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Results for “Ischemic Preconditioning”

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PubMed2005

Ischemic preconditioning as induction of ischemic tolerance after transient ischemic attacks in human brain: its clinical relevance.

Ischemic preconditioning has been well-established in different animal models of cerebral ischemia. Suggesting that transient ischemic attack (TIAs) may represent a clinical model of ischemic tolerance, patients with ipsilateral TIA before ischemic stroke may have a better neurological outcome compared to patients without TIA before ischemic stroke. A retrospective case-control study. Analysis of clinical and neuroradiological findings of 130 patients treated with local intra-arterial thrombolysis using urokinase after ischemic stroke between January 2000 and May 2002. Eleven patients (8%) demonstrated prestroke ipsilateral TIA in the same vascular territory. Despite no significant differences in baseline characteristics, independence (modified Ranking Scale score) and neurological outcome (NIHS score) were significantly associated with prior TIA in multivariante models. Patients with prestroke TIA, showing a similar clinical picture (NIHS score) on admission, demonstrated a more favorable outcome (NIHS score (p<0.001) and modified Ranking score (p<0.0001)) compared to patients with unheralded ischemic stroke. The interval between TIA and ischemic stroke (1-7 days), duration of TIAs (0-20 min) and number of TIAs (2-3) influenced the better outcome in this patients' subgroup. In addition, we could show an induction of ischemic tolerance by prestroke ASA treatment in patients without previous new-onset TIA. Two to three ipsilateral TIA of the same vascular territory and of up to 20 min duration within 1-7 days may lead to ischemic tolerance to a subsequent ischemic stroke as demonstrated by significantly diminished infarct extention throughout all cortical imagines in neuroradiological studies. The role of ASA has to been further elucidated.

Case-Control Studies↗

PubMed2006

Is remote preconditioning as effective as direct ischemic preconditioning in preventing spinal cord ischemic injury?

BACKGROUND: Spinal cord injury remains a devastating complication of thoracic and thoracoabdominal aortic operations. The aim of this study was to assess the affectivity of direct ischemic preconditioning (PC) and remote PC in preventing spinal cord ischemic injury in an experimental model. MATERIALS AND METHODS: Thirty-eight New Zealand white rabbits were divided into five groups: One group served as Sham group (n = 7). Rabbits in other groups had their abdominal aorta cross-clamped for 40 min. Before aortic occlusion, aorta was clamped twice at the same site of aortic occlusion for 5 min followed by 15 min of reperfusion after each ischemic episode in one group (Direct PC, n = 8), left renal artery was clamped twice for 5 min followed by 15 min of reperfusion after each renal ischemic episode in one group (Remote PC, n = 8), left renal artery was first clamped for 5 min followed by 15 min of reperfusion and then aorta was clamped for 5 min followed by 15 min of reperfusion in one group (Remote + Direct PC, n = 8), and no PC method was used in Control group (n = 7). RESULTS: In all PC groups, neurological status of rabbits (Tarlov score) at post-ischemia 24th and 48th hours was better than the control group (P < 0.05), but worse than Sham group (P < 0.05). Mean viability index values in PC groups were higher than control group (P < 0.01). Post-ischemia serum NSE and MDA levels obtained in all three PC groups were significantly lower than control group (P < 0.05 and P < 0.01). CONCLUSIONS: The use of direct ischemic PC and/or remote PC is an effective way of reducing spinal cord ischemic injury because of aortic occlusion, while direct PC is more effective. The combined use of direct PC and remote PC did not provide better protection.

Analysis of Variance↗

PubMed2006

Ischemic preconditioning protects cardiomyocytes against ischemic injury by inducing GRP78.

Ischemic preconditioning (IP) conferred by brief ischemia-reperfusion induces resistance to cell injury due to the following lethal ischemia. This study aimed to elucidate whether 78-kDa glucose-regulated protein (GRP78), a main ER molecular chaperone, contributes to IP-mediated protection against ischemic myocardial injury. In a rat coronary artery occlusion model, the GRP78 protein level increased to 210% of the sham level by early IP with three cycles of 4-min ischemia and 4-min reperfusion. The IP reduced infarct size in subsequent lethal ischemia. In primary cardiomyocytes, the simulated IP procedure, incubation in oxygen-glucose deprivation (OGD) medium, also increased the GRP78 expression and suppressed the cell death caused by lethal ischemia. Transfection of grp78 antisense oligonucleotide attenuated the IP-mediated resistance to ischemia. This study showed for the first time that early IP up-regulates myocardial GRP78. It was suggested that GRP78 induced by early IP contributes to protect cardiomyocytes against ischemic injury.

Animals↗

PubMed2001

Effect of ischemic preconditioning on myocardial protection in coronary artery bypass graft patients : can the free radicals act as a trigger for ischemic preconditioning?

OBJECTIVE: To investigate the interrelationship of free radicals (FRs), ischemic preconditioning (IP), and hemodynamic function in coronary artery bypass graft (CABG) patients. DESIGN: Prospective, randomized, and controlled clinical study. PATIENTS: Forty CABG patients were randomized into an IP group (n = 20) and a control group (n = 20). INTERVENTION: The IP group was preconditioned with two cycles of two-min ischemia followed by 3-min reperfusion before cross-clamping. MEASUREMENT AND RESULTS: FR content in coronary sinus blood was measured directly using alpha-phenyl-N-tert-butylnitrone-electron spin-trapped spectroscopy. A small amount of FRs was generated after the IP protocol (5.6% above the baseline) but not in control subjects. A larger amount was generated 10 min after declamping in both groups (8.4% in IP protocol and 7.7% in control subjects). Hemodynamic function recovered better in the IP group at 1 h and 6 h after declamping. There was a significant negative correlation between FR generation after declamping and left ventricular stroke work index (LVSWI) at 1 h and 6 h after declamping (r = -0.71 and - 0.59, respectively) in the control subjects but not in the IP group. There was a significant positive correlation between FR generation after the IP protocol and cardiac index at 1 h and 6 h (r = 0.50 and 0.61, respectively) and LVSWI at 1 h and 6 h (r = 0.56 and 0.54, respectively) after declamping in the IP group but not in the control subjects. CONCLUSION: FR generation after the operation correlates with ventricular functional depression in CABG patients. IP protects the stunning heart but does not alter FR generation. The association of better hemodynamic recovery after CABG with FR generation during the IP period suggests that FRs might act as one of the triggers for IP.

Aged↗

PubMed2005

Effects of 5-hydroxydecanoate and ischemic preconditioning on the ischemic-reperfused heart of fed and fasted rats.

This investigation aimed to assess whether the mitochondrial ATP-sensitive potassium channel blocker 5-hydroxydecanoate (5-HD) could abolish the protection conferred by fasting and ischemic preconditioning (IPC) and to ascertain whether these effects are associated with glycogen breakdown and glycolytic activity. Langendorff perfused hearts of fed and 24-h fasted rats were exposed to 25 min ischemia plus 30 min reperfusion. IPC was achieved by a 3 min ischemia plus a 5 min reperfusion cycle. 5-HD (100 microM) perfusion begun 5 min before IPC or 13 min before sustained ischemia in the non preconditioned groups. Fasting improved the reperfusion recovery of contraction, decreased the contracture and the lactate production, increased glycogenolysis and did not affect the percentage of viable tissue. 5-HD abolished the effects of fasting on the contractile recovery but did not affect the contracture. 5-HD decreased the lactate production in the fed group, increased the preischemic glycogen content in both nutritional groups and did not affect the ischemic glycogen fall. IPC improved the contractile function but prevented the contracture only in the fed group, reduced lactate accumulation and glycogenolysis and evoked an increase of the viable tissue. 5-HD abolished the effects of IPC on the contractile recovery and did not affect its effect on the contracture, lactate production, glycogenolysis and viable tissue. These data suggest that the mitocondrial ATP-sensitive potassium channel is involved in the effects of fasting and IPC on the contractile function but the other cardioprotective and metabolic effects appear evoked through other mechanisms. Also suggest that besides the inhibition of the mitochondrial potassium channel, other mechanisms mediate the effects of 5-HD.

Animals↗

PubMed2002

Influence of fasting on the effects of ischemic preconditioning in the ischemic-reperfused rat heart.

The effects of fasting and ischemic preconditioning (IP) on heart function of Langendorff-perfused rat hearts exposed to 25 min global ischemia plus 30 min reperfusion (RP), were correlated with lactate release and tissue-levels of long-chain acyl carnitine (LCCa) and CoA (LCCoA). IP was achieved by a 3 min ischemia plus a 5 min reperfusion cycle. Creatine kinase leakage was measured to assess the extent of cardiac injury. Fasting reduced the ischemic-induced contracture, improved RP recovery of mechanical function, reduced lactate release and increased the end-ischemia LCCoA and LCCa levels. Both in the fed and the fasted rat hearts IP delayed the pacemaker depression, reduced the amplitude of ischemic contracture and improved the RP recovery of contraction. However, IP reduced creatine kinase and lactate release only in the fed rat hearts. IP had no effects on tissue LCCa and LCCoA in both groups. These data suggest that: 1) beneficial effects of fasting may be ascribed, at least in part, to a reduced lactate production which may attenuate ischemic myocyte acidification and to the accumulation of fatty acyl esters which would favour citric acid cycle replenishment during RP. 2) beneficial effects of IP could be in part explained by the reduction of lactate production in the fed group although data obtained with the fasted rat heart indicate that another mechanisms must also be involved in the effects of IP. 3) accumulation of LCCoA and LCCa is not involved in the noxious effects of ischemia as well as in the protection effected by IP.

Animals↗

PubMed2005

[Effect of dipyridamole on the phenomenon of ischemic preconditioning in patients with ischemic heart disease during paired bicycle ergometer tests].

AIM: To assess effect of dipyridamole on ischemic preconditioning (IP) in patients with coronary artery disease by paired bicycle ergometer exercise tests (BETs). MATERIAL AND METHODS: Patients (men, n=12, age 51.7+/-2.5 years) with class II-III stable angina pectoris underwent paired BETs (tests 1 and 2 at 15 min intervals). Test 1 was regarded as baseline and test 2 as the preconditioning one. In 72 hours another pair of BETs was carried out (tests 3 and 4) with same time interval in between. Before second pair of tests the patients received 75 mg of dipyridamole orally. RESULTS: Significant improvements of several parameters of ECG were observed during repeat BETs (increased exercise duration, maximal heart rate and double product, decreased maximal ST-depression and number of ECG leads with >1 mm ST depression). These data suggested the presence of IP phenomenon in both paired BETs. However only test after dipyridamole was associated with significant increase of work load (from 82.4+/-10.5 to 96.4+/-10.1 W, p=0.033), shortening of ST-depression recovery time (from 367+/-45 to 254+30 s, p=0.032) and increase of increment of exercise duration (from 34+/-15 to 81+/-17 s, p=0.034). Number of ECG leads on with segment ST depression >0,1 mv was significantly less during test 4 compared with test 2 (2.6+/-0.4 and 3.4+/-0.5; p=0.045). This data reflected increase of ischemic threshold during test 4. CONCLUSION: Dipyridamole (75 mg orally) augmented IP in patients with coronary artery disease during repeated BETs.

Adult↗

PubMedDate not supplied

[Ischemic preconditioning improves post-ischemic function but not energy metabolism of skeletal muscles].

Ischemic preconditioning (IP) refers to a phenomenon whereby short periods of ischemia reduce tissue damage after a subsequent sustained ischemia. The effect of IP before tourniquet ischemia of the extremities has not yet been evaluated. We developed a rat model of skeletal muscle ischemia and measured the effect of IP on postischemic function and high-energy phosphate levels. IP consisted in three cycles of 10 min ischemia and 10 min reperfusion each. IP improved significantly skeletal muscle function after 3 hours of ischemia and 2 hours of reperfusion. High-energy phosphate levels, however, remained unchanged. This study shows a protective effect of IP in skeletal muscles. These results furthermore suggest that the protection of energy metabolism is not a mechanism of IP in this model. IP could be easily performed before surgery of the extremities under tourniquet ischemia. The protective effect on postischemic skeletal muscle has therefore to be further investigated.

Animals↗

PubMed2005

Ischemic preconditioning protects post-ischemic oxidative damage to mitochondria in rat liver.

This study examined the effect of ischemic preconditioning (IPC) in protecting against a hepatic ischemia/reperfusion (I/R) injury, with particular focus on mitochondrial damage. Rat liver was preconditioned by 10 min of ischemia and 10 min of reperfusion. Immediately after IPC, liver was subjected to 90 min of sustained ischemia followed by 5 h of reperfusion. The hepatic I/R increased serum aminotransferase activity and mitochondrial lipid peroxidation 5 h after reperfusion. IPC attenuated these increases. Whereas the mitochondrial glutathione content and glutamate dehydrogenase activities were lower in the I/R group, these decreases were attenuated by IPC. During IPC, the tissue peroxide levels increased after 10 min of ischemia and were normalized after 10 min of reperfusion. In association with the IPC-derived transient increase in the peroxide levels, the significant production of peroxides observed at 10 min of reperfusion after 90 min of ischemia was attenuated. Furthermore, whereas the mitochondria isolated from rat liver after 5 h of reperfusion were rapidly swollen, the swelling rate was attenuated in the mitochondria from rat liver subjected to IPC before the sustained ischemia. The hepatic ATP and adenosine levels were 38% and 46% lower during the reperfusion, respectively. These decreases were attenuated by IPC. Thus, these results suggest that IPC protects the mitochondria against the deleterious effects of I/R, and this protection is associated with the reduced oxidative stress.

Adenosine↗

PubMed2003

Dual preconditioning: effects of pharmacological plus ischemic preconditioning on skin flap survival.

To enhance skin flap viability, pharmacological and ischemic preconditioning methods were investigated intensively. This study was designed to determine whether combined local dexamethasone administration and pedicle clamping would result in an additive enhancement of skin flap survival in the rat model. Twenty-eight male Sprague-Dawley rats were included in dexamethasone injection, clamping, clamping plus dexamethasone injection, and control groups. A rectangular random skin flap (3 x 11 cm) was outlined as bipedicled on the back of the animals. The dexamethasone or saline injection points in the flap were standardized. In the dexamethasone injection group, after raising the flaps, a total of 2.5 mg/kg dexamethasone was injected into the flaps. In the ischemic preconditioning group, 1 hour after saline injection, the cranial pedicle was clamped for 20 minutes and then 40 minutes reperfusion was performed. The clamping-plus-dexamethasone injection group was the same as the clamping group except dexamethasone was injected instead of the saline. In the control group, saline was injected instead of dexamethasone. Regardless of the group, all flaps were cut at the cranial side at the end of the 2 hours and were sutured back. On day 7, the surviving area was significantly greater in all experimental groups compared with the control group (p<0.05). Furthermore, the clamping-plus-dexamethasone group demonstrated the highest flap viability.

Animals↗

PubMed2006

Effects of ischemic preconditioning on cyclinD1 expression during early ischemic reperfusion in rats.

AIM: To observe the effect of ischemic preconditioning on cyclinD1 expression in rat liver cells during early ischemic reperfusion. METHODS: Fifty-four SD rats were randomly divided into ischemic preconditioning group (IP), ischemia/reperfusion group (IR) and sham operation group (SO). The IP and IR groups were further divided into four sub-groups (n = 6). Sham operation group (SO) served as the control group (n = 6). A model of partial liver ischemia/reperfusion was used, in which rats were subjected to liver ischemia for 60 min prior to reperfusion. The animals in the IP group underwent ischemic preconditioning twice for 5 min each time prior to the ischemia/reperfusion challenge. After 0, 1, 2, and 4 h of reperfusion, serum and liver tissue in each group were collected to detect the level of serum ALT, liver histopathology and expression of cyclinD1 mRNA and protein. Flow cytometry was used to detect cell cycle as the quantity indicator of cell regeneration. RESULTS: Compared with IR group, IP group showed a significantly lower ALT level in 1 h to 4 h sub-groups (P < 0.05). Proliferation index (PI) indicated by the S-phase and G2/M-phase ratio [(S+G2/M)/(G0/G1+S+G2/M)] was significantly increased in IP group at 0 and 1 h (26.44 +/- 7.60% vs 18.56 +/- 6.40%, 41.87 +/- 7.27% vs 20.25 +/- 6.70%, P < 0.05). Meanwhile, cyclinD1 protein expression could be detected in IP group. But in IR group, cyclinD1 protein expression occurred 2 h after reperfusion. The expression of cyclinD1 mRNA increased significantly in IP group at 0 and 1 h (0.568 +/- 0.112 vs 0.274 +/- 0.069, 0.762 +/- 0.164 vs 0.348 +/- 0.093, P < 0.05). CONCLUSION: Ischemic preconditioning can protect liver cells against ischemia/reperfusion injury, which may be related to cell proliferation and expression of cyclinD1 during early ischemic reperfusion.

Alanine Transaminase↗

PubMed2006

The rat Apg3p/Aut1p homolog is upregulated by ischemic preconditioning in the retina.

PURPOSE: Retinas can be protected from subsequent severe ischemic injury by ischemic preconditioning. Ischemic preconditioning is dependent on gene expression and protein synthesis; however, it is not clear which genes are important in this process. In this study, we have identified and characterized the rat homolog of yeast Apg3p/Aut1p, an important autophagy protein encoded by the autophagy 3-like (APG3L) gene. We have also further characterized the homologous human APG3L gene. METHODS: A fragment of the rat Apg3 cDNA was identified by mRNA differential display from hypoxia-treated E1A-NR3, an immortalized cell line derived from rat retinal cells that manifests phenotypes of retinal neurons. The full length of rat Apg3 (rApg3) cDNA sequence (about 1.4 kb) encoding 341 amino acids was cloned from a rat retinal cDNA library and characterized using Southern and northern blot analysis, and a global GenBank search. Protein expression was determined by western blotting, and immunohistochemistry. Ischemic preconditioning was achieved by ligation of the retinal arteries of the right eye for 5 min followed by 5 h reperfusion. The prolonged retinal ischemia was induced by ligation of the retinal arteries for 45 min followed by 5 h reperfusion. The full-length homologous human APG3L gene was cloned and sequenced from a human genomic DNA library. RESULTS: The combination of genomic Southern blot analysis and a global GenBank search indicated that rat APG3L is a single copy gene. Rat Apg3 mRNA is expressed in the retina at a high level but is also detected in other tissues. In the process of comparing the rat and human APG3L genes we showed that the organization of the human APG3L gene includes a unique transcriptional start site, a coding region with 12 translated exons and 11 introns and is located on human chromosome 3q13.1. Subcellular localization studies showed that recombinant rat autophagocytosis protein (Apg3p) is a cytosolic protein. Rat Apg3 mRNA level was upregulated by ischemic preconditioning but downregulated by prolonged ischemia. CONCLUSIONS: Our results suggest that the upregulation of rApg3 is a specific response to ischemic preconditioning rather than to retina ischemia, and autophagy may contribute to the neuroprotective effect of ischemic preconditioning in the retina.

Amino Acid Sequence↗

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↗

PubMed1994

Ischemic preconditioning preserves end-ischemic ATP, enhancing functional recovery and coronary flow during reperfusion.

The mechanisms by which ischemic preconditioning (IPC) protects against reperfusion (RP) injury are unknown. The purpose of this study was to relate IPC to postischemic mechanical function, vascular reactivity, and bioenergetics. Isolated perfused rat hearts were randomized to two groups. Control (CTRL) hearts underwent 25 min of global, 37 degrees C ischemia and 40 min RP. IPC hearts underwent 2.5 min ischemia and 10 min RP followed by 25 min ischemia and 40 min RP (RP40). Left ventricular developed pressure (DP) and coronary flow were continuously measured. 31P NMR spectra determined phosphocreatine and ATP concentrations in parallel hearts every 5 min. Results are means +/- SEM; n = 6/group. Significance was assumed for P < 0.05 by paired (within groups) and unpaired (between groups) t test. CTRL heart DP recovered to 35 +/- 4% of preischemic (PI) DP by RP40 (P < 0.001), while IPC heart DP reached 99 +/- 4% (P = NS vs PI; P < 0.001 vs CTRL). CTRL coronary flow recovered to only 75 +/- 3% of PI (P < 0.001) by RP40. IPC coronary flow exceeded baseline during RP (RP40 = 118 +/- 3%, P < 0.001 vs CTRL; P < 0.05 vs PI). After 25 min ischemia, CTRL heart ATP fell to 40 +/- 4% of PI (P < 0.001) while the IPC group fell to only 60 +/- 4% (P < 0.05 IPC vs CTRL; P < 0.001 vs PI). IPC preserves more end-ischemic ATP compared to CTRL hearts with a resultant improvement in mechanical function during reperfusion. Only preconditioned hearts preserve the adaptive mechanism(s) responsible for postischemic vasodilatation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1996

Ischemic preconditioning improves post-ischemic skeletal muscle function.

Ischemic preconditioning (IP), using one or more brief periods of ischemia before a sustained ischemia, represents a new approach to reduce tourniquet ischemia-induced skeletal muscle damage. The aim of this study was to investigate the effect of IP on skeletal muscle function and high-energy phosphate tissues levels in a rodent model. IP protocols using one, two, or three preconditioning cycles were compared. IP was found to significantly improve force, performance, endurance, and contractility of postischemic skeletal muscle. The efficacy of IP-induced protection was correlated with the number of preconditioning cycles. Preconditioning with three cycles resulted in a more effective protection as compared to one or two cycles. Three cycles of IP significantly improved force (409 +/- 63 versus 240 +/- 47 mN), performance (2546 +/- 481 versus 1081 +/- 242 mN*sec), endurance (46.7 +/- 5.0 versus 29.6 +/- 3.4 sec) and contractility (59.9 +/- 4.2 versus 38.7 +/- 5.1) in postischemic m.extensor dig. long. when compared to nonpreconditioned muscles. In contrast, high-energy phosphate tissue levels remained unchanged after three cycles of preconditioning. Altogether, this study describes, for the first time, the efficacy of IP to improve postischemic muscle function. The respective clinical potential warrants further exploration.

Animals↗

PubMed1998

Hypothermia increases the threshold for ischemic preconditioning.

OBJECTIVES: Both hypothermia and ischemic preconditioning are known to provide tolerance to myocardial ischemia and reperfusion. The aim of this study was to determine whether hypothermia during the ischemic preconditioning period attenuates the protective effect of ischemic preconditioning. METHODS: Experiments were performed in buffer-perfused isolated rabbit hearts. All hearts underwent 45 minutes of regional ischemia, followed by 2 hours of reperfusion. Ischemic preconditioning was elicited by either one or four periods of 5 minutes of regional ischemia. Hypothermia (25 degrees C) was induced beginning either 20 or 50 minutes before the 45-minute period of regional ischemia; normothermia (38 degrees C) was restored 10 minutes before the 45-minute period of regional ischemia. Except for the hypothermic periods noted, hearts were maintained at 38 degrees C. RESULTS: Normothermic ischemic preconditioning with either one or four cycles of 5 minutes of coronary occlusion resulted in a profound reduction of infarct size (58% reduction with one cycle, p < 0.05; 95% reduction with four cycles, p < 0.01). Hypothermic ischemic preconditioning with one cycle of 5-minute coronary occlusion resulted in no reduction of infarct size but hypothermic ischemic preconditioning with four cycles of 5-minute coronary occlusions resulted in a 94% reduction of infarct size (p < 0.01). Myocardial glycogen and lactate levels were maintained near control levels during hypothermic ischemia. CONCLUSIONS: From these data we conclude that hypothermia during the preconditioning period increases the threshold for eliciting the infarct limitation of ischemic preconditioning.

Animals↗

PubMed2006

The antiarrhythmic effect and clinical consequences of ischemic preconditioning.

Potentially hazardous short ischemic episodes increase the tolerance of myocardium to ischemia paradoxically. This condition decreases the infarct area markedly caused by a longer duration of coronary occlusion. This phenomenon is known as 'ischemic preconditioning' and its powerful cardioprotective effect has been shown in experimental and clinical studies. Ischemic preconditioning decreases cardiac mortality markedly by preventing the development of left ventricular dysfunction and ventricular and supraventricular arrhythmias after acute myocardial infarction. Ischemia-induced opening of ATP-sensitive potassium channels and synthesis of stress proteins via activation of adenosine, bradykinin and prostaglandin receptors seem to be the possible mechanisms. By understanding the underlying mechanisms of ischemic preconditioning, it may be possible to develop new pharmacologic agents that cause ischemic preconditioning with antiischemic and antiarrhythmic properties without causing myocardial ischemia.

Angioplasty, Balloon, Coronary↗

PubMed1996

Ischemic preconditioning enhances donor heart preservation.

Ischemic preconditioning has not been assessed in an experimental model for myocardial preservation during heart transplantation. Using isolated working rat hearts, ischemic preconditioning was investigated as an adjunct to isolated hypothermic (group 1), crystalloid (group 2: University of Wisconsin solution; group 3: St. Thomas' Hospital cardioplegic solution II; group 4: Bretschneiders' cardioplegic solution), and noncrystalloid (group 5: cold blood cardioplegia) preservation during a 10-hr period of global ischemia at 4 degrees C. After acquisition of functional baseline data, ischemic preconditioning was induced with one cycle of 5 min of normothermic ischemia and 5 min of reperfusion before induction of global hypothermic ischemia (n= 10/group). Nonpreconditioned hearts (n= 10/group) were assessed for control. Ischemic preconditioning improved postischemic: functional recovery. Thus, aortic flow after 60 min of reperfusion recovered to 0%, 8%, 0%, 1% and 0% in control groups 1 to 5 without ischemic preconditioning and 21%, 25%, 10%, 8%, and 3% in groups 1 to 5 with ischemic preconditioning. The same pattern of recovery was observed in regard to postischemic maximum developed left ventricular pressure, which recovered to 21%, 56%, 30%, 36%, and 19% in groups 1 to 5 without preconditioning and 46%, 75%, 49%, 40%, and 47% in the corresponding groups with ischemic preconditioning. High-energy phosphate contents were not significantly different between preconditioned hearts and corresponding nonpreconditioned control hearts. Creatine kinase leakage during early reperfusion was found to be reduced with ischemic preconditioning. Thus, we have demonstrated that ischemic preconditioning can improve contractile function after global hypothermic ischemia in the isolated rat heart and we have shown that this protection is additive to that of hypothermia-induced protection during global ischemia at 4 degrees C. This endogenous mechanism of cardioprotection was effective regardless of whether preservation was accomplished using cardioplegic solution or topical hypothermia alone. This may have clinical implications in myocardial preservation for heart transplantation.

Adenosine↗