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Biomedical subjects

S Morooka

Publications and source records attributed to S Morooka.

At least 37 records · Page 2Linked to original sources
PubMed1999

Inhibition of P-selectin attenuates neutrophil-mediated myocardial dysfunction in isolated rat heart.

The expression of P-selectin on postischemic endothelium after reperfusion has been shown to trigger neutrophil attachment and the subsequent inflammatory responses. Extensive studies have demonstrated that P-selectin is involved in the progression of neutrophil-mediated myocardial infarction and no-reflow phenomenon. In the present study, we examined the effects of selectin inhibitors, sialyl Lewis X-oligosaccharide and anti-P-selectin monoclonal antibody, PB1.3 on neutrophil-dependent left ventricular dysfunction in isolated rat heart. The hearts were subjected to global ischemia for 20 min and then reperfused for 45 min with rat plasma in the presence of human neutrophils during the first 5 min of the reperfusion. Left ventricular developed pressure and other parameters of the left ventricular function deteriorated throughout the reperfusion period in a neutrophil-dependent manner. In contrast, the coronary flow was reduced early on (< 15 min) but recovered to the level in the hearts reperfused with no neutrophils 45 min after the reperfusion. We examined the effects of selectin inhibitors under experimental conditions in which the hearts were perfused with 30 million neutrophils. The treatment with sialyl Lewis X-oligosaccharide at a dose of 0.3 mg/min resulted in amelioration of left ventricular developed pressure to 57.2 +/- 14%, compared to 26.1 +/- 4.3% in the saline-treated group (P < 0.05). Similarly, the treatment with mouse anti-human P-selectin monoclonal antibody (IgG1) PB1.3 at a dose of 0.6 mg/min resulted in the prominent recovery of left ventricular developed pressure after 45 min of reperfusion (59.9 +/- 9.3% vs. 26.1 +/- 4.3% in the saline-treated group, P < 0.05). PB1.3 also attenuated the elevation of left ventricular end-diastolic pressure compared to that of the saline-treated group during the reperfusion period. Moreover, the treatment with PB1.3 ameliorated the recovery of coronary flow until 10 min after the reperfusion and the recovery of coronary flow 10 min after the reperfusion was 55.2 +/- 9.2%, as compared to 28.2 +/- 7.7% in saline-treated hearts (P < 0.05). To our knowledge, this is the first direct demonstration that the specific inhibition of P-selectin results in the inhibition of neutrophil-mediated left ventricular dysfunction or myocardial stunning.

Animals↗
PubMed1999

Cilostazol inhibits the expression of activation-dependent membrane surface glycoprotein on the surface of platelets stimulated in vitro.

Cilostazol is a newly developed antiplatelet drug that has been widely applied for clinical use. Its antiplatelet action appears to be mainly related to inhibition of intracellular phosphodiesterase activity. Our study was designed to investigate inhibitory effects of cilostazol on the expression of activation-dependent platelet membrane surface glycoproteins. We performed flow cytometric analysis using monoclonal antibodies, PAC-1 (antibody against activation dependent epitope of GPIIb/IIIa), anti-CD62P (P-selectin), and anti-CD63. In vitro ADP stimulation of platelets taken from seven healthy volunteers produced significant increases in the mean channel fluorescence intensities (MFI) for PAC-1 (148% increase) and CD62P (43% increase) but did not increase in that for CD63. The enhanced MFI for CD62P was suppressed to the control level by pretreatment with 1 microM (88% suppression), 3 microM (94% suppression), and 10 microM (95% suppression) of cilostazol. However, that of PAC-1 was suppressed to a lesser degree (12, 16, and 21% suppressions, respectively). Cilostazol may inhibit P-selectin release from alpha-granule, rather than activation-dependent conformational change of GPIIb/IIIa in platelets. Cilostazol inhibits cellular interaction among platelets, leukocytes, and vascular endothelial cells mediated by P-selectin.

Antigens, CD↗
PubMed1999

Enhancement of short wing formation and ovarian growth in the genetically defined macropterous strain of the brown planthopper, Nilaparvata lugens.

When JH II, III or methoprene was applied in the nymphal stages to two different strains of the brown planthopper which were selected to produce long (macropterous) or short (brachypterous) wing forms, no effect was observed on the molting profile or metamorphosis. Brachypterization of a majority of the presumptive macropters was, however, observed by application of these chemicals, although there was no effect on wing form in the presumptive brachypters. The results show that the sensitive periods for the brachypterization of the presumptive macropters falls between early antepenultimate instar and within 1 or 2days of the penultimate instar, and that the chemicals were effective, in the following order of potency: methoprene>JH III>JH II. Ovarian growth was greatly enhanced in the presumptive macropters when JH III or methoprene was applied twice, within 12h of the 3rd or 4th nymphal instar and 6h before adult emergence. JH II on the other hand had no effect on ovarian growth when applied to the presumptive macropters at any of the nymphal stages. None of the chemicals had any effect on ovarian growth in the presumptive brachypters.

Journal Article↗
PubMed1999

Serum levels of circulating adhesion molecules after coronary angioplasty.

The activation of platelets, leukocytes, and vascular endothelial cells mediated by cell adhesion molecules may play a role in the mechanism of restenosis, which is still a significant complication after coronary angioplasty. We observed serial changes in the circulating soluble forms of adhesion molecules in 25 patients with coronary artery disease who underwent coronary angioplasty for a single lesion of the left anterior descending artery. Serum levels of sICAM-1 (p < 0.05) and sP-selectin (p < 0.05) were significantly increased immediately after angioplasty in the coronary sinus blood samples. These increases continued during the 48-hour observation period, and the maximum increase was seen 48 h after angioplasty for sICAM-1 (p < 0.01) and 24 h after angioplasty for sP-selectin (p < 0. 01). The level of sL-selectin increased 24 h (p < 0.01) and 48 h (p < 0.001) after angioplasty. These changes were not observed in the peripheral blood samples. The sE-selectin level did not change after angioplasty. A multiple regression analysis showed that the late loss index obtained from quantitative angiographic (QCA) analysis was correlated with the changes in sICAM-1 (r = 0.31, p < 0.05), sL-selectin (r = 0.28, p < 0.05), and sP-selectin (r = 0.26, p < 0. 05) 48 h after angioplasty in the coronary sinus blood samples, but was not correlated with procedural variables, other QCA variables, or the change in the sL-selectin level. The measurements of these adhesion molecule levels may help to evaluate traumatic vessel wall injury and inflammation at the intervention site after coronary angioplasty.

Analysis of Variance↗
PubMed1999

Cyclic bursts of ventricular premature contractions of more than one minute intervals.

Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs.

Adolescent↗
PubMed1999

Secondary prevention with lipid lowering therapy in familial hypercholesterolemia: a correlation between new evolution of stenotic lesion and achieved cholesterol levels after revascularization procedures.

OBJECT: To assess the value of secondary prevention with lipid lowering therapy following either balloon angioplasty (PTCA) or bypass surgery (CABG) in familial hypercholesterolemia patients, the correlation of the new evolution of stenotic lesions and therapeutically achieved cholesterol levels was studied in 50 patients. METHODS: All surviving patients were followed angiographically after 5 years, and findings were correlated with the annually determined total serum cholesterol (TC) levels. RESULTS: New coronary atherosclerotic plaques were not observed in 18 patients in whom the TC was controlled to <220 mg/dl but in 19 of 32 patients in whom the TC was >220 mg/dl, a new evolution of stenotic lesions was observed angiographically. CONCLUSION: The new evolution of stenotic lesions following revascularization in patients with FH can be controlled significantly by lipid lowering therapy to maintain a TC level of <220 mg/dl, and if diet alone can not achieve it, aggressive medication and even LDL apheresis might be justified.

Aged↗
PubMed1999

[Evaluation of restenosis after percutaneous transluminal coronary angioplasty using a Doppler index, the Tei index].

Cardiac function and restenosis were evaluated after percutaneous transluminal coronary angioplasty (PTCA) using a Doppler index (the Tei index). Thirty-eight patients, 31 men and 7 women (mean age 57 years) with ischemic heart disease were studied. The underlying heart diseases were angina pectoris without left ventricular asynergy in 16 patients and old myocardial infarction (OMI) with left ventricular asynergy in 22 . Ejection fraction was measured by M-mode echocardiography and deceleration time, and the interval between cessation and onset of the mitral inflow velocity (a), ejection time at aortic valve (b), and the Tei index [(a-b)/b] were measured by M-mode echocardiography performed before and 6 months after PTCA. The ejection fraction, deceleration time and Tei index showed no changes after PTCA in patients with angina pectoris with or without restenosis. In patients with OMI with restenosis, the Tei index increased slightly after PTCA, from 0.56 +/- 0.15 to 0.61 +/- 0.13. The deceleration time changed from 0.23 +/- 0.03 to 0.24 +/- 0.02 msec, and the ejection fraction from 0.46 +/- 0.11 to 0.51 +/- 0.17, neither significantly. However, in patients with OMI without restenosis (15 out of 22 patients), the Tei index significantly improved after PTCA, from 0.55 +/- 0.13 to 0.48 +/- 0.12 (p < 0.05). In patients with left ventricular asynergy due to old myocardial infarction, without restenosis, the Tei index significantly improved after PTCA. The Tei index is useful for evaluating restenosis after PTCA in patients with OMI.

Angina Pectoris↗
PubMed1999

[A ruptured aneurysm of the anterior and posterior inferior cerebellar artery: a case report].

We report a case of an anterior and posterior-inferior cerebellar artery (AICA-PICA) aneurysm. The patient was a 62-year-old woman who suffered from sudden onset of severe headache and nuchalgia. Computed tomography (CT) scan revealed subarachnoid hemorrhage in the ambient cistern and blood clots in the 3rd and 4th ventricles. Vertebral angiography demonstrated an aneurysm located at the distal segment of the left AICA-PICA. Three demensional CT scan was very useful for the decision concerning surgical strategy. The patient underwent bilateral occipital craniectomy and the aneurysm was clipped successfully via the midline suboccipital approach. Her postoperative course was uneventful. Postoperative angiography showed successful clipping of the aneurysm. Distal AICA-PICA aneurysm is a very rare disease and only one case has been reported in the literature. The clinical features, CT findings, and surgical approach of distal AICA-PICA aneurysms are briefly discussed while reviewing the literature.

Aneurysm, Ruptured↗
PubMed1998

Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty.

BACKGROUND: The Cutting Balloon is a novel dilatation catheter for coronary angioplasty (InterVentional Technologies Inc). It produces longitudinal, microsurgical incisions in the vessel wall before the actual dilatation. It is assumed that these controlled surgical incisions relieve hoop stress and reduce vessel wall injury and eventually restenosis. However, no clinical indicator to support the theory of reduced injury has been described. Certain clusters of differentiation (eg, CD11, CD18 on the leukocytes) are implicated in leukocyte adhesion, increased permeability, and opsonization. Therefore, they might serve as clinical indicators of the injury level of the vessels after angioplasty. METHODS AND RESULTS: We randomly selected 64 patients with isolated left anterior descending coronary artery disease for either Cutting Balloon angioplasty or conventional balloon angioplasty. The expression of CD18 and CD11b on the surface of neutrophils was determined by flow cytometric analysis. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) were also measured. The expression of both the CD18 and CD11b in the coronary sinus blood gradually increased and reached its maximum at 48 hours after angioplasty. The sICAM-1 levels in the coronary sinus serum also increased after angioplasty. Percentage increases of CD18 and CD11b expression and the increase of the sICAM-1 levels at 48 hours after angioplasty (as ratios to baseline values before angioplasty) were less in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group (CD18, 1.10+/-0.05 versus 1.31+/-0.05, P<0.05; CD11b, 1.23+/-0.06 versus 1.72+/-0.10, P<0.001; sICAM-1, 1.12+/-0.05 versus 1.25+/-0.02, P<0.05). In all patients, the late lumen loss at follow-up angiogram positively correlated with the increased levels of CD11b (R=0.59, P<0.001) and sICAM-1 (R=0.38, P<0.05) at 48 hours after angioplasty. CONCLUSIONS: Balloon angioplasty upregulated Mac-1 (CD11b/CD18) on the surface of the neutrophils and increased sICAM-1 levels in association with late loss increase. These changes were significantly smaller in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group. This suggests that Cutting Balloon angioplasty may produce less vessel wall injury and, consequently, less neutrophil activation, which may account for the lower rate of restenosis.

CD18 Antigens↗
PubMed1998

Increased plasma P-selectin induced by intravenous administration of endotoxin in rats.

We developed a competitive enzyme immunoassay for detection of rat P-selectin and examined temporal changes of plasma P-selectin levels in an endotoxin-induced injury model in rats. Soluble P-selectin was detected in rat plasma after intravenous administration of lipopolysaccharide (LPS), and increased to a maximum level of five-fold over baseline after 24 hours. Plasma P-selectin was partially purified by gelfiltration and was identified as a 122 kDa band by Western blotting. Using the ELISA system we developed, monitoring of plasma P-selectin has become possible in the rat.

Animals↗
PubMed1998

The role of P-selectin, sialyl Lewis X and sulfatide in myocardial ischemia and reperfusion injury.

The role of P-selectin and the ligands of selectins such as sialyl Lewis X and sulfatide was studied in a myocardial ischemia and reperfusion injury model. Anesthetized rabbits underwent the occlusion of coronary artery (30 min) followed by reperfusion (5 h). The inhibitory effect on myocardial ischemia and reperfusion injury was examined with infarct size normalized by area-at-risk. Intravenous administration of an anti-P-selectin monoclonal antibody, PB1.3 (2 mg/kg), reduced infarct size by 38%. Similarly, the administration of sialyl Lewis X-oligosaccharide (10 mg/kg) reduced infarct size by 53% significantly. Finally, the infarct size was significantly reduced bv 39% in sulfatide-treated group (10 mg/kg). These results suggest that P-selectin plays an important role in myocardial ischemia and reperfusion injury and that the ligands of selectins, such as sialyl Lewis X-oligosaccharide and sulfatide, have cardioprotective effect on myocardial ischemia and reperfusion injury.

Animals↗
PubMed1998

Impaired endothelium-dependent acetylcholine-induced coronary artery relaxation in patients with high serum remnant lipoprotein particles.

Acetylcholine (Ach)-induced vascular relaxation is mediated by nitric oxide released from the endothelium. Hence, impaired Ach-induced relaxation reflects endothelial dysfunction. The action of lipoprotein lipase on chylomicrons and very low density lipoproteins produces remnant lipoproteins (RLP) rich in triglycerides (TG), cholesterol (C) and apolipoprotein E (apo E). Apo E on RLP serves as a ligand for uptake of RLP by macrophages, endothelial cells and other cells expressing the LDL receptor or the remnant receptor; uptake of RLP by vascular wall cells can promote atherosclerosis. Serum C, TG, Lp(a), apo E, apo A-I, apo B, HDL-C and RLP-C were measured in 652 patients who underwent diagnostic coronary angiography. Of these, 48 (32 males and 16 females, age 59 +/- 10 years) were suspected of having ischaemic heart disease because they had chest pain, but without angiographic evidence of atherosclerotic coronary artery disease defined as a discrete stenosis or intimal irregularity, and without any other known underlying heart disease. These were selected for acetylcholine provocation test in the left coronary artery. Nineteen of 48 patients had high RLP-C ( > or = 5 mg/dl, mean 8.7 +/- 3.1 mg/dl), 29 had normal RLP-C ( < or = 5 mg/dl, mean 2.4 +/- 0.4 mg/dl, P < 0.0001). The percent change (-, constriction, or +, dilation) in coronary artery diameter after intracoronary injection of Ach was smaller in the high RLP-C group, compared with the normal RLP-C group thus, in the left anterior descending artery, -33 +/- 23 vs -8 +/- 25 in the proximal segment (P <0.01), -30 +/- 37 vs -3 +/- 29 in the mid segment (P < 0.01), -17 +/- 47 vs 16 +/- 43 in the distal segment (P < 0.001); in the left circumflex artery, -29 +/- 46 vs -9 +/- 28 in the proximal segment (P < 0.01), -29 +/- 43 vs -5 +/- 34 in the mid segment (P < 0.01), -26 +/- 43 vs 10 +/- 31 in the distal segment (P < 0.001). There were no significant differences in other lipid levels. These results suggest that there is an association between high serum RLP-C and coronary vascular endothelial cell dysfunction and that RLP-C may be taken as a marker of early stage coronary artery atherosclerosis not detectable by angiography.

Acetylcholine↗
PubMed1998

Differential contribution of various adhesion molecules to leukocyte kinetics in pulmonary microvessels of hyperoxia-exposed rat lungs.

To elucidate the differential role of various adhesion molecules in distorting leukocyte behavior in the microvasculature of hyperoxia-exposed rat lungs, we investigated fluorescein-labeled leukocyte and erythrocyte kinetics in isolated lungs taken from the animals exposed to 90% O2 for 48 h under conditions in which endothelial intercellular adhesion molecule-1 (ICAM-1) and P-selectin were inhibited by appropriate monoclonal antibodies (1A29 for ICAM-1 and ARP2-4 for P-selectin), while leukocyte L-selectin was restrained with fucoidin. Measurements of blood cell kinetics were made by a confocal laser luminescence microscope coupled with a high-speed video camera. In addition, we histologically examined leukocyte accumulation within the alveolar septa and ICAM-1 as well as P-selectin expressions in the lung. We found that P-selectin expression was sparsely enhanced only in arterioles, whereas ICAM-1 was significantly induced in both venules and capillaries. Firm adhesion of leukocytes was not identified in arterioles and venules, whereas leukocyte rolling was evident in both the vessels. Arteriolar rolling was regulated via a P-selectin- and ICAM-1-independent but L-selectin-dependent mechanism, whereas venular rolling was mediated via a P-selectin-independent but ICAM-1- and L-selectin-dependent pathway. Leukocyte sequestration within capillaries was augmented by an ICAM-1-related mechanism. These findings may suggest that, in hyperoxia-exposed lungs, induction of adhesion molecules and their obstacles to leukocyte behavior are qualitatively different among arterioles, venules, and capillaries.

Animals↗
PubMed1998

Ischemic change on electrocardiogram induced by hypoglycemia in a diabetic patient.

A 34-year-old female patient who presented to our hospital had been treated with insulin for diabetes since she was 25 year old. For the previous year she had experienced chest pain on exertion and during hypoglycemia. During both chest pain and exercise tests, ST depression and flattening of the T wave were recognized in leads II, III, aVF, and V2-V6 on the electrocardiogram, and thus ischemic heart disease was suspected. Cardiac catheterization was performed, but no organic stenosis or spasms were found. Hypoglycemia (41 mg/dl) was induced by intravenous injection of rapid insulin (total 18 U, 0.4 U/kg). However, no coronary change was seen, although she felt chest pain and the same ischemic electrocardiographic changes occurred. We hypothesized the causes of the ischemic change to be both the effects of insulin on the cardiovascular system and the physiologic stress induced by the existence of microvascular abnormality. Special care should therefore be taken with diabetic patients being treated with insulin or hypoglycemic agents.

Adult↗
PubMed1998

Carbamazepine-induced sinus node dysfunction and atrioventricular block in elderly women.

We report on four elderly women in whom carbamazepine was suspected of inducing sinus node dysfunction (3 patients) and atrioventricular block (1 patient). Patients were treated with carbamazepine, 200 to 600 mg a day, for trigeminal neuralgia (n = 3) or epilepsy (n = 1). After 1 to 16 months of carbamazepine therapy, these patients were admitted to our emergency room because of bradyarrhythmia. Their conduction disturbances on electrocardiographic monitoring disappeared immediately after the cessation of carbamazepine intake. Provocation tests were performed on three patients. Because of renal insufficiency, one patient could not undergo the provocation test. Her carbamazepine clearance was markedly decreased. Carbamazepine induced sinus arrest in two patients within 48 hours after intake, but did not induce atrioventricular block in the remaining patient. In two patients, computer simulation of carbamazepine pharmacokinetics was performed and disclosed a clear-cut relationship between the plasma concentration of carbamazepine and the frequency of sinus arrest. During the test, the maximum plasma carbamazepine concentration in these two patients did not exceed the therapeutic range. However, it did exceed the range in the one with a negative test. Our results suggest that careful monitoring of ECG and plasma drug concentration is required with carbamazepine therapy, especially in elderly women.

Aged↗
PubMed1998

Clinical significance of neutrophil adhesion molecules expression after coronary angioplasty on the development of restenosis.

To investigate the neutrophil activation process following percutaneous transluminal coronary angioplasty (PTCA), we examined the expressions of Mac-1 (CD11b/CD18), L-selectin (CD62L), and sialyl-LewisX (SLX) on the surface of neutrophils after the PTCA procedure, by flow cytometric analysis. Twenty-nine patients with single vessel coronary artery disease of the left anterior descending artery who underwent elective PTCA were enrolled. In the 17 patients without restenosis at the follow-up angiography, the mean channel fluorescence intensity (MFI) for CD18, CD62L and SLX did not change after PTCA. Only the CD11b level was increased at 48 h after the PTCA. In the remaining 12 patients who developed restenosis, the MFI values for CD18 and CD11b were increased at 24 h and 48 h after the PTCA. The MFI value for CD62L was decreased and that for SLX was increased at 48 h after the PTCA. These changes were more prominent in the coronary sinus blood samples than in those of the peripheral blood samples. Our data indicate the down-regulation of L-selectin, probably by shedding, as well as the up-regulations of Mac-1 and sialyl-LewisX, especially in patients with restenosis. It is suggested that neutrophil activation by an interaction between the selectin family and carbohydrate ligands after PTCA may play a role in the development of restenosis, as does the integrin family.

Angioplasty, Balloon, Coronary↗
PubMed1998

Detection of platelets activated during acetylcholine-induced coronary vasospasm.

Although platelet activation may play a role in coronary artery spasm, platelets activated following coronary vasospasm have not been clinically detected. We performed flow cytometric analysis of activation-dependent granular proteins, CD62P (P-selectin), CD63, PAC-1 (activated glycoprotein [GP] IIb/IIIa) and thrombospondin on the platelet plasma membrane in patients who exhibited acetylcholine-induced coronary vasospasm and compared findings with those in control patients without vasospasm. We simultaneously investigated the plasma levels of thrombin anti-thrombin III complex (TAT), plasmin alpha2-plasmin inhibitor complex (PIC), and thrombomodulin. In patients with vasospasm, the expression of CD62P, CD63 and PAC-1 on the platelet membrane surface increased in coronary sinus blood samples following coronary vasospasm, although the expression in aortic samples did not change. The TAT level also increased in the coronary sinus after vasospasm. Platelets might be activated by coronary vasospasm within the coronary circulation. The platelet activation process may be modulated by thrombin generation.

Acetylcholine↗