Tetsuya Ishida
Louisiana State University
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Molecular and Cellular Biochemistry | 1998
Dean C. Gute; Tetsuya Ishida; Koji Yarimizu; Ronald J. Korthius
Skeletal muscle ischemia and reperfusion is now recognized as one form of acute inflammation in which activated leukocytes play a key role. Although restoration of flow is essential in alleviating ischemic injury, reperfusion initiates a complex series of reactions which lead to neutrophil accumulation, microvascular barrier disruption, and edema formation. A large body of evidence exists which suggests that leukocyte adhesion to and emigration across postcapillary venules plays a crucial role in the genesis of reperfusion injury in skeletal muscle. Reactive oxygen species generated by xanthine oxidase and other enzymes promote the formation of proinflammatory stimuli, modify the expression of adhesion molecules on the surface of leukocytes and endothelial cells, and reduce the bioavailability of the potent antiadhesive agent nitric oxide. As a consequence of these events, leukocytes begin to form loose adhesive interactions with postcapillary venular endothelium (leukocyte rolling). If the proinflammatory stimulus is sufficient, leukocytes may become firmly adherent (stationary adhesion) to the venular endothelium. Those leukocytes which become firmly adherent may then diapedese into the perivascular space. The emigrated leukocytes induce parenchymal cell injury via a directed release of oxidants and hydrolytic enzymes. In addition, the emigrating leukocytes also exacerbate ischemic injury by disrupting the microvascular barrier during their egress across the vasculature. As a consequence of this increase in microvascular permeability, transcapillary fluid filtration is enhanced and edema results. The resultant increase in interstitial tissue pressure physically compresses the capillaries, thereby preventing microvascular perfusion and thus promoting the development of the no-reflow phenomenon. The purpose of this review is to summarize the available information regarding these mechanisms of skeletal muscle ischemia/reperfusion injury.
Shock | 1997
Tetsuya Ishida; Koji Yarimizu; Dean C. Gute; Ronald J. Korthuis
Ischemic preconditioning (IPC) refers to a phenomenon in which a tissue is rendered resistant to the deleterious effects of prolonged ischemia by previous exposure to brief periods of vascular occlusion. While the beneficial effects of IPC were first demonstrated in the myocardium, it is now clear that preconditioning protects postischemic skeletal muscle, brain, and small intestine and may also occur in humans. Although first described over a decade ago, the mechanisms underlying the powerful protective effects of IPC remain uncertain. However, a growing body of evidence indicates that the beneficial actions of IPC involve the activation of adenosine A1 receptors during the period of preconditioning ischemia in most organs and species. Adenosine A1 receptor stimulation is thought to promote the translocation and activation of specific isoforms of protein kinase C, which in turn phosphorylate as yet unidentified cellular effector molecules. In the heart, it has been suggested that ATP-sensitive potassium channels may represent important effectors of the preconditioning phenomenon. In contrast, ATP-sensitive potassium channel activation does not seem to contribute to the beneficial effects of IPC in the small bowel and seems to play only a limited role in skeletal muscle. In these peripheral tissues, the beneficial effects of IPC are related to inhibition of leukocyte adhesion and emigration. In the small intestine, IPC seems to prevent postischemic leukocyte adhesion by maintaining the bioavailability of nitric oxide (a potent endogenous anti-adhesive agent) and preventing the expression of P-selectin (an adhesive molecule expressed by endothelial cells that is thought to modulate leukocyte rolling). In skeletal muscle, these actions are mediated by an effect of IPC to augment the production of adenosine (another potent endogenous anti-adhesive agent) during reperfusion. Thus, although adenosine-induced protein kinase C activation seems to play an important role in initiating the beneficial actions of IPC in most tissues, the effector of the preconditioning phenomenon seems to differ among tissues. Understanding the mechanisms of IPC has led to the recognition that tissues may also be preconditioned by administration of agents that act via the same signaling cascade (e. g., adenosine, bradykinin, α1-adrenergic agonists). The purpose of this review is to summarize the evidence regarding the mechanisms of IPC in different organs.
Journal of Gastroenterology and Hepatology | 2018
Fumihito Hirai; Tetsuya Ishida; Fuminao Takeshima; S. Yamamoto; Ichiro Yoshikawa; Shinya Ashizuka; Haruhiko Inatsu; Keiichi Mitsuyama; Suketo Sou; Ryuichi Iwakiri; Ryoichi Nozaki; Hidehisa Ohi; Motohiro Esaki; Mitsuo Iida; Toshiyuki Matsui
The aim of this study was to clarify the additional effect of a concomitant elemental diet (ED) for patients with Crohns disease on maintenance anti‐tumor necrosis factor‐α antibody (anti‐TNF).
Gastroenterology | 2016
Takayuki Matsumoto; Satoshi Motoya; Kenji Watanabe; Tadakazu Hisamatsu; Hiroshi Nakase; Naoki Yoshimura; Tetsuya Ishida; Shingo Kato; Tomoo Nakagawa; Motohiro Esaki; Masakazu Nagahori; Toshiyuki Matsui; Yuji Naito; Takanori Kanai; Yasuo Suzuki; Masanori Nojima; Mamoru Watanabe; Toshifumi Hibi
Gastrointestinal Endoscopy | 2018
Hiroto Suzuki; Takeshi Yamamura; Osamu Watanabe; Masanao Nakamura; Masanobu Matsushita; Tsunaki Sawada; Yasuyuki Mizutani; Eri Ishikawa; Yoshiki Niwa; Genta Uchida; Hiroyuki Otsuka; Takahiro Nishikawa; Tetsuya Ishida; Keisaku Yamada; Shun Hattori; Go Kajikawa; Hiroki Hashiguchi; Hiroki Suhara; Takuya Ishikawa; Kazuhiro Furukawa; Kohei Funasaka; Eizaburo Ohno; Hiroki Kawashima; Ryoji Miyahara; Yoshiki Hirooka; Hidemi Goto
Gastrointestinal Endoscopy | 2018
Takeshi Yamamura; Masashi Saito; Osamu Watanabe; Masanao Nakamura; Masanobu Matsushita; Tsunaki Sawada; Yasuyuki Mizutani; Yoshiki Niwa; Eri Ishikawa; Hiroto Suzuki; Hiroyuki Otsuka; Genta Uchida; Takahiro Nishikawa; Tetsuya Ishida; Takeshi Kuno; Keisaku Yamada; Shun Hattori; Hiroki Hashiguchi; Hiroki Suhara; Takuya Ishikawa; Kazuhiro Furukawa; Kohei Funasaka; Eizaburo Ohno; Ryoji Miyahara; Hiroki Kawashima; Yoshiki Hirooka; Hidemi Goto
Gastroenterology | 2018
Tadakazu Hisamatsu; Takayuki Matsumoto; Kenji Watanabe; Hiroshi Nakase; Satoshi Motoya; Naoki Yoshimura; Tetsuya Ishida; Shingo Kato; Tomoo Nakagawa; Motohiro Esaki; Masakazu Nagahori; Toshiyuki Matsui; Yuji Naito; Takanori Kanai; Yasuo Suzuki; Masanori Nojima; Mamoru Watanabe; Toshifumi Hibi
Gastrointestinal Endoscopy | 2017
Kenji Watanabe; Takayuki Matsumoto; Satoshi Motoya; Tadakazu Hisamatsu; Hiroshi Nakase; Naoki Yoshimura; Tetsuya Ishida; Shingo Kato; Tomoo Nakagawa; Masakazu Nagahori; Motohiro Esaki; Toshiyuki Matsui; Yuji Naito; Takanori Kanai; Yasuo Suzuki; Masanori Nojima; Mamoru Watanabe; Toshifumi Hibi
Gastroenterology | 2017
Hiroshi Nakase; Satoshi Motoya; Takayuki Matsumoto; Kenji Watanabe; Tadakazu Hisamatsu; Naoki Yoshimura; Tetsuya Ishida; Shingo Kato; Tomoo Nakagawa; Motohiro Esaki; Masakazu Nagahori; Toshiyuki Matsui; Yuji Naito; Takanori Kanai; Yasuo Suzuki; Masanori Nojima; Mamoru Watanabe; Toshifumi Hibi
Gastroenterology | 2016
Tetsuya Ishida