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Yoshihito Irie

Publications and source records attributed to Yoshihito Irie.

10 recordsLinked to original sources
PubMed2006

Effects of rabeprazole or famotidine during cardiac surgery on perioperative gastric and esophageal pH readings.

OBJECTIVES: Upper gastrointestinal bleeding, particularly from a stress-induced duodenal ulcer, is an extremely important perioperative complication in cardiovascular surgery. METHODS: In the present study, 33 patients undergoing elective open heart surgery between July 2000 and February 2001 were allocated to either a famotidine (FAM) or rabeprazole (RPZ) group to examine the perioperative gastric and esophageal pH readings, in conjunction with an investigation into the effect of infection with Helicobacter pylori (HP). RESULTS: Postoperative upper gastrointestinal bleeding did not occur in either group, and the intraoperative and postoperative mean gastric pH readings, as well as the holding time pH>6, suggested sufficient acid suppression by either drug. Gastric acid secretion was less strongly suppressed in HP-negative patients in the FAM group, but was unaffected by HP infection status in the RPZ group. CONCLUSION: The FAM group and RPZ group revealed a sufficient effect of gastric acid suppression. It was indicated that FAM had an insufficient effect of gastric acid suppression for HP-negative patients.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2006

[Aortic valve replacement through a partial sternotomy].

BACKGROUND: Instead of a median sternotomy which has been accepted as the standard approach to cardiaovascular surgery, we have selected a partial sternotomy as a minimally invasive surgery since 1997. Every technique and device must be reevaluated because the entire heart cannot be easily assessed. METHOD: In this paper we reported the pitfalls and results of 108 cases of aortic valve replacement through an upper and lower partial sternotomy. Single surgeon had used the single technique through the same operation field from 1997 to 2005. RESULTS: Mortality rate was 1.9% (2 patients). Aortic cross clamp time was a little longer in this series than in the conventional median sternotomy group. There were no differences in operating time, pumping time, intubation duration or bleeding. ICU stay and hospital stay were shorter in this series than in the conventional sternotomy group. The operating time was shorter in the regurgitation group than in the stenosis group. There were no differences in pumping time, intubation duration, bleeding, ICU stay or hospital stay. CONCLUSION: The minimally invasive cardiac surgery for the aortic valve replacement could be routinely and safely indicated.

Aortic Valve↗
PubMed2006

[Rupture of a chronic dissecting giant aneurysm into the pulmonary artery; report of a case].

Aortopulmonary fistula is an extremely rare complication of aortic dissection. We report a case of a chronic dissecting giant aneurysm with an aortopulmonary fistula. A 78-year-old woman experienced sudden onset chest pain and oppression. Chest X-ray showed ascending aortic and left ventricular enlargement and pulmonary congestion. Computed tomography (CT) confirmed the 100 mm ascending aortic aneurysm with dissection and aortopulmonary fistula. Operative repair was performed under profound hypothermic circulatory arrest with selective cerebral perfusion. The proximal and distal end were obliterated using a gelatin-resorcin-formaldehyde tissue glue and reinforced with a Teflon felt circumferential strip. The ascending aorta was replaced by a 30 mm coated Dacron vascular graft and the aortopulmonary fistula was closed with pledgeted vertical mattress suture. Postoperative CT showed a normally functioning vascular implant without any sign of aortopulmonary shunt or pulmonary artery stenosis.

Aged↗
PubMed2005

Kommerell's diverticular rupture complicated by aberrant left subclavian artery and right aortic arch successfully treated surgically.

We report a rare case of a rupture in Kommerell's diverticulum in a 73-year-old woman with Edwards IIIB aberrant left subclavian artery (A-LSA) and right aortic arch. This case was further complicated by an inferior vena cava defect. We performed an emergency operation through a right posterolateral approach. The descending aorta was replaced and the Kommerell's diverticulum was excised, followed by A-LSA reconstruction, performed under deep hypothermia with selective cerebral perfusion. We believe the prognosis was excellent.

Aged↗
PubMed2004

Combined blockade of the chemokine receptors CCR1 and CCR5 attenuates chronic rejection.

BACKGROUND: Chemokine-chemokine receptor interaction and the subsequent recruitment of T-lymphocytes to the graft are early events in the development of chronic rejection of transplanted hearts or cardiac allograft vasculopathy (CAV). In this study, we sought to determine whether blockade of chemokine receptors CCR1 and CCR5 with Met-RANTES affects the development of CAV in a murine model. METHODS AND RESULTS: B6.CH-2(bm12) strain donor hearts were transplanted heterotopically into wild-type C57BL/6 mice (myosin heavy chain II mismatch). Recipients were treated daily with either Met-RANTES or vehicle starting on postoperative day 4 and were euthanized on postoperative days 24 and 56. We found that Met-RANTES significantly reduced intimal thickening in this model of chronic rejection and that Met-RANTES markedly decreased the infiltration of CD4 and CD8 T lymphocytes and MOMA-2+ monocytes/macrophages into transplanted hearts. Met-RANTES also suppressed the ex vivo and in vitro proliferative responses of recipient splenocytes to donor antigens. Finally, Met-RANTES treatment was associated with a marked reduction in RANTES/CCL5 and monocyte chemoattractant protein-1 gene transcript levels in the donor hearts. CONCLUSIONS: Antagonism of the chemokine receptors CCR1 and CCR5 with Met-RANTES attenuates CAV development in vivo by reducing mononuclear cell recruitment to the transplanted heart, proliferative responses to donor antigens, and intragraft RANTES/CCL5 and monocyte chemoattractant protein-1 gene transcript levels. These findings suggest that chemokine receptors CCR1 and CCR5 play significant roles in the development of chronic rejection and may serve as potential therapeutic targets.

Animals↗
PubMed2003

Regulated interleukin-10 expression prevents chronic rejection of transplanted hearts.

OBJECTIVE: Interleukin-10 is a pleiotrophic cytokine with variable effects on the alloimmune response, depending on the experimental model system. The purpose of this study was to determine the role of regulated interleukin-10 expression on the development of chronic rejection in heart transplantation, or cardiac allograft vasculopathy. METHODS: Donor hearts from B6.C-H2(bm12) mice were transplanted into wild-type and interleukin-10 transgenic recipients. In interleukin-10 transgenic recipients, murine interleukin-10 cytokine is produced under the control of human interleukin-2 promoter. Donor hearts were sacrificed at days 7 and 24. No immunosuppression was used. Intimal proliferation was measured morphometrically. Intragraft cellular infiltrate was defined by both immunohistochemistry and flow cytometry. Intracellular cytokine staining assay was performed to determine both the type and source of intragraft cytokines. RESULTS: Hearts transplanted into wild-type recipients developed severe cardiac allograft vasculopathy by 24 days. Intimal lesions were absent in the donor hearts transplanted into interleukin-10 transgenic recipients. The number of graft-infiltrating T lymphocytes and the percentage of interleukin-2/interferon-gamma producing T lymphocytes were markedly reduced in interleukin-10 transgenic recipients. Finally, the overexpression of interleukin-10 resulted in the decline of graft-infiltrating macrophages at all time points. CONCLUSIONS: Regulated expression of interleukin-10 inhibits cardiac allograft vasculopathy development via reduction of mononuclear cell recruitment and alteration of their cytokine profile. This strategy may prove beneficial in controlling the alloimmune response in solid organ transplants.

Animals↗
PubMed2002

Indirect alloreactivity and chronic rejection.

BACKGROUND: The relative contribution of the direct versus indirect pathway of T-lymphocyte alloreactivity to the development of chronic rejection is incompletely understood. Utilizing a murine model of cardiac allograft vasculopathy (CAV) and a recipient strain with markedly reduced capacity for indirect alloreactivity, we sought to define the importance of indirect allorecognition in CAV. METHODS: The cells from H2-M mutant mice are unable to present intact protein antigens via class II molecules and have a markedly reduced capacity to present exogenous peptides. B6C.H-2(bm12) strain donor hearts were transplanted into either C57Bl/6 wild-type (WT) or H2-M mutant mice (on C57Bl/6 background). Recipients were killed on day 24. T lymphocyte and macrophage infiltration were graded immunohistochemically. Intimal lesions were measured morphometrically. RESULTS: Donor hearts in WT recipients developed significant intimal lesions, as expected (50+/-7%). Moreover, the donor hearts in H2-M mutant mice also developed comparable intimal lesions (52+/-9%, P=NS vs. WT). Furthermore, the extent of T lymphocyte and macrophage infiltration was similar in both groups. CONCLUSIONS: This study demonstrates that a markedly reduced capacity for indirect alloreactivity does not affect the severity of intimal lesions in this model of CAV. The findings of this study question the role of indirect alloreactivity as the sole pathway of allorecognition leading to chronic rejection.

Animals↗
PubMed2002

The role of MIG/CXCL9 in cardiac allograft vasculopathy.

T lymphocytes play a critical role in chronic rejection of transplanted hearts, or cardiac allograft vasculopathy (CAV). However, the molecular mediators of T lymphocyte recruitment in CAV are incompletely defined. We hypothesized that the chemokine, monokine induced by interferon-gamma (MIG/CXCL9), which induces T lymphocyte migration in vitro, participates in T lymphocyte recruitment in CAV. In a previously characterized MHC II-mismatched murine model of CAV, intragraft MIG/CXCL9 gene transcript and protein levels increased on days 7, 14, and 24 days after transplantation, paralleling T lymphocyte recruitment and preceding intimal thickening. Antibody neutralization of MIG/CXCL9 significantly reduced CD4(+) T lymphocyte infiltration and intimal thickening in this model. MIG/CXCL9 was produced by graft-infiltrating MOMA-2+ macrophages in early and late stages of CAV. And, although T lymphocytes did not produce MIG/CXCL9, recipient CD4(+) T lymphocytes were required for sustained intragraft MIG/CXCL9 production and CAV development. These findings demonstrate that 1) MIG/CXCL9 plays an important role in CD4(+) T lymphocyte recruitment and development of CAV, 2) MOMA-2+ macrophages are the predominant recipient-derived source of MIG/CXCL9, and 3) recipient CD4 lymphocytes are necessary for sustained MIG/CXCL9 production and CAV development in this model. Neutralization of the chemokine MIG/CXCL9 may have therapeutic potential for the treatment of chronic rejection after heart transplantation.

Animals↗
PubMed2002

Role of CD8+ lymphocytes in chronic rejection of transplanted hearts.

BACKGROUND: The contribution of CD8(+) lymphocytes to the pathogenesis of cardiac allograft vasculopathy, or chronic rejection in heart transplants, remains undefined. We used both major histocompatibility complex class I mismatched and major histocompatibility complex class II mismatched models of cardiac allograft vasculopathy to characterize the role of CD8(+) lymphocytes in the development of cardiac allograft vasculopathy. METHODS: Donor hearts from B10.A mice were transplanted into B10.BR recipients (major histocompatibility complex class I mismatched). Donor hearts were harvested at 1, 7, 14, and 30 days after transplantation and (1) quantitated morphometrically for lesion development, (2) stained immunohistochemically, or (3) digested for isolation of graft-infiltrating cells. The cytotoxic phenotype of graft-infiltrating CD8(+) lymphocytes was determined with flow cytometry. Intracellular cytokine staining of CD8(+) and CD4(+) lymphocytes for interleukin 2, interferon g, interleukin 4, and interleukin 10 was performed with 2-color flow cytometry. Finally, B6.C-H2(bm12) donor hearts were transplanted into either C57BL/6 wild-type (major histocompatibility complex class II mismatched) or CD8 -/- knockout recipients and examined for the development of cardiac allograft vasculopathy. RESULTS: In the major histocompatibility complex class I mismatched model, CD8(+) lymphocytes were the predominant T-lymphocyte subset that infiltrated the allografts and demonstrated markers of activation. The intracellular cytokine-staining assay demonstrated that CD8(+) lymphocytes were the primary sources of allograft interleukin 2 and interferon gamma. Intimal lesions developed in the allografts by day 14 (12.0% +/- 4.0%) and further increased by day 30 (44.0% +/- 5.0%). In the major histocompatibility complex class II mismatched model, the donor hearts in the CD8 -/- knockout recipients had substantially less severe intimal lesions when compared with the donor hearts in wild-type recipients (19.0% +/- 6.0% vs 50.0% +/- 7.0%, respectively; P <.05). CONCLUSIONS: In both major histocompatibility complex class I and II mismatched models, CD8(+) lymphocytes contribute significantly to chronic rejection. The findings of this study suggest that control of chronic rejection requires interventions directed at CD8(+) lymphocytes.

Animals↗