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Biomedical subjects

H Otani

Publications and source records attributed to H Otani.

At least 19 recordsLinked to original sources
PubMed2002

Fine reconstruction of the pancreatic ductular system at the onset of pancreatitis.

The three-dimensional structure of the pancreatic ductular system (from the intercalated duct to the intercellular secretory canaliculus) is controversial and unclear. The aim of this study is to reveal the three-dimensional structure of the pancreatic ductular sysytem at the onset of pancreatitis. One day following rat pancreatic duct ligation, dilated lumina from the pancreatic ductular system were reconstructed by light microscopic and scanning electron microscopic examination of pancreatic tissue serial sections. The existence of the intra-acinar duct, which is formed only by centroacinar cells and interconnects the adjacent central lumina in an acinus, was demonstrated. The intercellular secretory canaliculi, which are the terminal parts of the pancreatic ductular system, anastomose and end blindly in the intercellular space located between adjacent lateral surfaces of the acinar cells. The intercalated ducts, the intra-acinar ducts, the central lumina, and the intercellular secretory canaliculi are arranged together in a complex connecting and branching system. However, there were no anastomoses found among the central lumina or acini.

Animals↗
PubMed2002

Long-term results of chronic hemodialysis patients with isolated coronary artery bypass grafting performed by the same surgeon. A comparative study.

BACKGROUND: The aim of this study was to examine the long-term results of isolated coronary artery bypass grafting (CABG) patients who required chronic hemodialysis. METHODS: From May 1990 to June 2000, 23 hemodialysis patients received isolated CABG performed by the same surgeon. Postoperative follow-up was completed with maximum duration of 122 months. RESULTS: Operative deaths (n=2) were due to acute circulatory failure related to hemodialysis. The most frequent cause of late deaths (n=10) was infection. Five (50%) patients died of sepsis, and 80% of sepsis was caused by leg infection associated with arteriosclerosis obliterans. There were 6 late cardiac events including 3 cardiac deaths. The actual survival rates 1, 3, 5 and 7 years after CABG were 68.6%, 42.5%, 35.4% and 35.4%, respectively. And the actual cardiac event free rates 1, 3, 5 and 7 years after CABG were 77.6%, 77.6%, 46.6% and 46.6%, respectively. Operative mortality (p=0.019), long-term survival (p<0.001) and cardiac event free rate (p=0.002) were significantly poorer in hemodialysis patients than in non-hemodialysis patients. However, the long-term survival rate of our hemodialysis patients receiving isolated CABG was almost similar to that in dialysis patients without CABG. The etiology of chronic renal failure did not significantly affect long-term RESULTS. Using internal thoracic artery graft significantly (p=0.02) decreased the late cardiac event in hemodialysis patients, although it did not improve late survival. CONCLUSIONS: Primary CABG followed by aggressive re-intervention have the benefit of preventing late cardiac death in hemodialysis patients. However, prevention of sepsis and treatment of arteriosclerosis obliterans are important for improving the late survival in hemodialysis patients receiving isolated CABG.

Aged↗
PubMed2001

Involvement of interleukin-1beta/nitric oxide pathway in the postischemic impairment of long-term potentiation of the rat hippocampus.

To investigate whether postischemic cerebral dysfunction occurs via the interleukin-1 beta/nitric oxide (IL-1beta/NO) pathway, we examined the effects of an IL-1beta antagonist on long-term potentiation (LTP) impairment and excessive NO production in the rat hippocampus after 10-min global ischemia. Intracerebroventricilar administration of the IL-1beta antagonist attenuated NO production and rescued LTP impairment in the perforant path-dentate gyrus synapses, observed 1 day and 4 days after ischemic insult, respectively. There was an inverse relationship between LTP in the dentate gyrus synapses and hippocampal NO production. Centrally applied IL-1beta mimicked the consequences of transient ischemia in LTP formation and hippocampal NO production in non-ischemic rats. These findings indicate that the IL-1beta/NO pathway is involved in the hippocampal LTP impairment observed in the postischemic brain.

Animals↗
PubMed2001

Pertussis toxin-sensitive and -insensitive mechanisms of alpha1-adrenoceptor-mediated inotropic responses in rat heart.

In rat left ventricular papillary muscle, phenylephrine, an alpha1-adrenoceptor agonist, induced a triphasic inotropic response; an initial transient, small, positive inotropic effect followed by a transient chloroethylclonidine-sensitive negative inotropic effect and a sustained 2-(2,6-dimethoxyphenoxyethyl)aminomethyl-1,4-benzodioxane (WB4101)-sensitive positive inotropic effect. Treatment with pertussis toxin for 2 days significantly inhibited only the transient negative inotropic effect without changing the sustained positive inotropic effect. This treatment also prevented the acetylcholine (1 microM)-induced negative inotropic effect. Further, phenylephrine-induced transient negative inotropic effect was attenuated in the presence of ouabain. These results suggest that pertussis toxin-sensitive or -insensitive G-protein may be responsible for alpha1-adrenoceptor subtype-mediated negative inotropic effect or positive inotropic effect, respectively, in which the transient negative inotropic effect was produced via the stimulation of Na+, K+ pump, presumably through pertussis toxin-sensitive G-protein-dependent pathway.

Adrenergic alpha-Antagonists↗
PubMed2001

Developmental changes in Cl(-)-ATPase activity in rat brains.

Developmental changes in brain Cl(-)-ATPase activity were examined using fetal, neonatal and adult rats. The Cl(-)-ATPase activity rapidly increased over 20 postnatal days to a level four-fold higher than that in an 18-day-old fetus. On Western blot analysis using an anti-Cl(-)-ATPase/pump 51 kDa subunit (ClP51) antibody, the amount of ClP51 protein increased in parallel with Cl(-)-ATPase activity. Immunohistochemistry using the same antibody showed Cl(-)-ATPase-like immunoreactivity on the cell membranes of neurons such as cerebral and hippocampal pyramidal cells and cerebellar Purkinje cells, where the immunoreactivity increased with developmental changes in the size and shape of the neurons. These findings suggest that neuronal Cl(-)-ATPase activity markedly increases during early postnatal development with an increase in the amount of Cl(-)-ATPase protein, which may support the formation of inwardly directed neuronal Cl(-) gradients.

Adenosine Triphosphatases↗
PubMed2001

Bradycardia-induced long QT syndrome caused by a de novo missense mutation in the S2-S3 inner loop of HERG.

Long QT syndrome is a congenital disorder that presents with a defective cardiac ion channel and is either associated with prolonged action potential or, more commonly, known as an acquired form in which "torsades de pointes" type arrhythmias specifically occur after secondary causes. We report a case of a novel HERG mutation (A490T) that caused a bradycardia-associated form of long QT syndrome. A 27-year-old woman exhibited recurrent syncope due to torsades de pointes associated with a disturbance of the cardiac conduction system. By using polymerase chain reaction and single strand conformational polymorphism analyses, we identified a heterozygous single nucleotide substitution of HERG (G to A at nt 1468). This mutational change was not present in 140 Japanese control individuals. Electrophysiological assays for the A490T mutant HERG channel were conducted in the heterologous expression system with COS7 cells. The mutant channel was found to reconstitute functional channel currents, suggesting the homomeric mutant channel was functional. The mutation did not change the properties of the activation gate and inward rectification, however the current density of this mutant channel was small compared with that of wild type HERG. Taken together, this mutant may cause subtle changes in HERG channel functions (I(Kr)) in vivo. In this case, genetic background and unexpected bradycardia may have contributed to the development of long QT syndrome.

Adult↗
PubMed2001

Involvement of anion exchange in the hypoxia/reoxygenation-induced changes in pH(i) and.

The involvement of Cl(-)/HCO(3)(-) exchange in hypoxia/reoxygenation-induced changes in pH(i) and Ca(2+) concentration ([Ca(2+)](i)) was examined in rat ventricular myocytes. During 10-min hypoxia, the initial pH(i) (7.21+/-0.04) fell to below 6.8. Subsequent reperfusion with reoxygenated buffer returned this acidic pH(i) to the neutral range with increases in [Ca(2+)](i). These responses were reduced by the removal of Cl(-) or HCO(3)(-) and by the addition of anion exchange inhibitors, SITS (4-acetamido-4'isothiocyanato-stilbene-2,2'disulfonic acid) and DIDS (4,4'-diisothiocyano-stilbene-2,2'-disulfonic acid), while inhibitors for the Cl(-) channel and Na(+)/K(+)/2Cl(-) cotransport were without effects. The hypoxia-induced acidification was attenuated by protein kinase C inhibitors, calphostin C and chelerythrine, but not by a protein kinase A inhibitor, KT5720. Under normoxic condition, protein kinase C activation induced a SITS-sensitive acidification. Furthermore, in electrically driven rat papillary muscle, SITS and DIDS improved the recovery of developed tension during the reoxygenation. These results suggest that the hypoxia-induced decrease in pH(i) is mediated at least in part by anion exchange stimulation through protein kinase C activation, and this exchange takes part in the reoxygenation-induced Ca(2+) overload as well as contractile dysfunction.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2001

Hypoxia/reoxygenation promotes myocardial angiogenesis via an NF kappa B-dependent mechanism in a rat model of chronic myocardial infarction.

Therapeutic angiogenesis achieved either through the use of discreet angiogenic proteins or by gene therapy is fast emerging as a highly attractive treatment modality for ischemic heart disease. Herein we examine a novel method of stimulating myocardial angiogenesis by hypoxic preconditioning at both capillary and arteriolar levels, and the potential role of NF kappa B in mediating such a response. We also investigate the functional relevance of such treatment by assessing whether the induced neovascularization can help preserve left ventricular contractile functional reserve in the setting of developing heart failure secondary to myocardial infarction. Male Sprague-Dawley rats were randomly divided into eight groups: normoxia + sham surgery (NS), normoxia + permanent left anterior descending coronary artery (LAD) occlusion (NMI), hypoxic preconditioning + sham surgery (HS), hypoxic preconditioning + permanent LAD occlusion (HMI), PDTC (NF kappa B inhibitor) + hypoxic preconditioning + LAD occlusion (PHMI), PDTC+normoxia + LAD occlusion (PNMI), PDTC + hypoxic preconditioning + sham surgery (PHS) and PDTC + normoxia + sham surgery (PNS). Rats in the preconditioned groups were subjected to systemic hypoxemic hypoxic exposure (10+/-0.4% O2) for 4 h followed by a 24-h period of normoxic reoxygenation prior to undergoing LAD occlusion. Rats in the normoxia groups were time matched with the preconditioned group and maintained under normoxic conditions for the 28-h period prior to LAD occlusion. The HMI group displayed significant increases in capillary as well as arteriolar density after 2, 4 and 7 days post-operation compared to the NMI. Prior PDTC administration prevented such increases in the PHMI group and effectively abolished the pro-angiogenic effect of hypoxic preconditioning (HP). One week after sham surgery or LAD occlusion, rats underwent a pharmacological stress test with dobutamine in progressively increasing doses which revealed significantly elevated values of dp/dt(max) at each dose point in the HMI group compared to the NMI or PHMI groups. Hypoxic preconditioning also decreases endothelial cell injury as determined by the extent of endothelial cell apoptosis using anti-VWF factor labelling and TUNEL assay. The results suggest that HP stimulates myocardial angiogenesis via redox-regulated transcription factor, NF kappa B-dependent pathway to an extent sufficient to exert significant preservation of contractile functional reserve in a rat model of myocardial infarction progressing to heart failure.

Animals↗
PubMed2001

Characterization and subcellular localization of KCNQ1 with a heterozygous mutation in the C terminus.

Numerous mutations in KCNQ1, a gene encoding the alpha -subunit of cardiac delayed rectifier potassium channels, have been found in long QT syndrome (LQTS). Among them, several mutations in the C terminus have been shown to cause autosomal recessive or subclinical autosomal dominant LQTS. Here, we report a heterozygous mutation, T587M, which is also in the KCNQ1 C-terminal domain. The same mutation was found in three independent probands that were clearly symptomatic with family history of cardiac sudden death. Functional assay using a heterologous expression system with a mammalian cell line (COS7 cells) revealed that the mutant displayed neither functional channels when expressed alone nor dominant-negative effect when co-expressed with wild-type (WT) KCNQ1. To examine the cellular trafficking of KCNQ1, green fluorescent protein (GFP) was tagged to the cytoplasmic C terminus of WT or mutant KCNQ1. This procedure did not affect the essential properties of expressed WT KCNQ1 channels. On confocal microscopic images, GFP-tagged WT KCNQ1 showed a plasma membrane fluorescence pattern, whereas the GFP-tagged mutant showed a perinuclear fluorescence pattern. Co-expression of the mutant with GFP-tagged WT KCNQ1 did not influence its normal cellular transport. Therefore, the T587M mutant cannot traffic to the plasma membrane and may form no subunit assembly with WT KCNQ1. These findings provide a novel molecular basis for the clinical finding that this C-terminal mutation produced a severe form of RWS-type LQTS.

Adolescent↗
PubMed2001

Role of STAT3 in ischemic preconditioning.

We recently demonstrated that ischemic preconditioning (IPC) induced by cyclic episodes of short durations of ischemia and reperfusion potentiates a signal transduction cascade involving protein tyrosine kinases and MAP kinases. A rapid activation of janus kinase (JAK) and several signal transducers and activators of the transcription (STATs) including STAT3, STAT5A and STAT6 has been shown to occur during myocardial ischemia and reperfusion. This study sought to examine if JAK/STAT signaling pathway play any role in classical early phase of IPC. Isolated working rat hearts were perfused for 15 min with KHB buffer in the absence or presence of a JAK kinase inhibitor tyrphostin AG490 (5 microm) followed by IPC, 30 min global ischemia and 2 h of reperfusion. The results demonstrated extensive phosphorylation of JAK2 and STAT3 in the IPC hearts which was almost completely abolished by an inhibitor of JAK2, AG490. IPC displayed cardioprotection as evidenced by improved post-ischemic contractile recovery, decreased myocardial infarct size and reduced number of apoptotic cardiomyocytes. AG490 blocked IPC-mediated cardioprotection by altering the IPC-mediated survival signal into death signal. Thus, IPC-induced upregulation of antiapoptotic gene bcl-2 and downregulation of pro-apoptotic gene bax are decreased and increased, respectively, in the AG490 treated hearts. The results suggest that early phase of IPC potentiates JAK/STAT signaling by activating STAT3 which transmits a survival signal to the myocardium.

Animals↗
PubMed2001

Revascularization of left subclavian artery for coronary subclavian steal syndrome.

We have experienced 2 patients with coronary subclavian steal syndrome which progressed each to a different prognosis. Both cases received percutaneous transluminal angioplasty for subclavian artery stenosis after coronary artery bypass grafting. Although one case is doing well without any symptoms, the other case required axilloaxillary artery bypass grafting for the subclavian artery restenosis.

Aged↗
PubMed2001

Spontaneous loss of a conditionally dispensable chromosome from the Alternaria alternata apple pathotype leads to loss of toxin production and pathogenicity.

The Alternaria alternata apple pathotype causes Alternaria blotch of susceptible apple cultivars through the production of a cyclic peptide, host-specific toxin, AM-toxin. We recently cloned a cyclic peptide synthetase gene, AMT, whose product catalyzes the production of AM-toxin and showed that it resides on chromosomes of 1.8 Mb or less, depending on the A. alternata apple pathotype strain. Reverse transcriptase (RT)-PCR, using primers specific to AMT, on laboratory sub-cultured strains previously shown to produce AM-toxin, identified one isolate that did not express the gene. A leaf necrosis bioassay confirmed an AM-toxin-minus phenotype. However, an original isolate of this strain which had not undergone sub-culture gave a positive result by both RTPCR and bioassay. Contour-clamped homogeneous electric field electrophoresis and Southern hybridization demonstrated the loss of a 1.1-Mb chromosome in the non-toxin-producing isolate. Since this chromosome can be entirely lost without affecting growth, but is necessary for pathogenicity, we propose it is a conditionally dispensable chromosome.

Alternaria↗
PubMed2001

Evidence for a single nucleotide polymorphism in the KCNQ1 potassium channel that underlies susceptibility to life-threatening arrhythmias.

INTRODUCTION: Congenital long QT syndrome (LQTS) is a genetically heterogeneous arrhythmogenic disorder caused by mutations in at least five different genes encoding cardiac ion channels. It was suggested recently that common polymorphisms of LQTS-associated genes might modify arrhythmia susceptibility in potential gene carriers. METHODS AND RESULTS: We examined the known LQTS genes in 95 patients with definitive or suspected LQTS. Exon-specific polymerase chain reaction single-strand conformation polymorphism and direct sequence analyses identified six patients who carried only a single nucleotide polymorphism in KCNQ1 that is found in approximately 11% of the Japanese population. This 1727G>A substitution that changes the sense of its coding sequence from glycine to serine at position 643 (G643S) was mostly associated with a milder phenotype, often precipitated by hypokalemia and bradyarrhythmias. When heterologously examined by voltage-clamp experiments, the in vitro cellular phenotype caused by the single nucleotide polymorphism revealed that G643S-KCNQ1 forms functional homomultimeric channels, producing a significantly smaller current than that of the wild-type (WT) channels. Coexpression of WT-KCNQ1 and G643S-KCNQ1 with KCNE1 resulted in approximately 30% reduction in the slow delayed rectifier K+ current I(Ks) without much alteration in the kinetic properties except its deactivation process, suggesting that the G643S substitution had a weaker dominant-negative effect on the heteromultimeric channel complexes. CONCLUSION: We demonstrate that a common polymorphism in the KCNQ1 potassium channel could be a molecular basis for mild I(Ks) dysfunction that, in the presence of appropriate precipitating factors, might predispose potential gene carriers to life-threatening arrhythmias in a specific population.

Adult↗
PubMed2001

Protein kinase C isoform-dependent myocardial protection by ischemic preconditioning and potassium cardioplegia.

OBJECTIVE: Ischemic preconditioning combined with potassium cardioplegia does not always confer additive myocardial protection. This study tested the hypothesis that the efficacy of ischemic preconditioning under potassium cardioplegia is dependent on protein kinase C isoform. METHODS: Isolated and crystalloid-perfused rat hearts underwent 5 cycles of 1 minute of ischemia and 5 minutes of reperfusion (low-grade ischemic preconditioning) or 3 cycles of 5 minutes of ischemia and 5 minutes of reperfusion (high-grade ischemic preconditioning) or time-matched continuous perfusion. These hearts received a further 5 minutes of infusion of normal buffer or oxygenated potassium cardioplegic solution. The isoform nonselective protein kinase C inhibitor chelerythrine (5 micromol/L) was administered throughout the preischemic period. All hearts underwent 35 minutes of normothermic global ischemia followed by 30 minutes of reperfusion. Isovolumic left ventricular function and creatine kinase release were measured as the end points of myocardial protection. Distribution of protein kinase C alpha, delta, and epsilon in the cytosol and the membrane fractions were analyzed by Western blotting and quantified by a densitometric assay. RESULTS: Low-grade ischemic preconditioning was almost as beneficial as potassium cardioplegia in improving functional recovery; left ventricular developed pressure 30 minutes after reperfusion was 70 +/- 15 mm Hg (P <.01) in low-grade ischemic preconditioning and 77 +/- 14 mm Hg (P <.001) in potassium cardioplegia compared with values found in unprotected control hearts (39 +/- 12 mm Hg). Creatine kinase release during reperfusion was also equally inhibited by low-grade ischemic preconditioning (18.2 +/- 10.6 IU/g dry weight, P <.05) and potassium cardioplegia (17.6 +/- 6.7 IU/g, P <.01) compared with control values. However, low-grade ischemic preconditioning in combination with potassium cardioplegia conferred no significant additional myocardial protection; left ventricular developed pressure was 80 +/- 17 mm Hg, and creatine kinase release was 14.8 +/- 11.0 IU/g. In contrast, high-grade ischemic preconditioning with potassium cardioplegia conferred better myocardial protection than potassium cardioplegia alone; left ventricular developed pressure was 121 +/- 16 mm Hg (P <.001), and creatine kinase release was 8.3 +/- 5.8 IU/g (P <.05). Chelerythrine itself had no significant effect on functional recovery and creatine kinase release in the control hearts, but it did inhibit the salutary effects not only of low-grade and high-grade ischemic preconditioning but also those of potassium cardioplegia. Low-grade ischemic preconditioning and potassium cardioplegia enhanced translocation of protein kinase C alpha to the membrane, whereas high-grade ischemic preconditioning also enhanced translocation of protein kinase C delta and epsilon. Chelerythrine inhibited translocation of all 3 protein kinase C isoforms. CONCLUSIONS: These results suggest that myocardial protection by low-grade ischemic preconditioning and potassium cardioplegia are mediated through enhanced translocation of protein kinase C alpha to the membrane. It is therefore suggested that activation of the novel protein kinase C isoforms is necessary to potentiate myocardial protection under potassium cardioplegia.

Animals↗
PubMed2001

Insulin-like growth factor 1 prevents neuronal cell death and paraplegia in the rabbit model of spinal cord ischemia.

OBJECTIVE: Insulin-like growth factor 1 has been shown to be cytoprotective against ischemia-reperfusion injury in various organs. However, spinal cord protection by insulin-like growth factor 1 has not been tested. We have therefore examined the effect of insulin-like growth factor 1 on neuronal cell death and motor function after spinal cord ischemia. METHODS: Japanese white rabbits were subjected to spinal cord ischemia by clamping the abdominal aorta for 15 minutes. Insulin-like growth factor 1 (0.3 mg/kg) at a dose equipotent to insulin (0.3 IU/kg) in lowering blood glucose level or the control (phosphate-buffered saline solution as a vehicle) was administered intravenously 30 minutes before the aortic clamp. RESULTS: Hind-limb motor function had recovered normally 48 hours after the operation in all the rabbits (n = 8) treated with insulin-like growth factor 1. In contrast, all the control-treated (n = 8) and all but one of the insulin-treated (n = 6) rabbits had deteriorated to paraplegia by 48 hours after the operation. Histopathologic sections in the involved spinal cord segment showed that a significantly (P <.0001) greater number of motor neuron cells were preserved in the rabbits treated with insulin-like growth factor 1 (17.9 +/- 4.8 per section) than in those treated with the control (8.0 +/- 2.1). Although insulin was equipotent to insulin-like growth factor 1 in preserving the number of motor neuron cells (18.5 +/- 2.7), the percentage of motor neuron cells positive for terminal deoxynucleotidyltransferase-mediated deoxyuridine triphosphate-biotin nick-end labeling were significantly (P <.01) smaller in the rabbits treated with insulin-like growth factor 1 (6.0 +/- 4.6) compared with those treated with the control (54.6 +/- 33.8) and insulin (26.2 +/- 11.7). Immunohistochemical studies revealed that insulin-like growth factor 1 increased expression of the antiapoptotic Bcl-xL protein and inhibited expression of the proapoptotic Bax protein in motor neuron cells 24 and 48 hours after the operation. In contrast, expression of only Bax was increased after the operation in other groups of rabbits subjected to spinal cord ischemia. CONCLUSIONS: These results suggest that insulin-like growth factor 1, but not insulin with a conventional dose, protects motor neuron cells from ischemic spinal cord injury associated with differential regulation of Bcl-xL and Bax protein.

Animals↗
PubMed2001

An essential role of the antioxidant gene Bcl-2 in myocardial adaptation to ischemia: an insight with antisense Bcl-2 therapy.

Reperfusion of ischemic myocardium results in apoptotic cell death, which can be blocked by adapting the heart to ischemic stress induced by cyclic episodes of brief periods of ischemia and reperfusion. In concert, the antiapoptotic gene bcl-2 is decreased by ischemia/reperfusion, but increased in the ischemically adapted myocardium. To examine if bcl-2 plays a crucial role in cardioprotection, adaptive cardioprotection was further examined in the hearts treated with antisense bcl-2 oligodeoxynucleotides (ODN). Isolated Langendorff-perfused rat hearts were divided into three groups: control (perfused with Krebs-Henseleit bicarbonate buffer for 210 min); 30-min ischemia followed by 2-h reperfusion; ischemic adaptation followed by 30-min ischemia and 2-h reperfusion. The last (adapted heart) group was subdivided into another two groups: one was transfected 48 h earlier with antisense bcl-2 ODN, whereas the other group was transfected with sense bcl-2 ODN. Cardioprotection was examined by determining cardiomyocyte death due to necrosis and apoptosis. Antisense gene therapy almost completely abolished bcl-2 protein expression in the hearts. Bcl-2 mRNA was down-regulated in the ischemic/reperfused heart, but up-regulated in the adapted myocardium. Adapted myocardium showed decreased infarct size and reduced number of apoptotic cardiomyocytes. Ischemia/reperfusion resulted in increased oxidative stress as evidenced by increased malonaldehyde formation. Adapted myocardium had a reduced amount of malonaldehyde. Antisense bcl-2 ODN completely abolished the cardioprotective effects of adaptation by eliminating the antideath signal of bcl-2. In concert, reduced oxidative stress in the adapted myocardium no longer persisted. The results suggest an antioxidant role of bcl-2 that appeared to be essential for the cardioprotection achieved by ischemic adaptation.

Adaptation, Physiological↗