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Byline: Autocar Pro News Desk A combination of ATP technology and optimised biocide use saves costs and improves operational hygiene. LANXESS, one of the world's largest suppliers of antimicrobial protection [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.jtcvs.2008.08.020 Byline: Rajesh G. Katare (a), Motonori Ando (a)(c), Yoshihiko Kakinuma (a), Mikihiko Arikawa (a), Takemi Handa (a), Fumiyasu Yamasaki (b), Takayuki Sato (a) Abbreviations: ACh, acetylcholine; ATP, adenosine triphosphate; CABG, coronary artery bypass grafting; PTP, permeability transition pore; SS, sham stimulation; VS, vagal stimulation Abstract: In spite of recent advances in coronary interventional therapy, reperfusion injury is still considered to be a major problem in patients undergoing surgical procedures, such as bypass grafting. Here we demonstrate a novel therapeutic strategy against ischemia-reperfusion injury: vagally mediated prevention of reperfusion-induced opening of mitochondrial permeability transition pore. Author Affiliation: (a) Department of Cardiovascular Control, Kochi Medical School, Nankoku, Japan (b) Department of Clinical Laboratory, Kochi Medical School, Nankoku, Japan (c) Department of Science and Education, Okayama University, Okayama, Japan Article History: Received 20 September 2007; Revised 16 July 2008; Accepted 8 August 2008 Article Note: (footnote) Supported by a Health and Labor Sciences Research Grant (H14-NANO-002, H16-NANO-005) from the Ministry of Health, Labor, and Welfare of Japan and by a Grant-in-Aid for Scientific Research (15300165, 17790892) from the Ministry of Education, Science, Sports, and Culture of Japan.

Byline: Akira Koike, Toshiaki Akita, Yoshihiro Hotta, Kazumi Takeya, Itsuo Kodama, Mitsuya Murase, Toshio Abe, Junji Toyama Abstract: The effects of 5-(N,N-dimethyl)amiloride, a potent and specific Na.sup.+-H.sup.+ exchange inhibitor, were investigated in isolated perfused rabbit hearts subjected to ischemia and reperfusion. Phosphorus 31-nuclear magnetic resonance spectroscopy was used to monitor intracellular pH, creatine phosphate, [beta]-adenosine triphosphate, and inorganic phosphate. After cardioplegic arrest with St. Thomas' Hospital solution, normothermic (37A* C) global ischemia was induced for 45 minutes, and the hearts were reperfused for 50 minutes. Dimethyl amiloride at 10 [mu]mol/L, which has minimal inotropic and chronotropic effects on the nonischemic heart, was added to the cardioplegic solution. Treatment with dimethyl amiloride reduced the elevation of left ventricular end-diastolic pressure during and after the ischemia and improved the postischemic recovery of developed pressure from 76% [+ or -] 3.2% at 30 minutes of reperfusion in control hearts (n = 6) up to 99% [+ or -] 1.9% in hearts treated with dimethyl amiloride (n = 8). Dimethyl amiloride did not affect the decline in intracellular pH during ischemia for up to 30 minutes but enhanced the intracellular acidosis thereafter. The intracellular pH at the end of ischemia was 6.21 [+ or -] 0.05 in control hearts compared with 5.24 [+ or -] 0.17 in hearts treated with dimethyl amiloride (p < 0.05). During reperfusion, intracellular pH of hearts treated with dimethyl amiloride was less than control for 5 minutes, but subsequent recovery of intracellular pH was similar to control. Treatment with dimethyl amiloride did not affect creatine phosphate breakdown, inorganic phosphate accumulation, and [beta]-adenosine triphosphate depletion during 45 minutes of ischemia. The creatine phosphate resynthesis and inorganic phosphate reduction during reperfusion were also unaffected. These findings suggest that Na.sup.+-H.sup.+ exchange plays an important role not only during reperfusion but also during ischemia for the development of postischemic cardiac dysfunction most likely by inducing primary Na.sup.+ and secondary Ca.sup.2+ overload. Specific Na.sup.+-H.sup.+ exchange inhibitors like dimethyl amiloride would have a potential therapeutic profile in cardiac surgery, especially if added before ischemia. (J THORAC CARDIOVASC SURG 1996;112:765-75) Article History: Received 24 July 1995; Revised 14 November 1995; Revised 2 April 1996; Accepted 3 April 1996 Article Note: (footnote) [star] From the Department of Thoracic Surgery, School of Medicine, Nagoya University,a Nagoya, Japan; the Department of Pharmacology, Aichi Medical University,b Aichi, Japan; and the Departments of Circulation and Humoral Regulation,c Research Institute of Environmental Medicine, Nagoya University, Nagoya, Japan., [star][star] Address for reprints: Itsuo Kodama, MD, Department of Humoral Regulation, Research Institute of Environmental Medicine, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-01, Japan., a 0022-5223/96 $5.00 + 0, aa 12/1/73914