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

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preconditioned with the protocol attaining the greatest protection in studies I and 2, this was one single cycle of 5min ischaernia. Then the tissues were reoxygenated for 1,2,3, or 4 hr before the 90min of ischaernia. Figure 3.3 shows the experimental time course for the six study groups. Study, 4: In this study, the "delayed protection" or "second window of protection" was investigated. I have demonstrated in the previous chapter that the human right atrial preparation used in the present studies remains viable for at least 24 hr but is more sensitive to ischaernia following 24 hr aerobic incubation. For this reason, two periods of ischaerma, 30 min (Study 4A) and 90 min (Study 4B) were studied (n=6/group). Again the preconditioning protocol consisted of a single cycle of 5min ischaemia/5min reoxygenation. Figures 3.4A and 3.413 show the experimental time course. Assessment of tissue injury and viability: At the end of each experimental protocol, tissue injury was determined by measuring the leakage of creatinine kinase (CK) into the incubation medium and tissue viability by the reduction of 3- [4,5-Dimethylthiazol-2-yll-2,5 cliphenyltetrazolium bromide (MTT) to blue formazan product. In the following chapters In the thesis, LDH was replaced by release of CK because of technical problems relating to acquiring reagents from distfibutors. CK Leakage: The activity of CK leakage into the media during the reoxygenation period (U/g wet wt) was assayed by a kinetic ultraviolet method based on the formation of NAD (Sigma Catalogue No. 1340-K)- 69
A117'reduction- At the end of the experimental time, MTT analysis was performed as described in section 2.613 (Chapter 2) and the results expressed as OD/mg wet wt. 2.5 Statistical Analysis All data are presented as mean±SEM. All values were compared by ANOVA with application of a post hoc Tukey's test. Statistical significance was assumed at the p
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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
Page 35 and 36: and these proteins have been sugges
Page 37 and 38: K vi-1, channels were initially fou
Page 39 and 40: tissues the K.. %,.,, channels are
Page 41 and 42: Subsequently, Jaburek et al 1145] i
Page 43 and 44: venous capacitance vessels. At ther
Page 45 and 46: preconditioning to be investigated
Page 47 and 48: In the angioplasty model, Tomai et
Page 49 and 50: patients were randomized into two g
Page 51 and 52: CHAPTER 11 THE HUMAN RIGHT ATRIAL T
Page 53 and 54: inexpensive. Briefly in this model,
Page 55 and 56: of each ischemic period, slices wer
Page 57 and 58: 30 nini FO linlin L 60 min 120 inin
Page 59 and 60: In Study 3 (see Figure 2.4), slices
Page 61 and 62: D. Metabolite analysis Samples were
Page 63 and 64: leakage is calculated as the net LD
Page 65 and 66: B. Effect of the severity of ischae
Page 67 and 68: 2.11 DISCUSSION: The present studie
Page 69 and 70: clearly insufficient to induce myoc
Page 71 and 72: The present model may facilitate th
Page 73 and 74: 2.12 Conclusiow I have characterise
Page 75 and 76: 3.5 3 V 2.5 3: m Je m Z0 z 2 1.5 0.
Page 77 and 78: (3 3 2.5 a 1.5 - -r T 0 2 0.5 0 I P
Page 79 and 80: Q oro . 21 . 0 'a IP 10 '. R -C3 A
Page 81 and 82: =3 0 h X CD 0 x CD :3 0 , 7, CD 0 0
Page 83 and 84: CHAPTER III PRECONDITIONING THE HUM
Page 85: 3.2 MATERIALS AND METHODS-. 3.2.1 E
Page 89 and 90: -4 ýi r. () .1 a 0 1 tli n F5* - C
Page 91 and 92: v M. %; n C) .0 ý U ý ý - - - -2
Page 93 and 94: leakage resulting from precondition
Page 95 and 96: 3.5 DISCUSSION: The present studies
Page 97 and 98: during cardiac surgery totalling 10
Page 99 and 100: different. The cellular mechanisms
Page 101 and 102: cn Je 8 7 6 5 4 1 0 0.8 0.7 0.6 0.5
Page 103 and 104: 8 6 C) 2 0.7 0.6 Q) 0.5 0) E 25 0.4
Page 105 and 106: 6 5 CY) ,u3 CF) m -ýe m 2 1 0 -0.8
Page 107 and 108: CHAPTERIV THE ROLE OF THE KATPCHANN
Page 109 and 110: It has been reported that K.. %-I-p
Page 111 and 112: 0 a- I a 3 I cr =r Cl. 2 qQ 0'-ý 0
Page 113 and 114: Figure 4.7 shows that ischaemia alo
Page 115 and 116: Figure 4.2 Dosc-responsc experiment
Page 117 and 118: Figure 4.4 Dose-response experiment
Page 119 and 120: Figure 4.6 Dosc-response experiment
Page 121 and 122: 1 0.9 -ý 0.8 0.7 E 0.6 0.5 0.4 0.2
Page 123 and 124: activity, and showed that diazoxide
Page 125 and 126: Furthermore, Van den Hoek et al [3
Page 127 and 128: mechanism by which the opening of m
Page 129 and 130: 5.1 INTRODUCTION: Within the enormo
Page 131 and 132: 5.2 MATERIALS AND METHODS: 5.2.1 Ex
Page 133 and 134: M77'rechiction: At the end of the e
Page 135 and 136: 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
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myocardium. Several investigators [
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Table 7.2 - Patients haemod-v-namic
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(0 -I 3 CD CD CD 1 3 0 :3 0 0 =r w
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0 co t X 3 co 0 0 Cumulative Releas
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-& a) c) UT 0 =r w CD 3 CD 0 1ý (a
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When ischaernic preconditioning was
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evidence tbr the involvement ot'PKC
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institution o fcardiopu Imo nary by
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Biblioqraphv 1. Abete P, Ferrara N,
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14. Auchampach J, Cavero, I and Gro
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27. Becker LB, Van den Hoek TLV, Sh
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41. Bums PG, Krunkenkamp IB, Calder
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55. Cohen G, Shirai T, Weisel RD, e
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69. Currie RW and White FP (1983).
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83. Downey JM, Liu GS and Thornton
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97. Ganote C, Armstrong S and Downe
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110. Grover GJ, D'Alonzo A, Hess T,
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122. Hamilton T and Weston A (1989)
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137. Hu H, Sato T, Seharaseyon J, L
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151. Jennings R, Steenbergen C, Kin
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164. Kelpzig H, Kobert G, Mafter C,
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178. Lamping K, Christensen C, Pelc
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192. Liu GS, Thornton J, Van Winkle
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206. Maulik N, Yoshida T, Das DK. (
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219. Miyawaki H, Zhou X, Ashraf, M.
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233. Okazaki Y, Kodama K, Sato H, K
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248. Pryzlenk K, Li G, Whittaker P
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260. Saito S, Tamura Y, Moriuchi M,
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274. Schulz R, Post H, Valhaus C, e
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288. Stewart JR, Blackwell WH, Crut
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300. Tani M, Suganuma Y, Hasegawa H
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312. Tosaki A, Engelman DT, Engelma
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324. Walker D, Marber M, Walker J a
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337. Yamashita N, Nishida M, Hoshid
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351. Zhang JG, Lindup WE. (1993). R
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444 J. -G. Zhang and others are dif
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446 J. -G. Zhang and others Assessm
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448 J. -G. Zhang and others 0.9 0.8
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450 J. -G. Zhang and others C E 07
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4S2 J. -G. Zhang and othen effects
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ELSEVIER Abstract Cardiovascular Re
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936 S. Ghosh et al. / Cardiovascula
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938 S. Ghosh et al. / Cardiovascula
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940 S. Ghosh et al. [41 Goto M, Liu
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712 0" et &L h wcomMe geg in Obwa»
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714 Gbosb ot aL hmoo dmoWmbDbsnedH
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716 chmä et aL Pi unamOso äu In O
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718 ehe* et &L ditioning in the hum
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