administered to THM, all the parameters decreased significantly without lowering the systolic pressure. From these findings, it was demonstrated that RAS was playing a significant role in cardiac hypertrophy and renal disorders of THM and that lisinopril had inhibitory effects on cardiac hypertrophy and renal glomerular sclerosis by inhibiting RAS.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Short-acting nifedipine and diltiazem do not reduce the incidence of cardiac events in patients with healed myocardial infarction. Secondary Prevention Group.

BACKGROUND: The administration of calcium antagonists to patients with healed myocardial infarction is a controversial treatment. This study was conducted to elucidate the effect of short-acting nifedipine and diltiazem on cardiac events in patients with healed myocardial infarction. METHODS AND RESULTS: A controlled clinical open trial of 1115 patients with healed myocardial infarction was carried out between 1986 and 1994. The patients included 595 who received no calcium antagonist, 341 who received short-acting nifedipine 30 mg/d, and 179 who received short-acting diltiazem 90 mg/d. The primary end points were cardiac events, which were defined as fatal or nonfatal recurrent myocardial infarction; death from congestive heart failure; sudden death; and hospitalization because of worsening angina, congestive heart failure, or premature ventricular contractions. Cardiac events occurred in 51 patients (8.6%) in the no-calcium-antagonist group and 54 (10.4%) in the calcium-antagonist group (odds ratio, 1.24; 95% CI, 0.83 to 1.85), demonstrating that the calcium antagonists did not reduce the incidence of cardiac events. Subgroup analysis revealed no beneficial effects of these drugs for reducing cardiac events in patients with such complications as hypertension or angina pectoris. CONCLUSIONS: This study showed that use of short-acting nifedipine and diltiazem in this postmyocardial infarction population was associated with a 24% higher cardiac event rate, but this strong adverse trend did not reach statistical significance.

Aged↗
PubMed1997

Sematilide blocks the inward rectifier potassium channel in isolated guinea pig ventricular myocytes.

1. In whole-cell patch recording, the relative potency of the blocking action of sematilide on IK1 was found to be constant at each potential level of IK1 activation. Under more acidic condition, the degree of block was decreased. These results strongly suggested that the neutral form of sematilide may penetrate the cardiac cell membrane via hydrophobic pathway. 2. In cell-attached patches, sematilide prolonged the interburst interval and reduced the opening probabilities of the IK1 channel without affecting either the mean open time or the mean closed time within a burst.

Animals↗
PubMed1997

The blocking mechanism of sodium currents by a new class I antiarrhythmic drug, Ro 22-9194, in isolated guinea-pig ventricular myocytes.

1. Ro 22-9124 produced tonic block of sodium currents (INa) with a Hill coefficient of 1.01 and a dissociation constant of 0.12 microM at a holding potential of - 100 mV, and use-dependent block at 2 Hz in conjunction with an increase in pulse duration (5-300 msec). 2. Ro 22-9194 blocks INa, at least partially, due to binding to the activated state. 3. The course of recovery from the use-dependent block, which was not affected by the membrane potential, was 4.0 sec, suggesting that Ro 22-9194 belongs to the intermediate kinetic class I drugs and it probably acts via a hydrophobic pathway.

Animals↗
PubMed1997

Effect of thromboxane A2 synthetase inhibitor on metabolism and contractility in ischemic reperfused rabbit heart.

The effect of thromboxane A2 synthetase inhibitor (OKY-046) on myocardial metabolism and contractility during ischemia and reperfusion was examined by the phosphorus 31-nuclear magnetic resonance (31P-NMR) in Langendorff rabbit hearts with use of an artificial blood substitute, perfluorochemical emulsion Fluosol-43. After normothermic fifteen-minute global zero-flow ischemia or fifteen-minute global low-flow ischemia (coronary perfusion pressure = 20 mmHg), reperfusion of sixty minutes was carried out. OKY-046 was administered from forty-five minutes prior to the global ischemia. Adenosine triphosphate (ATP), creatine phosphate (CrP), inorganic phosphate (Pi), pH, left ventricular systolic developed pressure (LV Dev.P) and coronary flow were continuously measured. Twenty-eight heart were divided into four experimental groups consisting of 7 hearts each; Group I consisted of controls with zero-flow ischemia; Group II, perfusion with OKY-046 (10(-6) M) in zero-flow ischemia; Group III, controls with low-flow ischemia; and Group IV, perfusion with OKY-046 in low-flow ischemia. Group II showed a significant inhibition of the increase in Pi and of the decrease in ATP, CrP, and pH during global ischemia compared with Group I, and a suppression of the overshoot of CrP observed after postischemic reperfusion. Group IV also showed a significantly marked improvement of ATP, CrP, and pH and significant suppression in Pi during low-flow ischemia compared with Group III. These were no differences in LV Dev.P and coronary flow among any groups. In conclusion, OKY-046 has a significantly beneficial effect on metabolism during both myocardial ischemia and reperfusion.

Adenosine Triphosphate↗
PubMed1997

Aspirin plus either dipyridamole or ticlopidine is effective in preventing recurrent myocardial infarction. Secondary Prevention Group.

The efficacy of combining antiplatelet agents with low doses of aspirin to prevent cardiac events in patients with myocardial infarction was examined. A total of 1,083 patients with prior myocardial infarction were randomly divided into those who were (618) and were not (465) treated with antiplatelet agents, and observed for 12.5 +/- 18.5 months. Those treated with antiplatelet agents included 113 patients treated with aspirin (50 mg) plus dipyridamole (150 mg/day), 253 treated with aspirin (50 mg) plus ticlopidine (200 mg/day), and 252 treated with only 1 of the 3 antiplatelet agents. Cardiac events, including fatal or nonfatal recurrent myocardial infarction, death by congestive heart failure, and sudden death, occurred in 34 patients (7.3%) in the nontreatment group and in 19 patients (3.1%; p < 0.01) in the treatment group; odds ratio 0.40, 95% confidence interval 0.23-0.71. There were only 2 cardiac events (1.8%) in the aspirin + dipyridamole group (p < 0.05 vs nontreatment group: odds ratio 0.28: 0.08-1.03), and 5 such events (2.0%) in the aspirin + ticlopidine group (p < 0.01; odds ratio 0.28: 0.11-0.69). Subgroup analysis to exclude differences in the patients' background confirmed the efficacy of these antiplatelet agents. We conclude that combined treatment with low doses of aspirin plus either dipyridamole or ticlopidine is effective in preventing cardiac events in patients who have had prior myocardial infarction.

Aged↗
PubMed1997

Increased coronary vasomotor tone in acute myocardial infarction patients with spontaneous coronary recanalization.

To clarify the role of coronary spasm or dynamic coronary obstruction in the development of acute myocardial infarction (AMI) with spontaneous recanalization (SR), symptoms in 296 patients with AMI admitted within 24 h after the onset of chest pain were analyzed just before and after onset, and coronary angiograms were analyzed soon after onset. Patients were divided into 3 groups according to the initial angiographic findings in the infarct-related coronary artery (IRCA): group 1 comprised 172 patients with total occlusion (TIMI O); group 2 comprised 57 patients with subtotal occlusion (TIMI 1,2); and group 3 comprised 67 patients with SR (TIMI 3). The incidence of SR was 20.3% at 0-4 h after onset, 22.2% at 4-6 h, 19.7% at 6-12 h, 24.0% at 12-24 h, and 36.0% at 24 h or later. The incidence of SR did not increase significantly as time elapsed. The incidence of angina at rest and variable-threshold angina before the onset of infarction was only 16.2% in group 1, but was significantly higher in groups 2 (64.3%) and 3 (61.9%). The incidence of intermittent chest pain at onset in group 1 (8.4%) was significantly lower than in groups 2 (54.5%) and 3 (38.8%). Vasodilation of the proximal normal segment adjacent to the stenotic site of the IRCA induced by intracoronary nitroglycerin was significantly higher in groups 2 (11.7 +/- 1.2%) and 3 (20.7 +/- 2.6%) than in group 1 (4.0 +/- 0.6%). These results suggest that coronary spasm or dynamic obstruction may be involved in the pathogenesis of thrombus formation or coronary obstruction causing AMI in many Japanese patients.

Adult↗
PubMed1997

[Prevention of cardiac events by beta-blocking agents in elderly patients after myocardial infarction].

We retrospectively analyzed the effect of beta-blocking agents on the incidence of cardiac events in elderly patients who had had myocardial infarction. A total of 1169 patients who had had a myocardial infarction (age, 60.2 +/- 11.4 years) were followed for a mean of 18.0 +/- 19.7 months and the incidence of cardiac events (fatal or nonfatal myocardial infarction, sudden cardiac death, and death due to congestive heart failure) was computed. There were 21 cardiac events in 653 patients who received beta-blocking agents (3.2%) and 39 events in 516 patients who did not receive beta-blocking agents (7.6%, p < 0.01). Among patients less than 50 years old, the incidences of cardiac events were 4.1% in those who received beta-blocking agents and 7.6% in those who did not; among those 50 to 59 years old the incidences were 3.0% and 7.5%, respectively; among those 60 to 69 years old they were 4.3% and 6.0%, respectively; and among those 70 years old or older they were 0.8% and 11.4%, respectively (p < 0.01). We found that beta-blocking agents prevented cardiac events both in elderly and in younger patients after myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1997

[Long-term prognosis in patients with exercise-induced ST-segment elevation after myocardial infarction].

The present study investigated whether the exercise-induced ST-segment elevation can predict the prognosis for patients with myocardial infarction. Among 529 patients with myocardial infarction, 411 underwent treadmill exercise testing about 5 weeks after the onset. All patients were followed up (mean [+/-SD] 54 +/- 41 months) to compare the incidence of cardiac events. One hundred and eighteen patients (22%) could not perform the exercise test due to cardiac or noncardiac limitation. Ineligibility for exercise test was most useful for risk stratification. Multivariate analysis showed that elimination from the stress test with cardiac limitation was the most significant predictor for cardiac death. Excluding the 16 patients with bundle branch block, the 395 patients were classified into four groups of ST-segment elevation (107 cases, 27%), ST-segment elevation combined with depression (22 cases, 6%), ST-segment depression (106 cases, 27%), ST-segment unchanged (160 cases, 40%). Among the various stress test abnormalities, only low exercise duration was a predictor for cardiac death. ST-depression and ST-elevation combined with depression were independent risk predictors for all cardiac events. Most patients with ST-elevation had single-vessel disease with excellent exercise capacity and low incidence of cardiac events. ST-segment elevation during exercise 5 weeks after myocardial infarction is not associated with a poor prognosis.

Aged↗
PubMed1997

[Aortic valve insufficiency caused by nonpenetrating chest trauma difficult to distinguish from infective endocarditis with transesophageal echocardiography: a case report].

A 58-year-old man was involved in an automobile accident and suffered remittent fever, leukocytosis and high C-reactive protein level. He developed a diastolic murmur 2 months after the accident. Transesophageal echocardiography showed severe aortic regurgitation with a vegetation-like echo image attached to the right coronary cusp leaflet, suggesting infective endocarditis. Intensive medical treatment for 11 months did not improve the vegetation-like echo-image, so aortic valve replacement was performed. Disruption of the right coronary cusp leaflet was confirmed surgically. Prolapse had occurred as a result of disruption during diastole. The vegetation-like echo-image was considered to be the tip of this leaflet.

Aortic Valve Insufficiency↗
PubMed1996

Recombinant tissue plasminogen activator prevents intimal hyperplasia after balloon angioplasty in hypercholesterolemic rabbits.

The purpose of this study was to clarify whether continuous infusion of recombinant tissue plasminogen activator (rtPA) prevents intimal hyperplasia at the site of arterial injury. Forty-three Kurosawa and Kusanagi hypercholesterolemic (KHC) rabbits which underwent balloon angioplasty of the right common iliac artery were randomly divided into 2 groups; rtPA for 7 days (n = 29) and untreated (n = 14). The former group was subdivided into a high-dose group (n = 15) (2 mg/kg per day continuously for 7 days after 3 mg/kg for 4h) and a low-dose group (n = 14) (0.6 mg/kg per day for 7 days after 0.6 mg/kg for 4 h). Balloon angioplasty was performed with a 2.5-mm balloon (3 x 60-sec, 6-atm inflations at 60-sec intervals) 1 h after the initiation of rtPA infusion via an ear vein. The iliac arteries of the rabbits were histologically studied at 28 days. The cross-sectional areas of the intima, media, and adventitia were calculated at the site of intimal hyperplasia. The intimal cross-sectional area was 0.07 +/- 0.11 (mean +/- SD) mm2 for the high-dose rtPA group and 0.11 +/- 0.07 mm2 for the low-dose rtPA group, and both of these values were significantly less than that for the control group (0.57 +/- 0.21 mm2 p < 0.01). The ratio of the intimal to medial cross-sectional area was significantly (p < 0.01) lower for the rtPA groups than for the control group (high-dose rtPA; 0.10 +/- 0.13, low-dose rtPA; 0.21 +/- 0.19, control; 1.25 +/- 0.55). In conclusion, continuous infusion of rtPA for 7 days prevented intimal hyperplasia after balloon injury.

Angioplasty, Balloon↗
PubMed1996

Effect of acetylsalicylic acid on metabolism and contractility in the ischemic reperfused heart.

The effect of acetylsalicylic acid (ASA) on high-energy phosphates (adenosine triphosphate: ATP, creatine phosphate: CrP, inorganic phosphate: Pi) and intracellular pH during myocardial ischemia and reperfusion was studied using phosphorus 31-nuclear magnetic resonance (31P-NMR) in the isolated rabbit hearts. Coronary flow, left ventricular systolic developed pressure (LV Dev.P) and left ventricular end-diastolic pressure (LVEDP) were also measured. Langendorff hearts perfused at 37 degrees C with the perfluorochemical emulsion Fluosol-43 were subjected to 15 min and 30 min of zero-flow ischemia and to 15 min of low-flow ischemia (coronary perfusion pressure = 20 mmHg) followed by 65 min of reperfusion (control, Group I). ASA (0.28 mmol/L) was infused either for the entire experimental period from beginning 45 min prior to ischemia (Group II) and infused immediately after reperfusion (Group III). During ischemia, Group II showed a significant suppression of the decrease in the ATP level and pH with both zero-flow and low-flow ischemia compared to those in the other groups, and moreover the increase in Pi and the decrease in CrP in low-flow ischemia were also suppressed. In Group III, the ATP level during reperfusion was significantly higher than that in Group I, but was not significantly different from that in 30 min zero-flow ischemia. In 30 min zero-flow ischemia, Pi, CrP and coronary flow after reperfusion in Group II tended to recover to preischemic values. There were no differences in LV Dev.P among the 3 groups. In conclusion, ASA has a protective effect on myocardial high-energy phosphates during ischemia and reperfusion in rabbit hearts.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

[Hyperventilation and cold pressor stress echocardiography for diagnosis of vasospastic angina : report of five cases].

Two-dimensional echocardiography was used for diagnosing coronary vasospasm during the cold pressor stress test immediately after hyperventilation in five patients with suspected vasospastic angina. The test consisted of hyperventilation for 6 min and cold water pressor for 2 min under continuous electrocardiographic and echocardiographic monitoring. Coronary angiography with intracoronary injection of acetylcholine was performed in all patients within 1 month after the stress test. During the stress test, new asynergies of both the anterior and inferior walls were seen in three of the five patients, and new asynergy of the anterior wall in the other two patients. All acetylcholine induced coronary artery spasms occurred at the same locations as the new asynergies provoked by the stress test. In three patients, wall motion abnormality occurred earlier than ST segment elevation, and the other two patients had no ST changes. Chest pain was induced in three patients and delayed in comparison to electrocardiographic and echocardiographic changes. Echocardiographic monitoring during the stress test could detect spasms unaccompanied by either ST segment changes or chest pain, and could detect multivessel coronary spasms. Hyperventilation and cold pressor stress echocardiography may be used for the diagnosis of vasospastic angina.

Acetylcholine↗
PubMed1996

[Prevention of left ventricular aneurysm formation and left ventricular remodeling caused by percutaneous transluminal coronary angioplasty performed 24-48 hours after onset of acute myocardial infarction].

The prevention of left ventricular aneurysm formation and left ventricular remodeling by percutaneous transluminal coronary angioplasty (PTCA) performed 24 to 48 hours after onset of acute myocardial infarction was investigated. Left ventriculography and coronary angiography were performed in 25 patients within 24 hours of onset of acute myocardial infarction. The patients were divided into two groups; reperfusion group (n = 17) and successful PTCA group (n = 8). The reperfusion group and the PTCA group included patients whose infarct-related coronary arteries were successfully reperfused to 99%, Thrombolysis in Myocardial Infarction (TIMI) grade II or III, immediately after coronary thrombolysis. However, the reperfusion group did not include the patients with spontaneous reperfusion or reperfusion after PTCA. The PTCA group consisted of patients who underwent successful PTCA performed within 24 to 48 hours after onset of infarction (mean 28.4 +/- 6.0 hours). Non-reperfusion in the acute phase was defined as TIMI grade 0-I. The size of the ventricular aneurysm in the PTCA group was significantly reduced compared with the reperfusion group (PTCA group 4.2 +/- 8.7%, reperfusion group 27.2 +/- 6.6%; p < 0.01). The increase of left ventricular end-diastolic volume (delta LVEDVI) from the acute to chronic phases was calculated to estimate left ventricular remodeling. There was a significant difference between the two groups in delta LVEDVI (PTCA group 4 +/- 19 ml/m2, reperfusion group 19 +/- 17 ml/m2; p < 0.05). PTCA performed within 24 to 48 hours after onset in patients with acute myocardial infarction and infarct-related coronary arteries, resulting in reperfusion to 99% TIMI grade II or III immediately after coronary thrombolysis, prevents left ventricular aneurysm formation and remodeling.

Aged↗
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↗