AIM: Transmyocardial laser revascularization (TMR) and percutaneous transluminal myocardial laser revascularization (PTMR) have anti-anginal effects on certain groups of patients with ischemic heart disease, possibly by inducing myocardial neoangiogenesis through the mechanical injury. Here we examine the effects of TMR and PTMR on extracellular signal regulatory kinases (ERKs), which have been implicated in the control of neoangiogenesis in vitro. METHODS: Eight pigs were anesthetized with ketamine and fentanyl. In five pigs TMR was performed in the left ventricular anterior wall and PTMR in the posterior wall. Biopsies were taken either after 2 hours, 3, 7, 14, and 30 days. Three pigs served as controls and provided samples for baseline values and time-matched controls at 2 hours and 3 days. ERKs activity was determined by increased phosphorylation of myelin basic protein. Total ERKs protein abundance was determined by Western blot with an antibody against ERK1 and ERK2. RESULTS: It was found that ERKs activity was higher in all samples from the laser treated myocardium than in the control sample at baseline (TMR: >or=1878 pmol Pi x min(-1) mg pr(-1) vs 104 pmol Pi x min(-1) mg pr(-1), respectively, p<0.05. PTMR: >or=346 pmol Pi x min(-1) mg pr(-1) vs 136 pmol Pi min(-1) mg pr(-1), respectively, p<0.05). The time-matched samples showed increased activities of ERKs after laser treatment. The protein level of ERKs in myocardium treated with TMR and PTMR parallelled the data on ERKs activity. CONCLUSIONS: Our data suggest that the ERKs system is activated in the porcine heart by the mechanical injury of TMR and PTMR.
AIM: Transmyocardial laser revascularization (TMR) and percutaneous transluminal myocardial laser revascularization (PTMR) have anti-anginal effects on certain groups of patients with ischemic heart disease, possibly by inducing myocardial neoangiogenesis through the mechanical injury. Here we examine the effects of TMR and PTMR on extracellular signal regulatory kinases (ERKs), which have been implicated in the control of neoangiogenesis in vitro. METHODS: Eight pigs were anesthetized with ketamine and fentanyl. In five pigs TMR was performed in the left ventricular anterior wall and PTMR in the posterior wall. Biopsies were taken either after 2 hours, 3, 7, 14, and 30 days. Three pigs served as controls and provided samples for baseline values and time-matched controls at 2 hours and 3 days. ERKs activity was determined by increased phosphorylation of myelin basic protein. Total ERKs protein abundance was determined by Western blot with an antibody against ERK1 and ERK2. RESULTS: It was found that ERKs activity was higher in all samples from the laser treated myocardium than in the control sample at baseline (TMR: >or=1878 pmol Pi x min(-1) mg pr(-1) vs 104 pmol Pi x min(-1) mg pr(-1), respectively, p<0.05. PTMR: >or=346 pmol Pi x min(-1) mg pr(-1) vs 136 pmol Pi min(-1) mg pr(-1), respectively, p<0.05). The time-matched samples showed increased activities of ERKs after laser treatment. The protein level of ERKs in myocardium treated with TMR and PTMR parallelled the data on ERKs activity. CONCLUSIONS: Our data suggest that the ERKs system is activated in the porcine heart by the mechanical injury of TMR and PTMR.