Cell adhesion molecule mediation of myocardial inflammatory responses associated with ventricular pacing
| Autor: | Sang-Hyun Ihm, Robert L Thomas, Katrina Go Yamazaki, David M. Roth, Francisco Villarreal |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
medicine.medical_specialty
Pathology Physiology Vascular Biology and Microcirculation Inflammation In Vitro Techniques Ventricular Function Left Electrocardiography Mice Physiology (medical) Internal medicine Animals Medicine Cardiac structure Peroxidase Mice Knockout business.industry Cell adhesion molecule Cardiac Pacing Artificial Ventricular pacing Intercellular Adhesion Molecule-1 Glutathione Immunohistochemistry Electrodes Implanted Mice Inbred C57BL Myocarditis P-Selectin Data Interpretation Statistical Cardiology medicine.symptom Cardiology and Cardiovascular Medicine business Cell Adhesion Molecules |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 302:H1387-H1393 |
| ISSN: | 1522-1539 0363-6135 |
| Popis: | Poorly synchronized activation of the ventricles can lead to impairment of normal cardiac structure/function. We reported previously that short term (4 h) left ventricular (LV) pacing-induced ventricular dyskinesis led to an inflammatory response localized to the epicardium. Results from this study demonstrated that neutrophils may play a major role in this inflammatory process. Neutrophil recruitment to a site of injury is a process that is highly dependent on an upregulation of cell adhesion molecules (CAM). The dependence of ventricular dysynchrony-induced inflammatory responses on CAM upregulation has not been explored. To gain further insight, we used a mouse model of LV pacing to evaluate the role of CAM in mediating the inflammatory response associated with ventricular dyskinesis. We first examined the effects of LV pacing in wild-type mice. Results demonstrate that 40 min of LV pacing increases ICAM-1 immunostaining as well as myeloperoxidase activity and tissue oxidative stress by twofold in early-activated myocardium. Matrix metalloproteinase-9 activity also increased in the same region by ∼3.5-fold. To determine the role of CAM, mice null for ICAM-1 or p-selectin were subjected to 40 min LV pacing. Results demonstrate that the inflammatory response seen in the wild-type mice was significantly mitigated in the ICAM-1 and p-selectin null mice. In conclusion, results demonstrate that CAM expression plays a critical role in the triggering of LV pacing-induced inflammation, thus providing evidence of a vascular mechanism underlying this response. The mechanisms that trigger an upregulation of myocardial CAM expression and, therefore, inflammation await further investigation since they suggest a specific involvement of vascular events. |
| Databáze: | OpenAIRE |
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