Modulation of Na+/H+exchange isoform 1 mRNA expression in isolated rat hearts

1999 ◽  
Vol 277 (3) ◽  
pp. H993-H998 ◽  
Author(s):  
Xiaohong Tracey Gan ◽  
Subrata Chakrabarti ◽  
Morris Karmazyn
Keyword(s):  
Internal Standard ◽  
Ischemia And Reperfusion ◽  
Rt Pcr ◽  
Ischemia And Reperfusion Injury ◽  
Myocardial Ischemia And Reperfusion ◽  
Disease States ◽  
Pcr Product ◽  
Subsequent Response ◽  
Rat Hearts ◽  
Isolated Rat

Na+/H+exchange (NHE) has been demonstrated to mediate myocardial ischemia and reperfusion injury as well as injury produced by hydrogen peroxide (H2O2) or lysophosphatidylcholine (LPC). However, changes in gene expression in response to injurious factors have not been extensively studied. We examined Na+/H+exchange isoform 1 (NHE-1) expression using Southern detection of the RT-PCR product in response to 30 min of global ischemia with or without reperfusion in isolated rat hearts or to 30 min of exposure to either H2O2(100 μM) or LPC (5 μM). We also determined whether ischemic preconditioning (2× 5-min ischemia) alters basal NHE-1 expression or the subsequent response to insult. Ischemia with or without reperfusion increased NHE-1 expression approximately sevenfold ( P < 0.05), whereas either H2O2 or LPC increased expression approximately twofold. Preconditioning reduced NHE-1 message by ∼70% ( P < 0.05) and significantly attenuated the effects of ischemia, H2O2, or LPC. The internal standard, β-globin was unaffected by any treatment. Our results indicate that NHE-1 expression is rapidly increased in response to ischemia with or without reperfusion as well as in response to H2O2or LPC. In contrast, preconditioning was associated with downregulation of NHE-1. These results may be important in furthering our understanding of NHE-1 in cardiac disease states and suggest that the antiporter adapts rapidly to cardiac conditions associated with pathology.

Independent dual perfusion of left and right coronary arteries in isolated rat hearts

1991 ◽  
Vol 261 (6) ◽  
pp. H2082-H2090 ◽  
Author(s):  
M. Avkiran ◽  
M. J. Curtis
Keyword(s):  
High Energy ◽  
Low Flow ◽  
Blue Dye ◽  
Ischemia And Reperfusion ◽  
Langendorff Preparation ◽  
Rat Hearts ◽  
Left And Right ◽  
Conventional Models ◽  
Aortic Cannula ◽  
Isolated Rat

A novel dual lumen aortic cannula was designed and constructed to permit independent perfusion of left and right coronary beds in isolated rat hearts without necessitating the cannulation of individual arteries. Stability of the dual-perfusion preparation was shown to be similar to that of the conventional Langendorff preparation, in terms of coronary flow, heart rate, and high-energy phosphate content. The independence of left and right perfusion beds was confirmed by unilateral infusion of disulfine blue dye and spectrophotometric detection of the dye in ventricular homogenates. Transient cessation of flow to the left coronary bed resulted in severe ventricular arrhythmias upon reperfusion, as in conventional models of regional ischemia and reperfusion. The dual-perfusion model is technically undemanding, reproducible, inexpensive, and can be used in several species. It enables studies with 1) regional low flow ischemia, 2) regional zero-flow ischemia without coronary ligation (with attendant damage to vasculature), 3) selective application of drugs or interventions to the ischemic-reperfused zone, and 4) selective application of components of ischemia and reperfusion to a site anatomically relevant to ischemic heart disease.

Abstract 1712: The P2Y 12 Antagonist Cangrelor and the GP IIb/IIIa Blocker Abciximab Reduce Platelet-Mediated Myocardial Injury After Ischemia and Reperfusion

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jose A Barrabes ◽  
Javier Inserte ◽  
Maribel Mirabet ◽  
Adoracion Quiroga ◽  
Victor Hernando ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Myocardial Damage ◽  
Left Ventricular ◽  
Myocardial Salvage ◽  
Ischemia And Reperfusion ◽  
Activated Platelets ◽  
Rat Hearts ◽  
Developed Pressure ◽  
Enddiastolic Pressure ◽  
Isolated Rat

Objective: Platelets activated during experimental acute myocardial infarction (AMI) contribute to myocardial injury. We aimed to investigate whether platelets from patients with AMI increase myocardial damage after transient ischemia in isolated rat hearts and the modification of this effect by the P2Y 12 receptor antagonist cangrelor and the GPIIb/IIIa receptor blocker abciximab. Methods: Platelets were obtained from 9 AMI patients (7 thrombolyzed, all on aspirin) within 24 h after symptom onset. Incubation with 100 μM cangrelor or 50 μg/ml abciximab resulted, respectively, in 78 ± 4 and 90 ± 2% inhibition of aggregation (optical aggregometry). Isolated rat hearts (four simultaneous experiments per patient) were subjected to 40 min of global ischemia and 60 min of reperfusion. Hearts received no additional intervention (Control) or were infused during the 5 min prior to ischemia with platelets (22.5x10 6 /min), either untreated or treated with cangrelor or abciximab. Results: P-selectin expression (flow cytometry) in isolated platelets before infusion was 31 ± 3% (P = NS between groups). Platelets augmented myocardial injury, as demonstrated by worse left ventricular developed pressure (LVDevP), higher left ventricular enddiastolic pressure (LVEDP) and coronary resistance, and greater LDH release and infarct size (TTC staining), and both cangrelor and abciximab greatly attenuated these effects (Table ). Conclusions: Activated platelets from patients with AMI increase myocardial injury after ischemia and reperfusion, and cangrelor and abciximab attenuate this effect. The results support the notion that very early antiplatelet treatment may increase myocardial salvage by direct effects on the microcirculation in these patients.

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