Ischemic Preconditioning Control Research Articles

Ischemic Preconditioning Improves Resistance Training Session Performance.

da Silva Novaes, J, da Silva Telles, LG, Monteiro, ER, da Silva Araujo, G, Vingren, JL, Silva Panza, P, Reis, VM, Laterza, MC, and Vianna, JM. Ischemic preconditioning improves resistance training session performance. J Strength Cond Res 35(11): 2993-2998, 2021-The aim of this study was to investigate the acute effect of ischemic preconditioning (IPC) in a resistance exercise (RE) training session on the number of repetitions performed, total volume, and rating of perceived exertion in recreationally trained and normotensive men. Sixteen recreationally trained and normotensive men completed 3 RE sessions in a counterbalanced and randomized order: (a) IPC protocol using 220 mm Hg followed by RE (IPC), (b) IPC cuff control protocol with 20 mm Hg followed by RE (CUFF), and (c) no IPC (control) followed by RE (CON). RE was performed with 3 sets of each exercise (bench press, leg press, lateral pulldown, hack machine squat, shoulder press, and Smith back squat) until concentric muscular failure, at 80% of one repetition maximum, with 90 seconds of rest between sets and 2 minutes of rest between exercises. Ischemic preconditioning and CUFF consisted of 4 cycles of 5 minutes of occlusion/low pressure alternating with 5 minutes of no occlusion (0 mm Hg) using a pneumatic tourniquet applied around the subaxillary region of the upper arm. For each condition, the number of repetitions completed, total volume of work performed, and rating of perceived exertion were determined. No significant difference was found for rating of perceived exertion between any experimental protocol. Ischemic preconditioning significantly (p < 0.05) increased the number of repetitions across exercises. Consequently, total volume performed (sum of total number of repetitions x load for each exercise) was significantly higher in IPC (46,170 kg) compared with CON (34,069 kg) and CUFF (36,590 kg) across all exercises. This work may have important implications for athletic populations because it demonstrates increase in muscle performance outcomes during a single RE session. Therefore, performing IPC before RE could be an important exercise prescription recommendation to increase maximum repetition performance and total volume of work performed and thus potentially increase desired training adaptations (i.e., strength and hypertrophy).

Enhanced Metabolic Stress Augments Ischemic Preconditioning for Exercise Performance.

Purpose: To identify the combined effect of increasing tissue level oxygen consumption and metabolite accumulation on the ergogenic efficacy of ischemic preconditioning (IPC) during both maximal aerobic and maximal anaerobic exercise.Methods: Twelve healthy males (22 ± 2 years, 179 ± 2 cm, 80 ± 10 kg, 48 ± 4 ml.kg−1.min−1) underwent four experimental conditions: (i) no IPC control, (ii) traditional IPC, (iii) IPC with EMS, and (iv) IPC with treadmill walking. IPC involved bilateral leg occlusion at 220 mmHg for 5 min, repeated three times, separated by 5 min of reperfusion. Within 10 min following the IPC procedures, a 30 s Wingate test and subsequent (after 25 min rest) incremental maximal aerobic test were performed on a cycle ergometer.Results: There was no statistical difference in anaerobic peak power between the no IPC control (1211 ± 290 W), traditional IPC (1209 ± 300 W), IPC + EMS (1206 ± 311 W), and IPC + Walk (1220 ± 288 W; P = 0.7); nor did VO2max change between no IPC control (48 ± 2 ml.kg−1.min−1), traditional IPC (48 ± 6 ml.kg−1.min−1), IPC + EMS (49 ± 4 ml.kg−1.min−1) and IPC + Walk (48 ± 6 ml.kg−1.min−1; P = 0.3). However, the maximal watts during the VO2max increased when IPC was combined with both EMS (304 ± 38 W) and walking (308 ± 40 W) compared to traditional IPC (296 ± 39 W) and no IPC control (293 ± 48 W; P = 0.02).Conclusion: This study shows that in a group of participants for whom a traditional IPC stimulus was not effective, the magnification of the IPC stress through muscle contractions while under occlusion led to a subsequent exercise performance response. These findings support that amplification of the ischemic preconditioning stimulus augments the effect for exercise capacity.

Influence of diabetes mellitus duration on the efficacy of ischemic preconditioning in a Zucker diabetic fatty rat model.

Augmented mortality and morbidity following an acute myocardial infarction in patients with diabetes mellitus Type 2 (T2DM) may be caused by increased sensitivity to ischemia reperfusion (IR) injury or altered activation of endogenous cardioprotective pathways modified by T2DM per se or ischemic preconditioning (IPC). We aimed to investigate, whether the duration of T2DM influences sensitivity against IR injury and the efficacy of IPC, and how myocardial glucose oxidation rate was involved. Male Zucker diabetic fatty rats (homozygote (fa/fa)) at ages 6-(prediabetic), 12- (onset diabetes) and 24-weeks of age (late diabetes) and their age-matched non-diabetic controls (heterozygote (fa/+) were subjected to IR injury in the Langendorff model and randomised to IPC stimulus or control. T2DM rats were endogenously protected at onset of diabetes, as infarct size was lower in 12-weeks T2DM animals than in 6- (35±2% vs 53±4%; P = 0.006) and 24-weeks animals (35±2% vs 72±4%; P<0.0001). IPC reduced infarct size in all groups irrespective of the presence of T2DM and its duration (32±3%; 20±2%; 36±4% respectively; (ANOVA P<0.0001). Compared to prediabetic rats, myocardial glucose oxidation rates were reduced during stabilisation and early reperfusion at onset of T2DM, but these animals retained the ability to increase oxidation rate in late reperfusion. Late diabetic rats had low glucose oxidation rates throughout stabilisation and reperfusion. Despite inherent differences in sensitivity to IR injury, the cardioprotective effect of IPC was preserved in our animal model of pre-, early and late stage T2DM and associated with adaptations to myocardial glucose oxidation capacity.

Meta-analysis of ischemic preconditioning (IP) on postoperative outcomes after liver resections.

Background:The protective role (decrease ischemia-reperfusion injury) of ischemic preconditioning (IP) before continuous vascular occlusion in liver resection is controversial. This meta-analysis aimed to compare the advantages and any potential disadvantages of IP maneuver.Methods:A systematic search in the Embase, Medline, PubMed databases, and the Cochrane Library was performed using both medical subject headings (MeSH) and truncated word searches to identify all randomized controlled trials (RCTs) published on this topic. The primary outcomes were postoperative morbidity, mortality, postoperative aspartate aminotransferase (AST) level, alanine aminotransferase (ALT) level, and total bilirubin (TB) level. Pooled odds ratios (ORs) and weighted mean differences (WMDs) with 95% confidence intervals (95% CIs) were calculated using either the random effects model or fixed effects model.Results:Thirteen RCTs involving 918 patients were analyzed to achieve a summated outcome. The patients have been divided into IP group (n = 455) and no IP group (n = 463) before continuous vascular occlusion. No significant difference was found in postoperative mortality between both groups (P = .30). Subgroup analysis revealed that the postoperative morbidity in the cirrhosis subgroup was significantly less for the IP group compared with the control group (P = .01). In the cirrhosis subgroup, the result was stable (P = .04), without heterogeneity (P = .59; I2 = 0%). Meta-analysis of AST level on postoperative day (POD) 1 indicated lower postoperative AST level in the IP group (P = .04). The analysis of ALT level showed lower ALT level in the IP group versus control group (P = .02). However, there was no difference in postoperative AST and ALT level after excluding 1 study with statistical heterogeneity (all P > .05). With respect to postoperative TB level, there was no significant difference between 2 groups.Conclusion:IP cannot decrease the hospital mortality for patients undergoing hepatectomy. IP may be beneficial for patients with cirrhosis due to less morbidity in patients with liver cirrhosis. However, we cannot conclude that IP can decrease ischemia-reperfusion injury because it did not significantly decrease postoperative AST, ALT, and TB levels.

Ischemic preconditioning reduces the severity of ischemia-reperfusion injury of peripheral nerve in rats

Background and aimAllow for protection of briefly ischemic tissues against the harmful effects of subsequent prolonged ischemia is a phenomennon called as Ischemic Preconditioning (IP). IP has not been studied in ischemia-reperfusion (I/R) model of peripheral nerve before. We aimed to study the effects of acute IP on I/R injury of peripheral nerve in rats.Method70 adult male rats were randomly divided into 5 groups in part 1 experimentation and 3 groups in part 2 experimentation. A rat model of severe nerve ischemia which was produced by tying iliac arteries and all idenfiable anastomotic vessels with a silk suture (6-0) was used to study the effects of I/R and IP on nerve biochemistry. The suture technique used was a slip-knot technique for rapid release at time of reperfusion in the study. Cytoplasmic vacuolar degeneration was also histopathologically evaluated by light microscopic examination in sciatic nerves of rats at 7th day in part 2 study.Results3 hours of Reperfusion resulted in an increase in nerve malondialdehyde levels when compared with ischemia and non-ischemia groups (p < 0.001 and p < 0.0001 respectively). IP had significantly lower nerve MDA levels than 3 h reperfusion group (p < 0.001). The differences between ischemic, IP and non-ischemic control groups were not significant (p > 0.05). There was also a significant decrease in vacoular degeneration of sciatic nerves in IP group than I/R group (p < 0.05).ConclusionIP reduces the severity of I/R injury in peripheral nerve as shown by reduced tissue MDA levels at 3 th hour of reperfusion and axonal vacoulization at 7 th postischemic day.

Hepatic ischemic preconditioning increases portal vein flow in experimental liver ischemia reperfusion injury

Ischemic preconditioning (IPC) has been shown to decrease liver injury and to increase hepatic microvascular perfusion after liver ischemia reperfusion. This study aimed to evaluate the effects of IPC on hemodynamics of the portal venous system. Thirty-two rats were randomized into two groups: IPC group and control group. The rats of the IPC group underwent IPC by 10 minutes of liver ischemia followed by 10 minutes of reperfusion before liver ischemia, and the rats of the control group were subjected to 60 minutes of partial liver ischemia. Non-ischemic lobes were resected immediately after reperfusion. The animals were studied at 4 hours and 12 hours after reperfusion. Mean arterial pressure, heart rate, portal vein flow and pressure were analyzed. Blood was collected for the determination of the levels of aspartate aminotransferase, alanine aminotransferase, calcium, lactate, pH, bicarbonate, and base excess. IPC increased the mean portal vein flow at 4 hours and 12 hours after reperfusion. IPC recovered 78% of the mean portal vein flow at 12 hours after reperfusion. IPC decreased the levels of aspartate aminotransferase, alanine aminotransferase and lactate, and increased the levels of ionized calcium, bicarbonate and base excess at 12 hours after reperfusion. This study demonstrated that IPC increases portal vein flow and enhances hepatoprotective effects in liver ischemia reperfusion. The better recovery of portal vein flow after IPC may be correlated with the lower levels of transaminases and with the better metabolic profile.

Frequent biomarker analysis in the isolated perfused heart reveals two distinct phases of reperfusion injury

BackgroundReperfusion injury and its modulation are incompletely characterized. The purpose of the present study was to characterize the dynamics of reperfusion injury by portraying the temporal release of lactate dehydrogenase (LDH) during ischemia–reperfusion injury in an isolated heart model. MethodsWe studied infarct size and LDH release in the following groups: I) Effect of reperfusion length was evaluated in 79 rats subjected to 40minute ischemia and 60, 90, 120 or 180minute reperfusion and a) ischemic preconditioning (IPC) or b) No IPC (control). II) LDH release kinetics was studied in 6 rats subjected to calcium-paradox to verify the applicability of LDH as a dynamic marker of cellular injury. III) Ischemia–reperfusion injury modification was studied in 36 rats subjected to: a) ischemic postconditioning, b) prolonged ischemia, c) Reperfusion Injury Salvage Kinase (RISK) pathway inhibition with wortmannin in IPC hearts, d) RISK activation with insulin or e) mitochondrial permeability transition pore (mPTP) inhibition with cyclosporine A. ResultsInfarct size increased from 60 to 180minute reperfusion in control hearts. LDH was released in two separate peaks from 2 to 20 and 30 to 120min of reperfusion. IPC attenuated both peaks. Postconditioning and agents known to modify reperfusion injury attenuated the second peak. ConclusionsFrequent measurement of myocardial ischemia markers for 120min of reperfusion allows identification of two phases of reperfusion injury that are affected by cardioprotective stimuli. The second phase contributes significantly to final infarct size, which is modifiable and a potential target for cardioprotective interventions.

Remote ischemic preconditioning immediately before percutaneous coronary intervention does not impact myocardial necrosis, inflammatory response, and circulating endothelial progenitor cell counts: A single center randomized sham controlled trial

Percutaneous coronary intervention (PCI) is frequently accompanied by myocardial injury. The present study was performed to determine whether remote ischemic preconditioning (IP) induces cardioprotection during PCI. We enrolled 95 patients requiring nonemergency PCI for stable disease or unstable angina into this prospective clinical trial. Patients were randomized to either remote IP (induced by three 3-min cycles of blood pressure cuff inflations to 200 mm Hg around the upper arm, followed by 3-min of reperfusion n = 47) or sham control (n = 48) immediately preceding PCI. The primary outcome measure was the frequency of post-PCI myonecrosis, defined as a peak postprocedural cTnT T ≥ 0.03 ng/dL. Secondary outcome measures were the change in plasma high-sensitivity C-reactive protein (hsCRP) levels following PCI and in endothelial progenitor cells (EPC) counts following IP. There was no difference in the primary endpoint of the frequency of PCI related myonecrosis which occurred in 22 (47%) and 19 (40%) patients in the remote IP and control groups, respectively, P = 0.42. There was significant increase in hsCRP post-PCI in both groups (P < 0.001), but there was no difference between the groups (median %change in hsCRP 46% vs. 54%, P = 0.73). There was no significant change in circulating early (CD34 -/CD133+/KDR+), intermediate (CD34+/CD133+/KDR+), or late (CD34+/CD133-/KDR+) EPC in the two groups immediately following IP. The composite rate of death, myocardial infarction, and target lesion revascularization at 1 year was 14.1% versus 13.7% (P = 0.90). Our study indicates that remote IP immediately before PCI does not induce cardioprotection in low to moderate risk patients.

Ischemic Preconditioning Reduces Right Ventricular Infarct Size through Opening of Mitochondrial Potassium Channels

Objectives: We investigated whether ischemic preconditioning (IPC) protects the right ventricular (RV) myocardium against ischemic injury in hearts treated with the specific mitochondrial ATP-sensitive potassium (K_ATP) channel blocker 5-hydroxydecanoate (5-HD). Methods: Hearts from male Wistar rats (300 g, n = 39) were isolated and perfused with Krebs-Henseleit buffer and randomized to no IPC (control, n = 16), IPC (n = 16) or IPC preceded by addition of 5-HD (100 µ<smlcap>m</smlcap>, n = 7). IPC consisted of 2 × 5 min of global ischemia followed by 40 min of global ischemia and 120 min of reperfusion. The effect of IPC on RV myocardial infarct size was evaluated by measurement of the infarct size/area-at-risk ratio (RVIS/AAR). Postischemic RV function was evaluated by RV pressures. Results: IPC produced a marked decrease in RVIS/AAR (24.4 ± 8.1 vs. 42.6 ± 10.6%, p < 0.0001) and improved hemodynamic recovery of RV contractile function compared with the control group. We found no difference in RVIS/AAR (45.2 ± 4.4 vs. 42.6 ± 10.6, p > 0.05) or hemodynamic recovery between IPC + 5-HD and control hearts. Blockade of mitochondrial K_ATP channels by 5-HD abolished the cardioprotective response to IPC. Conclusion: IPC reduces RV myocardial infarct size and improves postischemic RV contractile function in the isolated rat heart, possibly through opening of the mitochondrial K_ATP channel.

The role of JNK in IP-induced tolerance against forebrain ischemia/reperfusion injury in gerbils

Kitagawa等[1]在沙土鼠脑缺血的实验研究中,首次观察到机体对短暂亚致死性缺血的适应性反应能增加神经元对致死性缺血的耐受性,由此提出了脑缺血预处理(ischemic preconditioning, IP)的概念.此后各国学者对IP的机制进行了广泛的研究,提出了许多假说.近年来,以受体激活为起点,以细胞内信号转导为主线,构成预处理保护机制研究的重点,其中丝裂原激活的蛋白激酶(mitogen activated protein kinase, MAPK)途径在IP中的作用引起了人们的关注。

Proteomic study on protective mechanism of ischemic preconditioning to ischemia-reperfusion lung injury

Objective To investigate the change of protein expression of lung tissue of rabbit after ischemic preconditioning (IP) and try to elucidate the potential protective mechanism of IP. Methods 12 domestic rabbits were randomly divided into group IP and group control (6 rabbits in each group). All the left lungs were afflicted by ische mia-reperfusion injury except that those in group IP were subject to IP prior to ischemic phase. 2-DE was employed to separate the total protein of the lung tissue. PDQuest analysis software was used to distinguish the differently expressed protein spot. MALDI-TOF-MS and Mascot database searching were exploited to identify these proteins. Results 1) IP attenuated the ischemia-reperfusion lung injury. 2) The proteomic analysis showed 35 target proteins, of which 17 were characterized such as phosphatidylinositol 3-kinase(PI3k) delta catalytic subunit. Conclusions 1) Proteomic is a promising tool to investigate the IP and ischemia-reperfusion lung injury. 2) That IP inhibits inflammatory cascades through phosphatidylinositol 3-kinase signal transduction pathway may be one of its protective mechanism.

Delta-opioid receptor activation mimics ischemic preconditioning in the canine heart.

The role of delta-opioid receptors in mediating ischemic preconditioning (IPC) in rats, rabbits, and pigs has been well-established; however, no studies have been performed in dogs. Therefore, the purpose of the present study was to determine if activation of delta-opioid receptors can mimic the cardioprotective effects of IPC in the canine heart and to determine if a nonselective opioid receptor antagonist could block IPC. All dogs were subjected to 60 minutes of left anterior descending (LAD) coronary artery occlusion and 3 hours of reperfusion. Ischemic preconditioning was produced by one 5-minute period of ischemia 10 minutes before LAD coronary artery occlusion. Infarct size (IS) expressed as a percent of the area at risk (AAR; IS/AAR) was determined by triphenyltetrazolium staining. Two selective delta-opioid receptor (DOR) agonists, TAN-67 and BW373U86, were administered by intracoronary infusion for 30 minutes before LAD occlusion and the opioid receptor antagonist naloxone was administered 30 minutes before IPC. Both TAN-67 and BW373U86 produced significant reductions in IS/AAR similar to that of IPC (control: 28+/-2.1; TAN: 12.3+/-2.2; IPC: 9.3+/-3.0: BW: 11.7+/-2.6). Naloxone attenuated the effect of IPC (control: 28+/-2.1; naloxone: 18.2+/-4.5). These results suggest that opioid receptors are important in IPC in dogs, and stimulation of delta-opioid receptors with selective agonists can mimic the cardioprotective effects of IPC and may have therapeutic potential.

Preconditioning of latissimus dorsi muscle flaps with monophosphoryl lipid a.

The use of dynamic myoplasty to restore function to failing organs is an exciting new application of skeletal muscle flaps. A complication of large flap elevation that can compromise flap function is ischemia-induced necrosis; one approach to minimizing this is to pretreat tissues with ischemic preconditioning. The purpose of this study was to determine whether systemic administration of monophosphoryl lipid A, a drug known to mimic late-phase ischemic preconditioning in the heart, could reduce ischemia-induced necrosis in latissimus dorsi muscle flaps. Forty latissimus dorsi muscle flaps from 20 Sprague-Dawley rats were allocated into four groups. In group I (n = 10), flaps were not preconditioned and served as controls. In group II (n = 10), flaps received ischemic preconditioning with two 30-minute periods of ischemia interspersed by 10 minutes of reperfusion. In group III (n = 10), rats received an intravenous bolus of approximately 0.3 ml of monophosphoryl lipid A vehicle only. In group IV (n = 10), rats received an intravenous bolus of 450 microg/kg of monophosphoryl lipid A and vehicle. Twenty-four hours after treatment, all latissimus dorsi muscle flaps were elevated on a single neurovascular pedicle and subjected to 4 hours of ischemia. After 72 hours of reperfusion, latissimus dorsi muscles were harvested, weighed, stained with nitroblue tetrazolium, and assessed for percent necrosis using digitized images of muscle sections and computerized planimetry. The percent necrosis in ischemic preconditioning-treated flaps (group II) was significantly reduced by 57 percent (p < 0.05) compared with control flaps (group I). The percent necrosis in flaps treated with monophosphoryl lipid A (group IV) was significantly reduced by 58 percent (p < 0.05) compared with vehicle-control flaps (group III). There was no difference in mean percent necrosis between ischemic preconditioning (group II) and monophosphoryl lipid A-treated (group IV) flaps or between ischemic preconditioning-control (group I) and monophosphoryl lipid A vehicle-control (group III) flaps. Intravenous administration of systemic monophosphoryl lipid A mimics the late-phase protective effect of ischemic preconditioning in the authors' rat latissimus dorsi muscle flap model.

Myocardial lactate production is not involved in the ischemic preconditioning mechanism in coronary artery bypass graft surgery patients

Objective: To study the relationship between ischemic preconditioning (IP) and lactate production and their impact on coronary artery bypass graft surgery patients. Design: Prospective, randomized, controlled study. Setting: University hospital. Participants: Eighty 3-vessel disease coronary artery bypass graft surgery patients with stable and unstable angina pectoris. Interventions: The IP patients were preconditioned with 2 periods of 2-minute ischemia followed by 3-minute reperfusion before aortic cross-clamping. Measurements and Main Results: The cardiac index (CI) after surgery was significantly higher in the IP group than in controls among stable patients (p = 0.013). IP was not effective in CI recovery in unstable patients. The baseline values of lactate production were 11.6%, 20.3%, −7.0%, and −2.9% in stable IP, stable control, unstable IP, and unstable control patients. Compared with baseline, lactate production increased significantly after the IP protocol (39.0% and 47.5% in the stable and unstable patients), and operation (47.5%, 31.7%, 35.4%, and 35.6% in stable IP, stable control, unstable IP, and unstable control patients) but not after 10 minutes of cardiopulmonary bypass (29.7% and 19.0% in the stable and unstable patients). There were no differences among the groups in lactate production after the operation. Lactate production after the IP protocol was negatively associated with CI recovery after surgery in the IP patients (p = 0.026). Conclusion: The IP effects do not include modulation of lactate production. IP induces lactate production, but it seems not to be involved in the triggering process. Copyright © 2001 by W.B. Saunders Company

Beneficial effects of ischemic preconditioning on right ventricular function after coronary artery bypass grafting

Background. Preservation of right ventricular myocardium is unsatisfactory in patients with critical stenosis or occlusion of the right coronary artery. The aim of this study was to investigate whether ischemic preconditioning (IP) improved the recovery of right ventricular function after coronary artery bypass grafting. Methods. Forty patients with three-vessel disease who had coronary artery bypass grafting were randomly assigned to the IP group (n = 20) or control group (n = 20). In the IP group, two cycles of two minutes of ischemia after three minutes of reperfusion were given before cross-clamping. Hemodynamic data were collected. Right ventricular ejection fraction was measured by thermodilution. Results. Right ventricular ejection fraction and right ventricular systolic volume index were decreased postoperatively (lowest value at 6 hours postoperatively). The changes in right ventricular ejection fraction were significantly milder in the IP group postoperatively ( p = 0.012). The decrease in right ventricular systolic volume index postoperatively was also less in IP patients ( p = 0.002). Fewer inotropic drugs were used in the IP group compared with controls. Conclusions. Ischemic preconditioning had a myocardial protective effect on recovery of right ventricular contractility in patients who had coronary artery bypass grafting.

Preconditioning during simulated MIDCABG attenuates blood flow defects and neutrophil accumulation

Background. Ischemic preconditioning (IP) may be cardioprotective in minimally invasive direct coronary artery bypass where cardioplegia is not used. This study tested the hypothesis that IP of the area at risk (AAR) would attenuate postischemic injury from transient coronary artery occlusion. Methods. In 19 anesthetized dogs, the left anterior descending coronary artery was occluded for 30 minutes (simulating coronary occlusion during anastomosis) followed by 3 hours of reperfusion. In 10 dogs, occlusion was preceded by 5 minutes of occlusion and 5 minutes of reperfusion (IP), whereas 9 other dogs had no IP (control, C). Results. Thirty minutes of left anterior descending occlusion caused comparable dyskinesis (systolic shortening, sonomicrometry) in the AAR in C (baseline, 29% ± 3% to 3% ± 2%) and in IP (baseline, 29% ± 2% to −0.3% ± 2%). After 3 hours of reperfusion, systolic shortening was significantly depressed in C (20% ± 4%), and was not significantly improved by IP (24% ± 3%, p = 0.8 versus C). Postischemic diastolic stiffness in the AAR was not altered by IP versus C (0.60 ± 0.12 versus 0.41 ± 0.13). Plasma creatine kinase activity was similar between C and IP at the end of reperfusion (20 ± 11 versus 16 ± 5 U/g). Postischemic AAR blood flow (in milliliters per minute per gram of tissue) at 180 minutes of reperfusion decreased by 56% versus baseline in C (from 1.04 ± 0.4 to 0.46 ± 0.12; p < 0.05) compared with no change in IP (from 0.74 ± 0.23 to 0.60 ± 0.10), but there was no significant group difference at this time. Myeloperoxidase activity as an index of neutrophil accumulation in AAR was decreased in IP versus C (0.4 ± 0.09 versus 0.7 ± 0.04 U/μg tissue). Conclusions. Ischemic preconditioning does not decrease postischemic wall motion and only modestly increases postischemic blood flow abnormalities in the AAR, but does significantly inhibit neutrophil accumulation.