Biomedical subjects

T Meguro

Publications and source records attributed to T Meguro.

At least 37 records · Page 2Linked to original sources

PubMed2001

Risk factors and predictors of coronary arterial lesions in Japanese hypertensive patients.

The morbidity rate of coronary artery disease has recently increased in Japan. This is attributable to changes from traditional to more westernized lifestyles. In this study, we therefore examined the risk factors and predictors of coronary arterial lesions in Japanese patients with essential hypertension. Coronary angiography was performed in 109 consecutive essential hypertension patients (57 men and 52 women; 66 +/- 8.0 years of age) with either angina pectoris or atypical chest pain, who were chosen from 485 consecutive hypertensive patients in a hypertension clinic in Sendai, Japan. Coronary arterial stenosis of greater than 50% was defined as significant and used as a dependent variable for the multiple regression analysis. Risk factors were defined as factors confirmed to have a causal relationship with coronary arterial lesions, whereas arteriosclerotic complications and hypertensive target organ damage were defined as predictors. Multiple logistic regression analysis was performed using these parameters as independent variables. Of 109 patients, 25 had a coronary arterial stenosis greater than 50%. A smoking habit (odds ratio (OR): 4.48; 95% confidence interval (CI): 1.13-17.82; p<0.05), hypercholesterolemia (OR: 5.34; 95% CI: 1.52-18.73; p<0.05), and 24-h diastolic blood pressure (OR: 2.33; 95% CI: 1.06-5.16; p<0.05) were significant risk factors, whereas carotid intima-media thickness (OR: 5.85; 95% CI: 1.48-23.2; p<0.05) was a significant predictor of coronary arterial lesion. When two of the major risk factors (a smoking habit, hypercholesterolemia, or impaired glucose tolerance including diabetes mellitus) were clustered in addition to the hypertension, the risk of coronary arterial lesions increased by 6.7 to 10.1 times. These findings indicate that the major risk factors established in Caucasians, i.e., a smoking habit, hypercholesterolemia and blood pressure level, are also risk factors for coronary arterial lesions in Japanese with essential hypertension. The presence of two or more risk factors increases the risk of coronary arterial lesions synergistically in the presence of hypertension.

Aged↗

PubMed2001

Mitral exposure technique for redo cardiac surgery. A left mediastinal pleurotomy and minimal adhesiotomy method.

We report an improved mitral exposure technique for mitral valve re-operation. Left mediastinal pleurotomy through a median sternotomy achieves rotation of the heart and excellent exposure of the mitral valve allowing the apex to drop posteriorly. We employed this technique in redo mitral valve surgeries for over a 3-year period. This minimal adhesiotomy method is technically simple, safe and time-saving.

Humans↗

PubMed2001

Change in the diameter of the radial artery transradial intervention using a 6 French system in Japanese patients.

We examined the change in the diameter of the radial artery after transradial intervention (TRI) using a 6 French system in 50 Japanese patients in order to investigate whether the radial artery would be preserved after TRI. In all cases, the Allen test was normal and repeated puncture was possible at the TRI site 3 months after TRI. Moreover, the appearance of new stenosis or thinning throughout the radial artery at the TRI site was not seen. The diameter of the radial artery 3 months after TRI tended to be somewhat smaller at both the proximal and distal sites; however, there was not a statistically significant change between the diameter before and 3 months after TRI. Our results show that the radial artery will be preserved after TRI using a 6 French system in selected Japanese patients.

Aged↗

PubMed2000

Response of the radial artery to three vasodilatory agents.

We examined the response of the radial artery to vasoactive agents (isosorbide dinitrate, ISDN, 1 mg, 3 mg, and 5 mg; verapamil, 1 mg, 3 mg, and 5 mg; and lidocaine, 10 mg, 30 mg, and 50 mg) in 100 consecutive patients admitted for elective coronary angiography. The drug solutions were directly injected into the radial artery from the puncture site. As a result, 5 mg of ISDN increased the diameter of the radial artery by 31% and 28.8% at the proximal and distal sites, respectively. Similarly, 5 mg of verapamil increased it by 9% and 10.8% at the proximal and distal site, respectively. But 10 mg of lidocaine decreased it by -15.6% and -12.1% at the proximal and distal site, respectively. At the doses utilized, ISDN was the most potent vasodilator for the radial artery and lidocaine caused paradoxical vasoconstriction.

Adult↗

PubMed2000

Deep circumflex iliac artery as a free arterial graft for myocardial revascularization.

When complete revascularization cannot be obtained with the internal thoracic artery and the other arterial grafts, the deep circumflex iliac artery (DCIA) may be an excellent alternative conduit. The deep circumflex iliac artery was used as a free graft for direct myocardial revascularization in 4 patients from January to July 1999. We describe our experience with this arterial conduit, review the anatomy of the artery, and present our harvesting technique.

Coronary Angiography↗

PubMed2000

Crystal structure of the low-humidity form of aspartame sweetener.

The low-humidity IB crystal form of aspartame (L-alphaaspartyl-L-phenylalanine methyl ester) is prepared via humidity-induced transition from the highly hydrated IA crystal form and is used widely as a sweetener. The crystal structure of the low-humidity IB form is determined at 1.05 A resolution (0.476 A(-1) in maximum sintheta/lambda) from an extremely fine fibrous crystal using synchrotron radiation. There are three aspartame molecules and two water molecules in the asymmetric unit of the monoclinic space group P2(1). Each aspartame molecule adopts an almost identical extended conformation which is commonly observed in other crystal forms of aspartame. Three aspartame molecules are assembled into a triangular trimer, and trimer units are stacked along the b-axis via hydrogen-bonding and electrostatic interactions in the main chains and also via hydrophobic contacts in the phenyl side-chains. Six trimer units are related by pseudo 6(1)-screw axis symmetry and form a hydrophilic channel at their center. The hydrophilic channel in the IB form contains only four water molecules in the unit cell, compared with 16 in the IA form. Although the IB form exhibits a trimer structure similar to that of the IA form, one aspartame molecule is rotated by approximately equals 20 degrees from the orientation in the IA form. This arrangement of the molecule implies that the humidity-induced transition is accompanied by a flapping motion of its methyl ester group. These structural differences may imply the stepwise transition from the IA to the IB forms.

Aspartame↗

PubMed2000

Curative treatment of cerebral arteriovenous malformations by embolisation using cellulose acetate polymer followed by surgical resection.

AIM: To investigate the usefulness of embolising cerebral arteriovenous malformations (AVMs) with a cellulose acetate polymer solution before surgical resection. METHODS: The cases of 12 patients with AVMs treated by embolisation before surgical resection were renewed. Two types of cellulose acetate polymer solutions were used to occlude 40 feeding vessels. All patients underwent surgical resection 1-51 days after embolisation. RESULTS: Reduction of the nidus volume after embolisation ranged from 20% to nearly 100%. Transient neurological deficits occurred in three patients, persistent deficits occurred in one and there were no haemorrhagic complications. All but one arteriovenous malformation were completely resected. Embolisation helped to identify feeding vessels and ease dissection. Histopathological examination of resected specimens disclosed mild inflammatory reactions in the acute stage and no unfavourable granulomatous changes in the chronic stage. CONCLUSION: Embolisation with cellulose acetate polymer solutions followed by surgical resection is safe and efficacious for treating cerebral AVMs.

Adult↗

PubMed2000

Adenovirus-mediated glial cell line-derived neurotrophic factor gene delivery reduces motor neuron injury after transient spinal cord ischemia in rabbits.

OBJECTIVE: Glial cell line-derived neurotrophic factor (GDNF) has protective effects on various injuries involving the central and peripheral nervous systems in vitro and vivo. However, the possible protective effect of GDNF on spinal cord ischemia and the exact mechanism involved in the ameliorative effect of GDNF on ischemic spinal cord injuries are not fully understood. Therefore, we investigated the possible protective effect of the adenovirus-mediated GDNF gene delivery on transient spinal cord ischemia in rabbits. METHODS: The adenoviral vector (lacZ gene as a control or GDNF gene contained) was injected directly into the lumbar spinal cord via a needle inserted into the dorsal spine 2 days before the animal was subjected to 15 minutes of spinal cord ischemia induced by infrarenal aortic occlusion. In situ terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick-end labeling (TUNEL staining) was performed, and temporal profiles of the GDNF and caspase-3 (caspase-3 is the marker of apoptotic change) immunoreactivity were investigated. RESULTS: In the control rabbit, the majority of motor neurons showed selective cell death at 7 days of reperfusion. Immunocytochemistry showed that in situ TUNEL staining was selectively detected at 2 days of reperfusion in motor neuron nuclei. GDNF and caspase-3 were selectively induced in the motor neuron cells at 8 hours of reperfusion. In the GDNF-treated group, a large population of motor neuron cells was still surviving at 7 days after having been subjected to 15 minutes of ischemia. Unlike the control group, the GDNF-treated group expressed GDNF persistently. Induction of TUNEL staining and immunoreactivity for caspase-3 were greatly reduced by the GDNF treatment. CONCLUSION: These results suggest that the reduction in motor neuron death by GDNF was greatly associated with a reduction in DNA fragmentation and apoptotic signals of the caspase-3 cascade; they further suggest a great potential for gene therapy for paraplegic patients in the future.

Adenoviridae↗

PubMed2000

Effect of external stenting and systemic hypertension on intimal hyperplasia in rat vein grafts.

OBJECTIVE: Overdistention of vein grafts in arterial circulation and systemic hypertension are thought to be influential risk factors contributing to vein graft failures. This study tested the effects of external stenting in preventing systemic hypertension and overdistention of the rat vein graft in the long term. METHODS: Jugular vein grafts were interposed into the carotid artery of normotensive (n = 39) and two-kidney, one-clip hypertensive (n = 30) rats. Jugular vein grafts wrapped with 1.5-mm-diameter polyester stents were used in normotensive (n = 26) and hypertensive (n = 25) rats. The vein grafts were harvested at 1, 2, 4, 8, 12, and 24 weeks after the grafting procedure. The neointimal area and wall thickness were measured by computerized planimetry, and Ki-67 immunohistochemistry was used to detect replicative smooth muscle cells in the graft wall. RESULTS: In each group, intimal hyperplasia was apparent at 1 week and increased gradually to 24 weeks. The number of Ki-67-positive cells was most increased at 2 weeks after the grafting procedure and gradually decreased thereafter. The numbers of Ki-67-positive cells and the extent of intimal hyperplasia were not significantly different between normotensive and hypertensive rats. Both neointima formation and cell proliferation in the graft wall were significantly reduced by external stenting as compared with the results with unstented grafts. CONCLUSION: Systemic hypertension by itself is not a risk factor for intimal hyperplasia and experimental vein graft failure in the long term. External stenting is effective against intimal hyperplasia, and it is possible to reduce the subsequent atherosclerotic change of the vein graft wall and improve the long-term patency of the vein graft with external stenting.

Animals↗

PubMed2000

Intermittent propofol sedation during embolization of cerebral arteriovenous malformations.

Embolization procedure was performed for a 12-year-old boy with a left parietal arteriovenous malformation. Although provocative tests for the feeders to be occluded were considered very informative, the patient had to be sedated during microcatheter insertion. We used intermittent sedation with propofol during the interventional procedure, and obtained successful embolization.

Anesthetics, Intravenous↗

PubMed2000

Age-adjusted heart rate variability as an index of the severity and prognosis of heart failure.

The age-adjusted, heart rate variability (HRV) was evaluated as a parameter for the severity of heart failure and its prognosis. HRV was obtained by 24-h Holter monitoring in patients with left ventricular dysfunction (LVD). New York Heart Association (NYHA) functional classification, echocardiography, radioisotope ventriculography, and blood examination were performed, and compared between patients and normal subjects. The evaluation was repeated during the follow-up period. Finally, using the lower limit of HRV, patients were divided into either normal or abnormal group for each low-frequency power (LF) and high-frequency power (HF) (age-adjusted HRV). Other parameters of heart failure and prognosis were compared between these 2 groups. HRV tended to be lower in patients with LVD. HF decreased at the early stage of heart failure, but did not decrease progressively. LF decreased progressively. HRV change paralleled the change of NYHA. The abnormal HRV group showed a poor prognosis for cardiac death, but not for sudden cardiac death. In patients with LVD, HRV was decreased compared with the normal subjects. Change in HRV correlated with the change in NYHA classification. Age-adjusted HRV correlated with cardiac-death prognosis, but not for sudden cardiac death.

Aged↗

PubMed2000

Urinary excretions of albumin and type IV collagen in normotensive and hypertensive subjects.

Plasma albumin leaks into urine as a result of glomerular hypertension and basement membrane injury, while urinary type IV collagen derives from mesangial matrix and glomerular basement membrane. The purpose of this study was to elucidate the pathophysiological significance of these urinary microproteins as an indicator of cardiovascular organ injuries in hypertension. In health-checkup participants without diabetes, proteinuria, or microhematuria, and who were not being treated for hypertension or any other disease at the time of enrollment, urinary albumin and type IV collagen were measured and their relations to organ injuries and cardiovascular risk factors were evaluated. Of 1,079 subjects (40- to 65-year-old; 256 men and 823 women) enrolled in the study, 120 (11.1%) had untreated hypertension exceeding 140/90 mmHg. Urinary albumin was positively correlated with both age (r=0.16, p<0.001) and systolic blood pressure (r=0.27, p<0.001). Urinary type IV collagen was not only positively correlated with age (r=0.12, p<0.001) and diastolic blood pressure (r=0.14, p<0.001) but also negatively correlated with blood hemoglobin (r=-0.12, p<0.001). Urinary albumin, but not type IV collagen, had a significant relation to electrocardiographic signs of left ventricular hypertrophy (p=0.012) and retinal arteriosclerosis on fundoscopy (p <0.001). Thus both albumin and type IV collagen would seem to have increased in association with age and hypertension in this cohort. It is suggested that urinary albumin is an indicator not only of renal injury, but also possibly of development of cardiac hypertrophy and arteriosclerotic changes. Urinary type IV collagen, on the other hand, may be associated with renal tissue injuries that affect erythrokinetics.

Adult↗

PubMed2000

Upregulation of rho A and rho kinase messenger RNAs in the basilar artery of a rat model of subarachnoid hemorrhage.

OBJECT: Rho A, a small guanosine triphosphate-binding protein, and rho kinases have been suggested to play an important role in the agonist-induced myofilament Ca++ sensitization and cytoskeletal organization of smooth-muscle cells. To discover their possible roles in the prolonged contraction seen in cerebral vasospasm, the authors investigated the messenger (m)RNA expressions of rho A and rho-associated kinases alpha and beta in the basilar artery (BA) of a rat double cisternal blood-injection model. METHODS: An experimental subarachnoid hemorrhage (SAH) was achieved in rats by twice injecting autologous arterial blood into the cisterna magna of each animal. The mRNAs for rho A and rho-associated kinases alpha and beta of the rat BA were analyzed using reverse transcription-polymerase chain reaction (RT-PCR). The cisternal blood injection induced a marked corrugation of elastic lamina and contraction of smooth-muscle cells observed with the aid of light and transmission electron microscopy in the rat BA on Days 3, 5, and 7. Results of the RT-PCR revealed that mRNAs for rho A and rho kinases alpha and beta were expressed in the rat BA and that they were significantly upregulated and reached their peaks on Day 5. CONCLUSIONS: The mRNA upregulation of these proteins indicates that activation of rho A/rho kinase-related signal transduction pathways is involved in the development of long-lasting contraction of cerebral arteries after SAH.

Animals↗

PubMed2000

Role of calcium channels in oxyhemoglobin-induced apoptosis in endothelial cells.

OBJECT: Oxyhemoglobin (OxyHb) released from hemolysed erythrocytes has been considered to be responsible for cerebral vasospasm after subarachnoid hemorrhage. The authors previously reported that OxyHb produced apoptosis in cultured vascular endothelial cells. The change in intracellular Ca++ homeostasis was expected to be one of the possible mechanisms of the cytotoxic effects of OxyHb. This study was undertaken to investigate the protective effects of Ca++ channel blockers on OxyHb-induced apoptosis. METHODS: Cultured bovine coronary artery and brain microvascular endothelial cells (passages 5-9) were used. A cell density study, immunohistochemical staining, and DNA fragmentation analysis were performed to confirm apoptosis. Various concentrations (1-50 microM) of OxyHb were used for 24- to 72-hour incubations with and without Ca++-channel blockers. Oxyhemoglobin produced cytotoxicity leading to cell detachment from the culture dish in time- and concentration-dependent manners. The highest dose (50 microM) of OxyHb produced cell detachment after a 24-hour incubation, and the lower doses (1-10 microM) produced cell detachment after 48 to 72 hours. Immunohistochemical analysis showed that apoptosis occurred in cells that were still attached to the side of the culture dish after 48 to 72 hours of OxyHb treatment (5 microM). The OxyHb (10 microM) produced DNA ladders at 48 to 72 hours. Three Ca++-channel blockers were used to prevent the toxic effect of OxyHb. The voltage-dependent Ca++-channel blocker nicardipine (1 microM), the voltage-independent Ca++-channel blocker econazole (10 microM), and the inorganic Ca++-channel blocker lanthanum (100 microM) all failed to prevent cell detachment or DNA ladders produced by OxyHb. These results were similar in both cell lines. CONCLUSIONS: Oxyhemoglobin produced apoptotic changes in cultured vascular endothelial cells, and Ca++-channel blockers did not prevent OxyHb-induced apoptosis.

Animals↗

PubMed2000

Effects of mitogen-activated protein kinase inhibitors on cerebral vasospasm in a double-hemorrhage model in dogs.

OBJECT: Mitogen-activated protein kinase (MAPK) may be involved in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. This study was conducted to investigate the ability of the MAPK inhibitors PD-98059 and U-0126 to reverse vasospasm in a double-hemorrhage model in dogs. METHODS: Twenty-two adult mongrel dogs of either sex, each weighing 18 to 24 kg, were divided randomly into four groups: control SAH (four dogs), vehicle- (dimethyl sulfoxide, six dogs), PD-98059- (six dogs), and U-0126-treated groups (six dogs). The double-hemorrhage model was created by an autologous blood injection into the cisterna magna on Days 0 and 2. An intracisternal injection of MAPK inhibitors was administered once per day on Days 3 through 6. Cerebral angiography was performed on Days 0 and 7 before the animals were killed. Western blot analysis was used to study the effects of hemorrhage and drug treatment on the MAPK immunoprecipitation. Severe vasospasm developed in the dogs in the control and vehicle-treated groups (basilar artery [BA] diameter reduction 46.6 +/- 5.5% and 49.3 +/- 4.6%, respectively). In the PD-98059-treated group, most of the dogs developed mild vasospasm (18.9 +/- 6.2%). In the U-0126-treated group, severe vasospasm was observed despite treatment (39.6 +/- 6.4%). The PD-98059 but not the U-0126 abolished MAPK immunoprecipitation in the spastic BAs. However, treatment with either PD-98059 or U-0126 improved the clinical scores of the dogs. CONCLUSIONS: The present study is the first in which the effects of MAPK inhibitors on vasospasm have been investigated in vivo. The authors demonstrate that MAPK may play a role in vasospasm and that PD-98059 is a potential candidate for the treatment of cerebral vasospasm.

Animals↗

PubMed1999

Induction of glial cell line-derived neurotrophic factor and c-ret porto-oncogene-like immunoreactivity in rabbit spinal cord after transient ischemia.

The mechanism of spinal cord injury has been thought to be related with tissue ischemia, and spinal motor neuron cells are suggested to be vulnerable to ischemia. To evaluate the mechanism of such vulnerability of motor neurons, we attempted to make a reproducible model of spinal cord ischemia. Using this model, the inductions of glial cell line-derived neurotrophic factor (GDNF) and the c-ret porto-oncogene (RET) receptor tyrosine kinase were investigated with immunohistochemical analyses for up to 7 days of the reperfusion following 15 min of ischemia in rabbit spinal cord. Spinal cord sections from animals sacrificed at 8 h, 1, 2, and 7 days following the 15 min of ischemia were immunohistochemically evaluated using monoclonal antibodies for GDNF and RET. Following the 15 min of ischemia, the majority of the motor neurons showed selective cell death at 7 days of reperfusion. Immunoreactivity of GDNF and RET were induced at 8 h of reperfusion selectively in motor neuron cells. No glial cells were stained in the spinal cord sections. The induction of GDNF and RET proteins at the early stage of reperfusion may be related to the transient functional recovery of neurons after ischemia.

Animals↗

PubMed1999

Cyclosporine attenuates pressure-overload hypertrophy in mice while enhancing susceptibility to decompensation and heart failure.

Left ventricular hypertrophy (LVH) is a compensatory mechanism to cope with pressure overload. Recently, a calcineurin pathway mediating LVH and its prevention by cyclosporine was reported. We examined whether calcineurin mediates LVH due to pressure overload in mice. Pressure overload was induced by aortic banding in 53 mice (32 treated with cyclosporine [25 mg. kg-1. d-1], 21 treated with vehicle). There were 17 sham-operated mice (9 treated with vehicle, 8 treated with cyclosporine). At 3 weeks after surgery, LV weight to body weight was greater in the nontreatment banded group (4.39+/-0. 16 mg/g) than in the cyclosporine-treated banded group (3.95+/-0.14 mg/g, P<0.05), with both groups being greater compared with the entire group of sham-operated mice (3.02+/-0.04 mg/g). The pressure gradient between the ascending and abdominal aorta was not different between the cyclosporine-treated (49.6+/-6.1 mm Hg) and nontreatment groups (48.7+/-4.6 mm Hg). Although LV systolic pressure was lower in the cyclosporine-treated banded animals, LV systolic wall stress was similar in the nontreatment banded group and in the cyclosporine-treated group. However, LV dP/dt was lower (P=0.05) in the cyclosporine-treated banded group (4774+/-656 mm Hg/s) than in the nontreatment banded group (6604+/-516 mm Hg/s). During the protocol, 23 of 32 mice in the cyclosporine-treated group and 9 of 21 mice in the nontreatment group died. All deaths occurred within 10 days after surgery. Deaths caused by heart failure were 7.2-fold higher (P<0.05) in the cyclosporine-treated group, whereas deaths due to other causes were not different between the 2 groups. In addition, LV function of mice was assessed at 48 hours after banding; LV ejection fraction measured with echocardiography was lower (P<0.05) in the cyclosporine-treated banded group (66+/-3.0%) than in the nontreatment banded group (79+/-1.5%), whereas LV systolic wall stresses were similar. Calcineurin phosphatase activity was depressed similarly in both cyclosporine-treated groups compared with both nontreatment groups. Thus, cyclosporine could attenuate, but not prevent, LVH at the expense of inhibiting an important compensatory mechanism in response to pressure overload, resulting in reduced LV wall stress and function and increased susceptibility to decompensation and heart failure.

Animals↗

PubMed1999

Experimental study of intracisternal administration of tissue-type plasminogen activator followed by cerebrospinal fluid drainage in the ultra-early stage of subarachnoid haemorrhage.

This experimental study evaluated the effect of intrathecal injection of tissue-type plasminogen activator followed by cisternal drainage in the ultra-early stage of aneurysmal subarachnoid haemorrhage to prevent vasospasm. Twenty Japanese white rabbits were divided into five groups. Either tPA (groups A, B, and E) or saline (groups C and D) was injected intrathecally 1 hour (groups A, B, C, and D) or 21 hours (group E) after the intrathecal injection of blood. Cerebrospinal fluid was drained 2, 4, and 6 hours after the intrathecal injection of blood (groups A, C, and E). On day 4, the angiographic caliber of the basilar artery in each group was as follows (mean +/- SD): A, 85.9 +/- 5.0%; B, 74.6 +/- 5.3%; C, 69.1 +/- 2.7%; D, 64.0 +/- 4.9%; E, 80.2 +/- 2.7% (compared with baseline). In the two groups in which CSF was drained (groups A and C), fibrinolysis with tPA significantly suppressed vasospasm. In the two groups treated with tPA (groups A and B), cisternal drainage significantly suppressed vasospasm. In the two groups treated with saline (groups C and D), however, cisternal drainage did not suppress vasospasm. Examination of the series of CSF samples (groups A and C) showed that fibrinolysis with tPA effectively cleared clots early. In the two groups treated with tPA and CSF drainage (groups A and E), early removal of subarachnoid clots reduced the degree of vasospasm. Early fibrinolysis with tPA and early removal of subarachnoid clots by drainage is effective for preventing vasospasm.

Angiography, Digital Subtraction↗