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Biomedical subjects

H Itoh

Publications and source records attributed to H Itoh.

At least 469 records · Page 26Linked to original sources
PubMed1998

Endothelial nitric oxide synthase gene is positively associated with essential hypertension.

Essential hypertension has a genetic basis. Accumulating evidence, including findings of elevation of arterial blood pressure in mice lacking the endothelial nitric oxide synthase (eNOS) gene, strongly suggests that alteration in NO metabolism is implicated in hypertension. There are, however, no reports indicating that polymorphism in the eNOS gene is associated with essential hypertension. We have identified a missense variant, Glu298Asp, in exon 7 of the eNOS gene and demonstrated that it is associated with both coronary spastic angina and myocardial infarction. To explore the genetic involvement of the eNOS gene in essential hypertension, we examined the possible association between essential hypertension and several polymorphisms including the Glu298Asp variant, variable number tandem repeats in intron 4 (eNOS4b/4a), and two polymorphisms in introns 18 and 23. We performed a large-scale study of genetic association using two independent populations from Kyoto (n=458; 240 normotensive versus 218 hypertensive subjects) and Kumamoto (n=421; 223 normotensive versus 187 hypertensive subjects), Japan. In both groups, a new coding variant, Glu298Asp, showed a strong association with essential hypertension (Kyoto: odds ratio, 2.3 [95% confidence interval, 1.4 to 3.9]; Kumamoto: odds ratio, 2.4 [95% confidence interval, 1.4 to 4.0]). The allele frequencies of 298Asp in hypertensive subjects were significantly higher than those in normotensive subjects in both groups (Kyoto: 0.103 versus 0.050, P<0.0017; Kumamoto: 0.120 versus 0.058, P<0.0013, respectively). No such disequilibrium between genotypes was significantly associated with any other polymorphisms we examined; the Glu298Asp variant was also not linked to any other polymorphisms. In conclusion, the Glu298Asp missense variant was significantly associated with essential hypertension, which suggests that it is a genetic susceptibility factor for essential hypertension.

Adult↗
PubMed1998

Pulmonary epithelioid haemangioendothelioma in 21 patients, including three with partial spontaneous regression.

This investigation studied the general conditions and prognostic factors of pulmonary epithelioid haemangioendothelioma (PEH), which is a rare disease. Twenty-one patients were collected throughout Asia by a questionnaire. Age at the detection or onset of symptoms of PEH was 14-64 yrs (mean 44 yrs). Males were more likely to be detected by symptoms (4/8, 50%) than were females (1/13, 8%). Fifteen showed bilateral multiple nodular opacities. Partial spontaneous regression occurred in three asymptomatic patients (one male and two females, all with bilateral multiple nodular opacities) 5, 13 and 15 yrs after detection. Two of the three patients with pleural effusion died within 1 yr, while the 16 patients with no effusion were alive more than 1 yr later (p<0.05). Histologically, two patients with fibrinofibrous pleuritis and extrapleural proliferation of tumour cells died within 2 yrs, while only one of 14 patients lacking such manifestations died within the same period (p<0.05). All three patients without spindle tumour cells survived for 12 yrs after the diagnosis, while all four patients with such cells died during the same period (p<0.05). In conclusion, 21 patients with pulmonary epithelioid haemangioendothelioma were reported, of whom three demonstrated partial spontaneous regression, and adverse prognostic features were identified.

Adolescent↗
PubMed1998

Idiopathic nonspecific interstitial pneumonia/fibrosis: comparison with idiopathic pulmonary fibrosis and BOOP.

Based on past difficulties in clinically differentiating patients with idiopathic pulmonary fibrosis (IPF), bronchiolitis obliterans-organizing pneumonia (BOOP), and nonspecific interstitial pneumonia/fibrosis (NSIP), which all manifest clinically as interstitial lung disease, experience with pathologically confirmed examples of the three diseases was reviewed to compare clinical profiles and prognosis and to define NSIP more clearly. Thirty-one patients (15 males and 16 females) were pathologically identified as NSIP and subclassified into either the cellular (n=16) or fibrotic group (n=15). All 31 patients were clinically considered to be idiopathic NSIP cases. Patients with idiopathic BOOP (n=16) and IPF (n=64) were compared with the NSIP patients. Subacute presentation of interstitial lung disease characterized both idiopathic NSIP and idiopathic BOOP. NSIP patients showed volume loss on a chest radiograph (29.0%) and honeycombing on a computed tomography scan (25.8%); these features were not found in BOOP patients. Bronchoalveolar lavage lymphocytosis was characteristic of both BOOP and NSIP. Two subgroups of NSIP can be recognized histologically: patients in the fibrotic group had a less favourable outcome than those in the cellular group. BOOP and NSIP had a more favourable outcome than IPF. In conclusion, idiopathic nonspecific interstitial pneumonia can be differentiated from other types of idiopathic interstitial pneumonia, both pathologically and clinically.

Adult↗
PubMed1998

Regulation of endothelial production of C-type natriuretic peptide by interaction between endothelial cells and macrophages.

We demonstrated endothelial production of C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family, and its regulation by cytokines, including tumor necrosis factor-alpha (TNF alpha). We thus proposed that CNP can control vascular tone and growth as an endothelium-derived relaxing peptide. We also revealed the marked elevation of plasma CNP concentration in patients with septic shock, in which TNF alpha plays a significant part. As the interaction between endothelial cells (EC) and monocytes-macrophages plays a pivotal role in the pathogenesis of atherosclerosis, we investigated the effect of coculture of EC and macrophages on endothelial production of CNP. We used a human monocytic leukemia cell line, THP-1, which differentiates into macrophages when treated with phorbol 12-myristate 13-acetate. The coculture of EC and THP-1-derived macrophages enhanced CNP secretion by more than 10-fold compared with the single culture of EC or the coculture of EC and THP-1 without phorbol 12-myristate 13-acetate treatment. Prevention of direct contact between EC and THP-1-derived macrophages did not attenuate the increase in CNP secretion. Northern blotting revealed the augmentation of CNP messenger RNA expression in EC in the coculture. We detected TNF alpha in the conditioned medium from the coculture of EC and THP-1-derived macrophages. Furthermore, anti-TNF alpha antibody inhibited the stimulation of CNP secretion in the coculture. CNP at a concentration of 1 nM did not stimulate cGMP production in EC or THP-1-derived macrophages, but it elevated cGMP production significantly in vascular smooth muscle cells. These results indicate that endothelial production of CNP is stimulated mainly by TNF alpha released from THP-1-derived macrophages in the coculture. Endothelial CNP at the enhanced level may be one of the vascular mediators to regulate local vascular tone and growth through cGMP production by vascular smooth muscle cells, suggesting the potential significance of endothelial CNP in atherosclerosis.

Animals↗
PubMed1998

Pregnancy increases soluble and particulate guanylate cyclases and decreases the clearance receptor of natriuretic peptides in ovine uterine, but not systemic, arteries.

Pregnancy increases uterine blood flow by 30- to 50-fold and uterine production of cGMP by 38-fold. Moreover, cGMP causes potent vasodilatation. We hypothesized that pregnancy up-regulates soluble and particulate guanylate cyclases (sGC and pGC) in ovine uterine arteries. Activities of sGC and pGC were compared by measuring cGMP production (37 C; 10 min) by uterine arteries from nonpregnant (n = 5) and pregnant (n = 4, 120 +/- 2 days' gestation; term = 145 +/- 3 days; mean +/- SE) ewes after sodium nitroprusside (100 microM), atrial natriuretic peptide (1 microM), or C-type natriuretic peptide (CNP; 1 microM) treatment. The protein and/or messenger RNA expressions of sGC beta1-subunit, pGC-A, pGC-B, the clearance receptor of natriuretic peptide (CR), and CNP were investigated in uterine and systemic (renal and/or omental) arteries from nonpregnant (n = 29) and pregnant (n = 21; 125 +/- 2 days' gestation) ewes. The potencies of uterine arterial GC activities were sGC >> pGC-A > pGC-B. Activities as well as protein expression of sGC, pGC-A, and pGC-B in pregnant uterine arteries were increased 48-128% above those in nonpregnant controls concomitant with a 34% down-regulation of CR protein expression; systemic arterial protein expressions were unaltered. These changes in uterine arterial GC-B and CR were confirmed using RT-PCR. Immunohistochemical staining of CNP in uterine, but not systemic, arterial endothelium from pregnant ewes was much stronger than that from nonpregnant ewes. Thus, two distinct GC pathways are present in ovine uterine artery, and both may be specifically upregulated during pregnancy and so contribute to the tremendous local increase in cGMP production during pregnancy.

Animals↗
PubMed1998

Augmented placental production of leptin in preeclampsia: possible involvement of placental hypoxia.

Preeclampsia (PE) is a hypertensive disorder, which develops in late pregnancy and is usually associated with placental hypoxia and dysfunction. We have recently demonstrated that leptin is a novel placenta-derived hormone in humans and suggested its significance in human pregnancy (see Ref. 19). To explore the changes in the leptin production in placenta in PE, we measured the plasma leptin level and placental leptin messenger RNA expression in pregnant women with PE. Plasma leptin levels in preeclamptic women were elevated significantly, compared with gestational age- and body mass index-matched normal pregnant women (P < 0.0001). Plasma leptin levels in the severe PE group were significantly higher than those in the mild PE group (P < 0.0001). Plasma leptin levels in preeclamptic women were reduced, soon after the placental delivery, to those expected for their body mass indices. Northern blot analysis revealed that leptin messenger RNA levels are increased in the placentas from preeclamptic women, compared with normal pregnant women. Leptin secretion was increased significantly in a human trophoblastic cell line (BeWo cells) cultured under hypoxic conditions (5% O2), compared with those cultured under standard conditions (20% O2; P < 0.01). The present study demonstrated that placental production of leptin is augmented in severe PE, probably because of placental hypoxia, thereby suggesting the possible significance of leptin as a marker of placental hypoxia in severe PE.

Adult↗
PubMed1998

Efficacy of oral magnesium administration on decreased exercise tolerance in a state of chronic sleep deprivation.

We have previously reported that chronic sleep deprivation causes a deficiency of intracellular magnesium (Mg) and decreased exercise tolerance. The aim of this study was to clarify whether oral administration of Mg could be effective in restoring the exercise tolerance that is decreased by chronic sleep deprivation. A bicycle ergometer cardiopulmonary exercise test was performed by 16 healthy volunteers (mean age 21.9 years). They were divided into 2 groups: 8 received doses of 100 mg of Mg orally per day for 1 month (Mg group) and the remaining 8 received no Mg and served as the control group. The study conditions were designed as follows: (1) the usual state (good sleep); and (2) the sleep-deprived state (sleeping time up to 60% less than the usual state for 1 month). The ratio of intracellular Mg content of the sleep-deprived state to the usual sleep state was significantly higher in the Mg group (p<0.05) than the untreated control group. There was no difference between the sleep-deprived state and the usual state with regard to anaerobic threshold and peak oxygen uptake in the Mg group, whereas both of these decreased in the sleep-deprived state in the control group. These results indicate that decreased exercise tolerance observed in the sleep-deprived state could be improved by oral Mg administration.

Administration, Oral↗
PubMed1998

Influence of aerobic exercise training on brain natriuretic peptide secretion in patients in the chronic phase of myocardial infarction.

Brain natriuretic peptide (BNP) secretion increases after myocardial infarction (MI); its plasma level may reflect the degree of left ventricular dysfunction. This study examines how aerobic exercise therapy for MI influences BNP secretion. Subjects included 70 patients (mean age, 62.0+/-11.3 years) who were divided into four groups: (1) 20 patients with an anterior MI and exercise training; (2) 20 patients with an anterior MI and no exercise training; (3) 15 patients with an inferior MI and exercise training; and (4) 15 patients with an inferior MI and no exercise training. The training groups performed aerobic exercise 3 times a week for 2 months. Exercise intensity was defined as a heart rate of anaerobic threshold (AT), derived from the treadmill cardiopulmonary exercise testing at 1 month after the onset of MI. The subjects underwent cardiopulmonary exercise testing again at 3 months after the onset of MI. To measure BNP, blood samples were obtained in the resting state and immediately after the peak exercise. AT and peak oxygen uptake increased in the training group with anterior MI and in both the training and nontraining groups with inferior MI. Significant serial change in plasma BNP level was not observed in the inferior MI groups. Plasma BNP level decreased longitudinally only in the nontraining anterior MI group. It was concluded that exercise training in patients with an anterior MI could delay the recovery of left ventricular function, but will increase exercise tolerance.

Aged↗
PubMed1998

Improved oxygen utilization during mild exercise in heart failure.

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.

Aged↗
PubMed1998

Effects of intravenously administered C-type natriuretic peptide in humans: comparison with atrial natriuretic peptide.

We have previously reported that C-type natriuretic peptide (CNP), the third member of the natriuretic peptide family, is produced in vascular endothelial cells and suggested that CNP might be a local regulator of vascular tone and growth. To evaluate the biological actions of CNP as compared with human atrial natriuretic peptide (hANP), we intravenously administered synthetic CNP (0.43 nmol/kg) and alpha-hANP (0.43 and 0.043 nmol/kg) to healthy humans. The experiments were done on different days in the same five healthy volunteers (31+/-1 yr old). CNP injection caused a transient but significant decrease in both systolic and diastolic blood pressure (-4.3+/-1.3, -4.1+/-1.0 mmHg) with a significant increase in heart rate (+7.6+/-2.6 bpm), and exerted significant diuretic and natriuretic activities (+130+/-80%, +160+/-100% over the basal level). These effects of CNP (0.43 nmol/kg) were comparable to, or less than, those of alpha-hANP (0.043 nmol/kg). CNP injection also significantly suppressed aldosterone secretion (22% reduction as compared with the basal level). Our results demonstrate that intravenously-administered CNP acts as a natriuretic peptide with less potency than ANP.

Adult↗
PubMed1998

Canine mesenchymal chondrosarcoma of the ribs.

The tumor of the thoracic cavity, which arose from the ribs, was diagnosed as mesenchymal chondrosarcoma. No distant metastasis was observed. Histologically, the tumor was characterized by the nests of well-defined cartilaginous tissue within a proliferation of primitive mesenchymal cells. Additionally, the deformed blood vessels compressed by the proliferating mesenchymal cells exhibited clear stag-horn appearance. Immunohistochemically, most neoplastic cells that formed multifocal cartilaginous islands were positive for S-100 protein, while the surrounding mesenchymal cells were negative. This is the first report of canine mesenchymal chondrosarcoma of the ribs.

Animals↗
PubMed1998

Importance of intrapulmonary lymph nodes in the differential diagnosis of small pulmonary nodular shadows.

STUDY OBJECTIVE: The objectives of the present study were to evaluate the importance of intrapulmonary lymph nodes (IPLNs) in the differential diagnosis of small pulmonary nodules and to review the CT findings of IPLNs. DESIGN: Retrospective analysis of patient records. SETTING: Chest Disease Research Institute Hospital, Kyoto University. PATIENTS: Between January 1991 and May 1996, we examined 26 patients with pulmonary nodular shadows smaller than 1 cm in diameter that could not be diagnosed before surgery. All patients (19 men, 7 women) underwent chest CT (28 to 72 years old; mean, 52.3 years). RESULTS: The pathologic diagnoses were IPLNs in 46.2% (12/26), pulmonary hamartoma in 23.1% (6/26), lung cancer in 11.5% (3/26), pulmonary tuberculoma in 11.5% (3/26), and metastatic lung tumor in 7.7% (2/26). IPLNs were located in the lower lobe in 72%. The characteristic CT findings of IPLNs were a clear border and location close to the pleura. Two of them resembled lung cancer. The CT features in these two IPLNs and in three small lung cancers overlapped. CONCLUSIONS: In the present study, we investigated small nodular shadows <1 cm in diameter and found that IPLNs located underneath the pleura are important to consider in the differential diagnosis of lung cancer. The CT scan findings of IPLNs were not necessarily specific and sometimes resembled those of lung cancer. Because of their location, video-assisted thoracic surgery is useful in making a definite diagnosis.

Adult↗
PubMed1998

A case of Gitelman's syndrome with chondrocalcinosis.

A 45-year-old Japanese woman, treated for Bartter's syndrome for 14 years, presented with complaints of numbness in her extremities and polyarthralgia. She was diagnosed to have Gitelman's syndrome with chondrocalcinosis, which were effectively treated with spironolactone and magnesium supplementation. Gitelman's syndrome is a primary renal tubular disorder characterized by hypomagnesemia and hypocalciuria with normal calcemia. The persistent hypomagnesemia is one of the causes of chondrocalcinosis, and many cases of Bartter's syndrome with hypomagnesemia are associated with chondrocalcinosis attributed to a tubular magnesium defect. We summarize the reported cases with Bartter's syndrome and chondrocalcinosis, referring to the possibility of Gitelman's syndrome.

Bartter Syndrome↗
PubMed1998

Severe diabetic scleredema with extension to the extremities and effective treatment using prostaglandin E1.

We report a 49-year-old woman with severe diabetic scleredema (DS). The patient had non-insulin-dependent diabetes mellitus (NIDDM) for 9 years and noticed thickened skin on her back 3 years previously. Her DS rapidly extended to her back and extremities with pain and immobility. Her symptoms of DS improved dramatically after establishing strict glycemic control and intravenous administration of prostaglandin E1 (PGE1). However, the histological findings of her skin biopsy did not change even after the treatment for 12 weeks, and her symptoms worsened again after discontinuation of glycemic control and PGE1 treatment. The causes of DS have been considered to be metabolic abnormalities associated with hyperglycemia and hypoxia in the skin due to diabetic microangiopathy. PGE1 was an effective treatment for DS in our patient. Strict control of hyperglycemia and PGE1 treatment may be sufficient to manage DS, although a very long treatment period is necessary.

Acupuncture Analgesia↗
PubMed1998

Relationship between maximal pulmonary ventilation and arterialized venous blood potassium and dopamine concentrations obtained at exhaustion in man.

This study was performed to test the hypothesis that potassium concentration in arterialized blood may be closely related to maximal pulmonary ventilation (V.Emax) obtained at exhaustion during maximal exercise in man. Eleven healthy men performed bicycle exercise with incremental loading at 60 rpm until exhaustion. Pulmonary ventilation (V.E), oxygen uptake (V.O2), and heart rate (HR) were determined continuously throughout the experiment. Arterialized venous blood samples were collected to measure potassium ([K+]), lactate ([La]), hydrogen ion (pH), catecholamine ([CA]), and dopamine ([DA]) concentrations. A significant correlation (r = 0.98-0.88) between V.E and [K+], [La], and pH during exercise was observed in all subjects. Furthermore, a close relationship was found in this study between dopamine concentration measured at exhaustion ([DA]0) and maximal pulmonary ventilation per kilogram of body weight (V.Emax/W) (r = -0.668, p < 0.05) or maximum oxygen uptake per kilogram of body weight (VO2MAX/W) (r = 0.720, p < 0.05). However, no significant correlation was found between V. Emax/W and [K+]0 (r = 0.202, NS), [La]0 (r = -0.096, NS), and pH0 (r = 0.344, NS). These results suggest that dopamine may play a more important role in the determination of maximal pulmonary ventilation during exercise in man than K+ or pH.

Adolescent↗
PubMed1998

Increased adipose expression of the uncoupling protein-3 gene by thiazolidinediones in Wistar fatty rats and in cultured adipocytes.

Uncoupling protein (UCP) 3 and UCP2, mitochondrial carrier proteins dissipating electrochemical gradient across the mitochondrial inner membrane, have been implicated in the regulation of energy metabolism. The UCP3 gene is expressed abundantly in the skeletal muscle, while the UCP2 gene is detected in the white adipose tissue (WAT) with diffuse localization throughout the body. Uncoupling of electron transport and ATP synthesis has been reported to increase glucose uptake, suggesting that UCP may be involved in glucose metabolism. Thiazolidinediones (TZDs), which are insulin-sensitizing agents for NIDDM, have been reported to increase energy expenditure. To elucidate the pathophysiologic significance of UCP3 and UCP2 in the effect of TZDs on glucose metabolism and energy expenditure, we examined their basal mRNA levels in the WAT, brown adipose tissue (BAT), and skeletal muscle from Wistar fatty rats, a rat model of NIDDM and obesity with leptin receptor defect, and investigated expression of the genes encoding UCP3 and UCP2 in Wistar fatty rats and in Wistar lean rats with 2-week oral administration of 3 mg x kg(-1) x day(-1) pioglitazone, a TZD derivative. Basal UCP3 mRNA levels were significantly lower (38 +/- 8, 45 +/- 13, and 76 +/- 6%) in the retroperitoneal WAT, BAT, and skeletal muscle from Wistar fatty rats than in those from Wistar lean rats, while basal UCP2 mRNA levels were significantly higher by 2.1-, 1.8-, and 2.5-fold in the subcutaneous WAT, retroperitoneal WAT, and BAT from Wistar fatty rats, respectively, than in those from Wistar lean rats. In pioglitazone-treated Wistar fatty rats, UCP3 mRNA levels were significantly increased by 2.1-, 2.0-, and 1.6-fold in the epididymal WAT, retroperitoneal WAT, and BAT, respectively, as compared with those in nontreated fatty rats. In pioglitazone-treated lean rats, UCP3 mRNA levels were significantly increased by 1.3-fold in the BAT as compared with those in nontreated lean rats. No significant change of UCP2 mRNA levels was observed in pioglitazone-treated fatty and lean rats. In addition, to examine the direct effect of TZDs on adipocytes, we examined the regulation of UCP3 and UCP2 gene expression using the primary culture of rat mature adipocytes from Sprague-Dawley rats. In rat cultured mature adipocytes, UCP3 mRNA levels were increased in a dose-responsive manner by 10(-5) to 10(-4) mol/l pioglitazone, while there was no significant change of UCP2 mRNA levels. These results clearly demonstrate that UCP3 gene expression is upregulated by TZDs in the WAT and BAT in Wistar fatty rats, an obese model with leptin receptor defect, and that adipose UCP3 gene expression is increased in response to TZDs in vitro. The present study suggests the involvement of UCP3 in the effects of TZDs on energy and glucose metabolism.

Adipocytes↗
PubMed1998

[Repair of left ventricular free wall rupture with GRF glue associated with acute myocardial infarction: report of a case].

Histopathological examination of a repair of left ventricular free wall rupture associated with acute myocardial infarction using GRF glue was reported. A 63-year-old male with cardiac rupture due to LMT total occlusion was referred to our ward after unsuccessful PTCA with institution of IABP and PCPS. Left ventricular rupture repair by GRF glue and xenograft pericardial patch with concomitant myocardial revascularization (SVG-LAD, CX) was performed under cardiopulmonary bypass. Hemostasis around the ventricular rupture was easily accomplished. Unfortunately, the patient died at 14 POD because of low output syndrome caused by broad myocardial infarction. At autopsy, rupture site was examined histologically and was revealed that GRF glue made a tight adhesion between patch and myocardium. Neither abnormal inflammatory cells nor giant cells were found. We concluded that GRF glue might be a effective histocompatibly in hemostasis for left ventricular rupture associated with acute myocardial infarction.

Cardiac Surgical Procedures↗