scholarly journals Sevoflurane Confers Additional Cardioprotection after Ischemic Late Preconditioning in Rabbits

2003 ◽  
Vol 99 (3) ◽  
pp. 624-631 ◽  
Author(s):  
Jost Müllenheim ◽  
Dirk Ebel ◽  
Mirco Bauer ◽  
Florian Otto ◽  
André Heinen ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Katp Channels ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Area At Risk ◽  
Late Preconditioning ◽  
Infarct Size Reduction ◽  
Artery Disease ◽  
Conscious Animals

Background Sevoflurane exerts cardioprotective effects that mimic the early ischemic preconditioning phenomenon (EPC) by activating adenosine triphosphate-sensitive potassium (KATP) channels. Ischemic late preconditioning (LPC) is an important cardioprotective mechanism in patients with coronary artery disease. The authors investigated whether the combination of LPC and sevoflurane-induced preconditioning results in enhanced cardioprotection and whether opening of KATP channels plays a role in this new setting. Methods Seventy-three rabbits were instrumented with a coronary artery occluder. After recovery for 10 days, they were subjected to 30 min of coronary artery occlusion and 120 min of reperfusion (I/R). Controls (n = 14) were not preconditioned. LPC was induced in conscious animals by a 5-min period of coronary artery occlusion 24 h before I/R (LPC, n = 15). Additional EPC was induced by a 5-min period of myocardial ischemia 10 min before I/R (LPC+EPC, n = 9). Animals of the sevoflurane (SEVO) groups inhaled 1 minimum alveolar concentration of sevoflurane for 5 min at 10 min before I/R with (LPC+SEVO, n = 10) or without (SEVO, n = 15) additional LPC. The KATP channel blocker 5-hydroxydecanoate (5-HD, 5 mg/kg) was given intravenously 10 min before sevoflurane administration (LPC+SEVO+5-HD, n = 10). Results Infarct size of the area at risk (triphenyltetrazolium staining) was reduced from 45 +/- 16% (mean+/-SD, control) to 27 +/- 11% by LPC (P < 0.001) and to 27 +/- 17% by sevoflurane (P = 0.001). Additional sevoflurane administration after LPC led to a further infarct size reduction to 14 +/- 8% (LPC+SEVO, P = 0.003 vs. LPC; P = 0.032 vs. SEVO), similar to the combination of LPC and EPC (12 +/- 8%; P = 0.55 vs. LPC+SEVO). Cardioprotection induced by LPC+SEVO was abolished by 5-HD (LPC+SEVO+5-HD, 41 +/- 19%, P = 0.001 vs. LPC+SEVO). Conclusions Sevoflurane administration confers additional cardioprotection after LPC by opening of KATP channels.

Adenosine A1-receptor induced late preconditioning and myocardial infarction: reperfusion duration is critical

2002 ◽  
Vol 283 (1) ◽  
pp. H38-H43 ◽  
Author(s):  
Renaud Tissier ◽  
Rachid Souktani ◽  
Patrick Bruneval ◽  
Jean-François Giudicelli ◽  
Alain Berdeaux ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride ◽  
Receptor Stimulation ◽  
Late Preconditioning ◽  
Adenosine A1 ◽  
A1 Receptor

We investigated the influence of coronary artery reperfusion (CAR) duration on the infarct-limiting properties of adenosine A1-receptor stimulation-induced delayed preconditioning (A1-DPC) compared with ischemia-induced delayed preconditioning (I-DPC). Sixty-one chronically instrumented conscious rabbits successfully underwent the following protocol. On day 1, rabbits were randomly divided into four groups: control (saline, iv), I-DPC (six 4-min coronary artery occlusion/4-min reperfusion cycles), A1-DPC100( N 6-cyclopentyladenosine, 100 μg/kg iv), and A1-DPC400( N 6-cyclopentyladenosine, 400 μg/kg iv). On day 2 (i.e., 24 h later), rabbits underwent a 30-min coronary artery occlusion after which CAR was started and maintained for either 3 or 72 h. Infarct size (percentage of the area at risk) was determined by triphenyltetrazolium chloride staining. After 3 h of CAR, I-DPC, A1-DPC100, and A1-DPC400 significantly decreased infarct size (36 ± 5, 41 ± 4, 38 ± 5%, respectively) compared with control (55 ± 3%). After 72 h of CAR, infarct sizes were not significantly different among the four groups. This result was confirmed by histologic analysis. Thus A1-DPC at the two investigated doses, as well as I-DPC, decreased infarct size after 3 h but not 72 h of CAR.

Responses to coronary artery occlusion in conscious dogs with selective cardiac denervation

1988 ◽  
Vol 255 (3) ◽  
pp. H525-H533 ◽  
Author(s):  
Y. T. Shen ◽  
D. R. Knight ◽  
S. F. Vatner ◽  
W. C. Randall ◽  
J. X. Thomas
Keyword(s):  
At Risk ◽  
Blood Flow ◽  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Conscious Dogs ◽  
Wall Thickening ◽  
Area At Risk ◽  
Cardiac Denervation

The extent to which cardiac denervation alters responses to myocardial ischemia remains controversial. This study compared responses to 24-h coronary artery occlusion (CAO) on measurements of wall thickness (ultrasonic crystals), regional myocardial blood flow (microspheres), and infarct size (triphenyltetrazolium chloride technique) in three groups of conscious dogs with 1) selective posterior left ventricular (LV) wall denervation, 2) selective ventricular denervation, or in 3) intact dogs. After CAO, hemodynamic changes were not different among the three groups. Wall thickening in the ischemic zone became akinetic or paradoxical early after CAO and did not recover in any group over the 24-h monitoring period. Blood flow in the area at risk fell similarly in all groups. Infarct size, as a percentage of the area at risk, was 45 +/- 7% in intact, 48 +/- 6% in posterior LV wall-denervated, and 48 +/- 8% in ventricular-denervated group. There was, however, a lower (P less than 0.05) frequency of arrhythmic beats per minute after 3 h of CAO in the ventricular-denervated group (3.2 +/- 1.4) compared with the intact (11.3 +/- 4.1) or posterior wall-denervated (12.6 +/- 3.2) group. An additional group of ventricular-denervated dogs was studied to determine the effects of sequential, brief 2-min CAO at 2, 4, and 8 wk after denervation. Responses of regional wall thickening to CAO were not affected significantly even after 8 wk following ventricular denervation. Thus, in conscious dogs, neither selective ventricular denervation nor selective denervation of the posterior LV wall improved collateral blood flow, affected regional function favorably, or reduced infarct size after CAO.

Differential effects of postconditioning on myocardial stunning and infarction: a study in conscious dogs and anesthetized rabbits

2006 ◽  
Vol 291 (3) ◽  
pp. H1345-H1350 ◽  
Author(s):  
Nicolas Couvreur ◽  
Laurence Lucats ◽  
Renaud Tissier ◽  
Alain Bize ◽  
Alain Berdeaux ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Myocardial Stunning ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Segment Length ◽  
Wall Thickening ◽  
Area At Risk

Postconditioning, i.e., brief intermittent episodes of myocardial ischemia-reperfusion performed at the onset of reperfusion, reduces infarct size after prolonged ischemia. Our goal was to determine whether postconditioning is protective against myocardial stunning. Accordingly, conscious chronically instrumented dogs (sonomicrometry, coronary balloon occluder) were subjected to a control sequence (10 min coronary artery occlusion, CAO, followed by coronary artery reperfusion, CAR) and a week apart to postconditioning with four cycles of brief CAR and CAO performed at completion of the 10 min CAO. Three postconditioning protocols were investigated, i.e., 15 s CAR/15 s CAO ( n = 5), 30 s CAR/30 s CAO ( n = 7), and 1 min CAR/1 min CAO ( n = 6). Left ventricular wall thickening was abolished during CAO and similarly reduced during subsequent stunning in control and postconditioning sequences (e.g., at 1 h CAR, 33 ± 4 vs. 34 ± 4%, 30 ± 4 vs. 30 ± 4%, and 33 ± 4 vs. 32 ± 4% for 15 s postconditioning, 30 s postconditioning, and 1 min postconditioning vs. corresponding control, respectively). We confirmed this result in anesthetized rabbits by demonstrating that shortening of left ventricular segment length was similarly depressed after 10 min CAO in control and postconditioning sequences (4 cycles of 30 s CAR/30 s CAO). In additional rabbits, the same postconditioning protocol significantly reduced infarct size after 30 min CAO and 3 h CAR (39 ± 7%, n = 6 vs. 56 ± 4%, n = 7 of the area at risk in postconditioning vs. control, respectively). Thus, contrasting to its beneficial effects on myocardial infarction, postconditioning does not protect against myocardial stunning in dogs and rabbits. Conversely, additional episodes of ischemia-reperfusion with postconditioning do not worsen myocardial stunning.

KATP channels are common mediators of ischemic and calcium preconditioning in rabbits

1998 ◽  
Vol 274 (4) ◽  
pp. H1106-H1112 ◽  
Author(s):  
Ichiro Kouchi ◽  
Tomoyuki Murakami ◽  
Ryuzo Nawada ◽  
Masaharu Akao ◽  
Shigetake Sasayama
Keyword(s):  
Infarct Size ◽  
Channel Blocker ◽  
Myocardial Infarct ◽  
Katp Channels ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Myocardial Infarct Size ◽  
Area At Risk ◽  
Channel Activation ◽  
Calcium Infusion

Calcium preconditioning (CPC), like ischemic preconditioning (IPC), reduces myocardial infarct size in dogs and rats. ATP-sensitive potassium (KATP) channels induce cardioprotection of IPC in these animals. To determine whether KATP channels mediate both IPC and CPC, pentobarbital sodium-anesthetized rabbits received 30 min of coronary artery occlusion followed by 180 min of reperfusion. IPC was elicited by 5 min of occlusion and 10 min of reperfusion, and CPC was elicited by two cycles of 5 min of calcium infusion with an interval period of 15 min. Infarct size expressed as a percentage of the area at risk was 38 ± 3% (mean ± SE) in controls. IPC, CPC, and pretreatment with a KATP channel opener, cromakalim, all reduced infarct size to 13 ± 2, 17 ± 2, and 12 ± 3%, respectively ( P < 0.01 vs. controls). Glibenclamide, a KATP channel blocker administered 45 min (but not 20 min) before sustained ischemia, attenuated the effects of IPC and CPC (31 ± 4 and 41 ± 6%, respectively). Thus KATP channel activation appears to contribute to these two types of cardioprotection in rabbits.

Role of the β1-Adrenergic Pathway in Anesthetic and Ischemic Preconditioning against Myocardial Infarction in the Rabbit Heart In Vivo 

2006 ◽  
Vol 105 (3) ◽  
pp. 503-510 ◽  
Author(s):  
Markus Lange ◽  
Thorsten M. Smul ◽  
Christoph A. Blomeyer ◽  
Andreas Redel ◽  
Karl-Norbert Klotz ◽  
...  
Keyword(s):  
Signal Transduction ◽  
Coronary Artery ◽  
Infarct Size ◽  
Ischemic Preconditioning ◽  
Myocardial Infarct ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Myocardial Infarct Size ◽  
Area At Risk

Background Anesthetic and ischemic preconditioning share similar signal transduction pathways. The authors tested the hypothesis that the beta1-adrenergic signal transduction pathway mediates anesthetic and ischemic preconditioning in vivo. Methods Pentobarbital-anesthetized (30 mg/kg) rabbits (n = 96) were instrumented for measurement of systemic hemodynamics and subjected to 30 min of coronary artery occlusion and 3 h of reperfusion. Sixty minutes before occlusion, vehicle (control), 1.0 minimum alveolar concentration desflurane, or sevoflurane, and esmolol (30.0 mg x kg(-1) x h(-1)) were administered for 30 min, respectively. Administration of a single 5-min cycle of ischemic preconditioning was instituted 35 min before coronary artery occlusion. In separate groups, the selective blocker esmolol or the protein kinase A inhibitor H-89 (250 microg/kg) was given alone and in combination with desflurane, sevoflurane, and ischemic preconditioning. Results Baseline hemodynamics and area at risk were not significantly different between groups. Myocardial infarct size (triphenyltetrazolium staining) as a percentage of area at risk was 61 +/- 4% in control. Desflurane, sevoflurane, and ischemic preconditioning reduced infarct size to 34 +/- 2, 36 +/- 5, and 23 +/- 3%, respectively. Esmolol did not alter myocardial infarct size (65 +/- 5%) but abolished the protective effects of desflurane and sevoflurane (57 +/- 4 and 52 +/- 4%, respectively) and attenuated ischemic preconditioning (40 +/- 4%). H-89 did not alter infarct size (60 +/- 4%) but abolished preconditioning by desflurane (57 +/- 5%) and sevoflurane (61 +/- 1%). Ischemic preconditioning (24 +/- 7%) was not affected by H-89. Conclusions The results demonstrate that anesthetic preconditioning is mediated by the beta1-adrenergic pathway, whereas this pathway is not essential for ischemic preconditioning. These results indicate important differences in the mechanisms of anesthetic and ischemic preconditioning.

Diabetes and hyperglycemia impair activation of mitochondrial KATP channels

2001 ◽  
Vol 280 (4) ◽  
pp. H1744-H1750 ◽  
Author(s):  
Judy R. Kersten ◽  
Matthew W. Montgomery ◽  
Tannaz Ghassemi ◽  
Eric R. Gross ◽  
Wolfgang G. Toller ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Katp Channels ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
High Dose ◽  
Myocardial Infarct Size ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride

Hyperglycemia is an important predictor of cardiovascular mortality in patients with diabetes. We investigated the hypothesis that diabetes or acute hyperglycemia attenuates the reduction of myocardial infarct size produced by activation of mitochondrial ATP-regulated potassium (KATP) channels. Acutely instrumented barbiturate-anesthetized dogs were subjected to a 60-min period of coronary artery occlusion and 3 h of reperfusion. Myocardial infarct size (triphenyltetrazolium chloride staining) was 25 ± 1, 28 ± 3, and 25 ± 1% of the area at risk (AAR) for infarction in control, diabetic (3 wk after streptozotocin-alloxan), and hyperglycemic (15% intravenous dextrose) dogs, respectively. Diazoxide (2.5 mg/kg iv) significantly decreased infarct size (10 ± 1% of AAR, P < 0.05) but did not produce protection in the presence of diabetes (28 ± 5%) or moderate hyperglycemia (blood glucose 310 ± 10 mg/dl; 23 ± 2%). The dose of diazoxide and the degree of hyperglycemia were interactive. Profound (blood glucose 574 ± 23 mg/dl) but not moderate hyperglycemia blocked the effects of high-dose (5.0 mg/kg) diazoxide [26 ± 3, 15 ± 3 ( P < 0.05), and 11 ± 2% ( P < 0.05), respectively]. There were no differences in systemic hemodynamics, AAR, or coronary collateral blood flow (by radioactive microspheres) between groups. The results indicate that diabetes or hyperglycemia impairs activation of mitochondrial KATP channels.

Aspirin before reperfusion blunts the infarct size limiting effect of atorvastatin

2007 ◽  
Vol 292 (6) ◽  
pp. H2891-H2897 ◽  
Author(s):  
Yochai Birnbaum ◽  
Yu Lin ◽  
Yumei Ye ◽  
Juan D. Martinez ◽  
Ming-He Huang ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Clinical Setting ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Blue Dye ◽  
Sprague Dawley ◽  
Area At Risk ◽  
Triphenyltetrazolium Chloride ◽  
Coronary Syndromes

We assessed whether aspirin (acetylsalicylic acid, ASA), administered before reperfusion, abrogates the infarct size (IS)-limiting effect of atorvastatin (ATV). Statins reduce IS. This dose-dependent effect is mediated by upregulation of cycloxygenase-2 (COX2) and PGI2 production. Administration of selective COX2-inhibitors either with ATV for 3 days or immediately before coronary occlusion blocks the IS-limiting effect of ATV. Sprague-Dawley rats received 3-day ATV (10 mg·kg−1·day−1) or water alone. Rats underwent 30 min coronary artery occlusion and 4 h reperfusion (IS protocol, n = 8 in each group), or rats underwent 30 min coronary artery occlusion and 10 min reperfusion (enzyme expression and activity protocol, n = 4 in each group). Immediately before reperfusion rats received intravenous ASA (5, 10, or 20 mg/kg) or saline. Area-at-risk (AR) was assessed by blue dye and IS by triphenyltetrazolium chloride. ATV reduced IS (10.1 ± 1.4% of the AR) compared with controls (31.0 ± 2.2%). Intravenous ASA alone did not affect IS (29.0 ± 2.6%); however, ASA dose dependently (5, 10, and 20 mg/kg) attenuated the protective effect of ATV on IS (15.8 ± 0.9%, 22.0 ± 1.6%, and 23.7 ± 3.8%, respectively). ASA dose dependently blocked the upregulation of COX2 by ATV. COX2 activity was as follows: control, 8.93 ± 0.90 pg/mg; ATV, 75.85 ± 1.08 pg/mg; ATV + ASA5, 34.39 ± 1.48 pg/mg; ATV + ASA10, 19.87 ± 1.10 pg/mg; and ATV + ASA20, 9.36 ± 0.94 pg/mg. ASA, administered before reperfusion in doses comparable to those used in the clinical setting, abrogates the IS-limiting effect of ATV in a model with mechanical occlusion of the coronary artery. This potential adverse interaction should be further investigated in the clinical setting of acute coronary syndromes.

Innate protection of baboon myocardium: effects of coronary artery occlusion and reperfusion

1996 ◽  
Vol 270 (5) ◽  
pp. H1812-H1818 ◽  
Author(s):  
Y. T. Shen ◽  
J. T. Fallon ◽  
M. Iwase ◽  
S. F. Vatner
Keyword(s):  
Blood Flow ◽  
Coronary Artery ◽  
Infarct Size ◽  
Diastolic Pressure ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Area At Risk ◽  
Protective Mechanisms ◽  
Reperfusion Period

To determine whether the extent of myocardial infarction differs in conscious baboons and pigs, both devoid of performed collaterals, the effects of 40 and 90 min of coronary artery (CA) occlusion (O) both followed by 4-7 days of CA reperfusion (R) were examined in both species. CAO reduced subendocardial and subepicardial blood flows similarly, almost to zero, in baboons and pigs for the entire CAO period. At 24 h of CAR, subendocardial blood flow had almost returned to pre-CAO control levels in baboons but remained significantly depressed in pigs. The major difference in hemodynamics during CAO and CAR was in left ventricular end-diastolic pressure, which rose by 6 +/- 1 mmHg in pigs over the initial 24-h reperfusion period but did not change significantly in baboons. These data on recovery of subendocardial blood flow and left ventricular end-diastolic pressure suggest larger infarcts in pigs than in baboons. Indeed, infarct size expressed as a function of area at risk (IF/AAR) was significantly greater (P <0.05) in pigs (53 +/- 4.9%) than in baboons (17 +/- 2.9%) with 90 min of CAO and 4-7 days of CAR. With 40 min of CAO and 4-7 days of CAR, IF/AAR was 46 +/- 3.6% in pigs, whereas in baboons the IF/AAR was minimal, i.e., 2 +/- 0.6%. Thus pigs and baboons were characterized by minimal coronary collateral circulation, but infarct size was significantly less in conscious baboons than in conscious pigs. Potentially, these differences could be explained, in part, by natural protective mechanisms and/or less reperfusion injury in primates. These results in primates may also help explain the salutary effects of CAR in patients at intervals longer than have been demonstrated to be beneficial in other experimental animals.

Adenosine-Supplemented Blood Cardioplegia Attenuates Postischemic Dysfunction After Severe Regional Ischemia

Circulation ◽  
1999 ◽  
Vol 100 (suppl_2) ◽  
Author(s):  
Vinod H. Thourani ◽  
Russell S. Ronson ◽  
David G.L. Van Wylen ◽  
Steven T. Shearer ◽  
Sara L. Katzmark ◽  
...  
Keyword(s):  
At Risk ◽  
Coronary Artery ◽  
Infarct Size ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Area At Risk ◽  
Blood Cardioplegia ◽  
Regional Ischemia ◽  
Myocardial Area ◽  
Group 5

Background —Various studies have reported that the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but this timing may not utilize ADO’s potential against myocardial reperfusion injury. This study tested the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusion reduces postischemic dysfunction after severe regional ischemia. Methods and Results —After 75 minutes of left anterior descending coronary artery occlusion, total cardiopulmonary bypass was initiated; cold (4°C) antegrade BCP (8:1 blood:crystalloid) was delivered every 20 minutes for the first 3 doses, and 27°C BCP was delivered for the terminal infusion. Dogs (n=6 per group) received unsupplemented BCP, ADO (100 μmol/L/L) supplemented in all infusions of BCP (ADO-CP), or ADO (100 μmol · L −1 · L −1 ) supplemented only in the terminal infusion of BCP followed by intravenous ADO (140 μg · kg −1 · min −1 ) infusion for the first 30 minutes of reperfusion (ADO-R). Postischemic regional systolic shortening was significantly greater in the ADO-R group (5±2.0%) than in the BCP group (−3±1.0%), but not in the ADO-CP group (2±0.2%). Postischemic regional diastolic stiffness in the area at risk during end reperfusion was lower with ADO-R (1.8±0.3%) than with ADO-CP (2.7±0.3%) or BCP (4.4±0.5%). Infarct size was reduced in the ADO-CP (29±2%) and ADO-R (21±2%) groups compared with the BCP group (42±4%). Edema in the myocardial area at risk was decreased in the ADO-CP (82±0.2%) and ADO-R (80±0.4%) groups compared with the BCP group (86±0.7%). Adherence of fluorescently labeled neutrophils (PMNs) to postischemic coronary artery endothelium was attenuated by ADO-R (55±2 PMNs/mm 2 ), but not by ADO-CP (114±5 PMNs/mm 2 ), compared with BCP (118±3 PMNs/mm 2 ). Conclusions —The results show that BCP supplemented with ADO reduces infarct size, preserves postischemic systolic and diastolic regional function but does not attenuate coronary artery endothelial dysfunction unless administered during reperfusion.

Mechanical Unloading Properties of Axial Flow Pumps and their Effect on Myocardial Stunning

1995 ◽  
Vol 18 (12) ◽  
pp. 766-771 ◽  
Author(s):  
F. R. Waldenberger ◽  
B. Meyns ◽  
P. Wouters ◽  
E. De Ruyter ◽  
E. Pongo ◽  
...  
Keyword(s):  
Coronary Artery ◽  
Myocardial Stunning ◽  
Myocardial Dysfunction ◽  
Axial Flow ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Wall Thickening ◽  
Myocardial Wall Motion ◽  
Mechanical Unloading ◽  
Artery Disease

Postischemic myocardial dysfunction affects morbidity and mortality in patients with coronary artery disease. It is known that mechanical unloading of the left heart ventricle can positively influence postischemic myocardial dysfunction. In this respect we tested two miniaturised axial flow pumps, i.e. the 14-F and the 21-F Hemopump®. An experimental study was carried out on 30 open chest sheep where regional myocardial wall motion was followed using sonomicrometry in a preparation of transient coronary artery occlusion. Only the larger 21-F Hemopump® showed hemodynamically significant unloading of the left ventricle. Furthermore, as far as stunning is concerned, systolic wall thickening recovered better when this type of pump was used during reperfusion. Also postejection thickening, which is an indication of diastolic postischemic dysfunction, is reduced significantly in the postischemic area (ANOVA, p<0.05). Thus, the 21F Hemopump®, but not the 14F Hemopump®, provides adequate mechanical unloading in order to beneficially influence myocardial stunning.

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