ischaemic preconditioning of the human heart. - Leicester Research ...

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240. Paulson DJ (1997). The diabetic heart is more sensitive to ischernic injury. Cardiovasc Res. 34: 104-112. 241. Pepine CJ and Pepine A (1992). Intervention therapy for coronary artery disease in the elderly. Cardiovasc Chn 22: 175-187. 242. Perrault LP, Menasch6 P, Bel A et al (1996). Ischemic preconditioning in cardiac surgery: a word of caution. J Thorac Cardiovasc Surg 112,1378- 1386. 243. Piper, HM, Probst 1, Hutter JF, Spieckermann PG. (1982). Culturing of calcium stable adult cardiac myocytes. J CeY MoM Cardiol 14,397-412. 244. Piot CA, Padmanaban D, Ursell PC, Sievers RE, Woffe CL. (1997). Ischernic preconditioning decreases apoptosis in rat hearts in vivo. Circulation 96,1598-1604. 245. Pombo CM, Bonventre JV, Avruch J, Woodgett JR, Kyriakis JM, Force T (1994). The stress activated protein kinases are major c-Jun amino-terminal kinases activated by ischemia and reperfusion J Biol Chem 269: 26546-51. 246. Prasad K and Callaghan J (1969). Effect of replacement of potassium by rubidium on the transmembrane action potential and contractility of human papillary muscle. Cif-c Research 24: 157-166. 247. Pryzlenk K and Kloner R (1995). Preconditioning: a balanced perspective. British Head Journal 74: 575-577. 206
248. Pryzlenk K, Li G, Whittaker P (2001). No loss in the in-vivo efficacy of ischernic preconditioning in middle-aged and old rabbits. J Am Cog Cardiol, 38: 1741-1747. 249. Qian YZ, Bernado NL, Nayeem MA, et al (1999). Induction of 72-kDa heat shock protein does not produce a second window of ischemic preconditioning in rat heart. Am. J. Physiol. 276: H224-H234. 250. Rainio P, Sormunen R, Lepojarvi M, Nissinen J, Kaukoranta P and Peuhkurinen K (1995). Ultrastructural changes during retrograde warm and mild hypothermic blood cardioplegia for coronary bypass operations. Thorac Cardiovasc Surg I 10 : 81-88. 251. Reimer K, Jennings R and Hill M (1981). Total ischaemia in dog hearts, in vitro: 2) High energy phosphate depletion and associated defects in energy metabolism, cell volume regulation, and sarcolemmal integrity. Circ Research 49: 901-911. 252. Reimer KA, Murry CE, Yamasawa 1, Hill ML and Jennings RB (1986). Four brief periods of ischaemia causes no cumulative ATP loss or necrosis. Am J Physiol 251 :H 1306-1315. 253. Richard VJ, Murry CE, Jennings RB, Reimer KA (1990). Oxygen- derived free radicals and postischemic myocardial reperfusion: therapeutic implications. Fundam Clin Pharmacol. 4: 85-103. 207 J
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ISCHAEMIC PRECONDITIONING OF THE HU
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ABSTRACT Ischaemic preconditioning
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andomised clinical study with the f
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CHAPTERI Introduction 35 Matefials
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Discussion 151 CHAPTER Vill Conclus
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44 CK leakage and MTT reduction on
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The Wellcome Trust and The British
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Presentations International "The Ef
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Abbreviations An attempt has been m
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1.1 Introduction Ischaernic heart d
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1.2 Myocardial Ischaemia Myocardial
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hours up to several days to complet
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phosphates and its influence on hyd
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1.4 Myocardial Protection This refe
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performed. This process is repeated
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1.6 Possible Mechanisms of Ischaemi
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kilodalton stress proteins. These p
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and these proteins have been sugges
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K vi-1, channels were initially fou
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tissues the K.. %,.,, channels are
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Subsequently, Jaburek et al 1145] i
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venous capacitance vessels. At ther
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preconditioning to be investigated
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In the angioplasty model, Tomai et
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patients were randomized into two g
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CHAPTER 11 THE HUMAN RIGHT ATRIAL T
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inexpensive. Briefly in this model,
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of each ischemic period, slices wer
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30 nini FO linlin L 60 min 120 inin
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In Study 3 (see Figure 2.4), slices
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D. Metabolite analysis Samples were
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leakage is calculated as the net LD
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B. Effect of the severity of ischae
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2.11 DISCUSSION: The present studie
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clearly insufficient to induce myoc
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The present model may facilitate th
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2.12 Conclusiow I have characterise
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3.5 3 V 2.5 3: m Je m Z0 z 2 1.5 0.
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(3 3 2.5 a 1.5 - -r T 0 2 0.5 0 I P
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Q oro . 21 . 0 'a IP 10 '. R -C3 A
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=3 0 h X CD 0 x CD :3 0 , 7, CD 0 0
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CHAPTER III PRECONDITIONING THE HUM
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3.2 MATERIALS AND METHODS-. 3.2.1 E
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A117'reduction- At the end of the e
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-4 ýi r. () .1 a 0 1 tli n F5* - C
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v M. %; n C) .0 ý U ý ý - - - -2
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leakage resulting from precondition
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3.5 DISCUSSION: The present studies
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during cardiac surgery totalling 10
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different. The cellular mechanisms
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cn Je 8 7 6 5 4 1 0 0.8 0.7 0.6 0.5
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8 6 C) 2 0.7 0.6 Q) 0.5 0) E 25 0.4
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6 5 CY) ,u3 CF) m -ýe m 2 1 0 -0.8
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CHAPTERIV THE ROLE OF THE KATPCHANN
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It has been reported that K.. %-I-p
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0 a- I a 3 I cr =r Cl. 2 qQ 0'-ý 0
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Figure 4.7 shows that ischaemia alo
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Figure 4.2 Dosc-responsc experiment
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Figure 4.4 Dose-response experiment
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Figure 4.6 Dosc-response experiment
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1 0.9 -ý 0.8 0.7 E 0.6 0.5 0.4 0.2
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activity, and showed that diazoxide
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Furthermore, Van den Hoek et al [3
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mechanism by which the opening of m
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5.1 INTRODUCTION: Within the enormo
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5.2 MATERIALS AND METHODS: 5.2.1 Ex
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M77'rechiction: At the end of the e
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oc 0 0 cr F; * 10 eb I ý; o I 5 0
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Pages missing original in the
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esulted in a decrease of CK leakage
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are on long-term hypoglycaernics or
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absence of uniformity of expeniment
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5.7 Conclusion Preconditioning is a
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0.9 0.8 07 m 0.6 E -0 0t 4 0.3 02 0
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-0 1.2 1 &8 0.6 04 0.2 o Aerobic Is
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6.1 INTRODUCIFION' Life expectancv
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(MI-T) to blue t'()rmazan product C
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The demonstration that ischaemic in
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Table 61 Patients' demographic and
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Nure 6,1: Creatine Kinase (CK) leak
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CHAPTER VII IN VIVO STUDIES ON T"E
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The apparent discrepancy bet,.,,, e
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In the off-pump group, coronary byp
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eduction as described in section 3.
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7.4.2 In vitro studies Figures 7.3A
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preconditioning stimulus in man is
Page 173 and 174: myocardium. Several investigators [
Page 175 and 176: Table 7.2 - Patients haemod-v-namic
Page 177 and 178: (0 -I 3 CD CD CD 1 3 0 :3 0 0 =r w
Page 179 and 180: 0 co t X 3 co 0 0 Cumulative Releas
Page 181 and 182: -& a) c) UT 0 =r w CD 3 CD 0 1ý (a
Page 183 and 184: When ischaernic preconditioning was
Page 185 and 186: evidence tbr the involvement ot'PKC
Page 187 and 188: institution o fcardiopu Imo nary by
Page 189 and 190: Biblioqraphv 1. Abete P, Ferrara N,
Page 191 and 192: 14. Auchampach J, Cavero, I and Gro
Page 193 and 194: 27. Becker LB, Van den Hoek TLV, Sh
Page 195 and 196: 41. Bums PG, Krunkenkamp IB, Calder
Page 197 and 198: 55. Cohen G, Shirai T, Weisel RD, e
Page 199 and 200: 69. Currie RW and White FP (1983).
Page 201 and 202: 83. Downey JM, Liu GS and Thornton
Page 203 and 204: 97. Ganote C, Armstrong S and Downe
Page 205 and 206: 110. Grover GJ, D'Alonzo A, Hess T,
Page 207 and 208: 122. Hamilton T and Weston A (1989)
Page 209 and 210: 137. Hu H, Sato T, Seharaseyon J, L
Page 211 and 212: 151. Jennings R, Steenbergen C, Kin
Page 213 and 214: 164. Kelpzig H, Kobert G, Mafter C,
Page 215 and 216: 178. Lamping K, Christensen C, Pelc
Page 217 and 218: 192. Liu GS, Thornton J, Van Winkle
Page 219 and 220: 206. Maulik N, Yoshida T, Das DK. (
Page 221 and 222: 219. Miyawaki H, Zhou X, Ashraf, M.
Page 223: 233. Okazaki Y, Kodama K, Sato H, K
Page 227 and 228: 260. Saito S, Tamura Y, Moriuchi M,
Page 229 and 230: 274. Schulz R, Post H, Valhaus C, e
Page 231 and 232: 288. Stewart JR, Blackwell WH, Crut
Page 233 and 234: 300. Tani M, Suganuma Y, Hasegawa H
Page 235 and 236: 312. Tosaki A, Engelman DT, Engelma
Page 237 and 238: 324. Walker D, Marber M, Walker J a
Page 239 and 240: 337. Yamashita N, Nishida M, Hoshid
Page 241 and 242: 351. Zhang JG, Lindup WE. (1993). R
Page 243 and 244: 444 J. -G. Zhang and others are dif
Page 245 and 246: 446 J. -G. Zhang and others Assessm
Page 247 and 248: 448 J. -G. Zhang and others 0.9 0.8
Page 249 and 250: 450 J. -G. Zhang and others C E 07
Page 251 and 252: 4S2 J. -G. Zhang and othen effects
Page 253 and 254: ELSEVIER Abstract Cardiovascular Re
Page 255 and 256: 936 S. Ghosh et al. / Cardiovascula
Page 257 and 258: 938 S. Ghosh et al. / Cardiovascula
Page 259 and 260: 940 S. Ghosh et al. [41 Goto M, Liu
Page 261 and 262: 712 0" et &L h wcomMe geg in Obwa»
Page 263 and 264: 714 Gbosb ot aL hmoo dmoWmbDbsnedH
Page 265 and 266: 716 chmä et aL Pi unamOso äu In O
Page 267: 718 ehe* et &L ditioning in the hum
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