ABSTRACT
BACKGROUND: Idiopathic dilatation of the pulmonary artery (IDPA) is a rare condition in which the pulmonary artery dilates without an obvious cause. Pulmonary artery replacement is indicated in severe cases to prevent serious complications. CASE PRESENTATION: A 59-year-old man was diagnosed with an IDPA of 64 mm and Kommerell's diverticulum (aortic aneurysm located at the aberrant left subclavian artery). A computed tomography scan revealed slight compression of the aneurysm to the trachea, although not interfering with airway management. The surgical approach was a median sternotomy, and cardiopulmonary bypass was established through aortic and bicaval cannulations. The perioperative course was uneventful. CONCLUSIONS: To prevent injury to the dilated pulmonary artery, a strategy for cardiopulmonary bypass and a surgical approach should be discussed beforehand. As dilatation of the pulmonary artery is often complicated by anatomic abnormalities, preoperative evaluation should be aimed at appropriate assessments using imaging modalities.
ABSTRACT
BACKGROUND: The application of pulsed radiofrequency (PRF) current to peripheral nerves with conditions related to neuropathic pain is considered to be clinically safe, while it has been reported that the destruction of mitochondria after PRF application was observed by electron microscopy. If it occurs reproducibly, PRF applied to peripheral nerves should provoke neurolysis because the impairment of mitochondria is known as the primary cause of apoptosis. METHODS: Human monocytic cells THP-1 loaded with 100 nM tetramethylrhodamine methyl ester (TMRM), a fluorescent dye that proves the mitochondrial membrane potential (MMP), were exposed to the electric field of continuous radiofrequency (CRF) or PRF current. The TMRM-related fluorescence from THP-1 cells was measured by flow cytometry. RESULTS: The exposure of THP-1 cells to a PRF electric field generated by NeuroTherm NT500 for 15 min with maximum power did not decrease MMP in these cells, nor did it cause the induction of apoptosis. By contrast, the application of CRF current at 70 °C for 3 min significantly decreased MMP and induced apoptosis within 10 min after CRF application. CONCLUSION: We conclude from these findings that PRF application does not provoke mitochondrial injury in various types of mammalian cells because the size and the subcellular structure of the plasma membrane or mitochondria are similar among those. However, the present results cannot address the effect of PRF current on organic structure around the nervous system. Further study is required to solve the question of whether PRF current causes neurolysis or not.
ABSTRACT
BACKGROUND: The enhanced expression of endogenous opioid peptides, including ß-endorphin, has been implicated in the mechanism of action of pulsed radio frequency (PRF) application in pain modulation. Because thermal effects cannot be separated from the physical property of PRF application to biological tissues, we evaluated whether temperatures higher than that of the normal body temperature (37°C) modulate mRNA expression for the precursor of ß-endorphin, proopiomelanocortin (POMC) in human monocytic cells THP-1. We also attempted to examine whether mechanisms other than thermal effects also modulate such gene expression. METHODS AND RESULTS: The mRNA for POMC in THP-1 cells increased by a 15-minutes incubation at 42°C, 45°C, or 70°C without PRF application as compared with that in cells incubated at 37°C. On the other hand, gene expression for POMC in cells incubated at 20°C as well as at 37°C with PRF application for 15 minutes increased as compared to that in cells incubated at 37°C without PRF application. Continuous radio frequency at 70°C but not PRF provoked apoptotic cell death at 1-2 hour, and necrotic cell death at 24 hours after the RF application. CONCLUSION: A simple experimental system using human monocytic cells in culture demonstrated that a 15 minute elevation of temperature above 37°C enhanced gene expression for POMC in THP-1 cells, while a 15 minute application of PRF to these cells incubated at 37°C or lower, also enhanced gene expression, indicating that temperature-independent mechanisms as well as thermal effects may be involved in such gene expression.
ABSTRACT
It is known that a variety of sized procoagulant vesicles that express tissue factor are released from several types of cells including monocytes by mechanisms related to the induction of apoptosis, while it has not yet been evaluated whether superoxide is involved in the production of such vesicles. Here, we report that a local anesthetic bupivacaine induces apoptosis in human monocytic cells THP-1 within a short observation period, where the shedding of procoagulant vesicles is associated. The property as procoagulant vesicles was evaluated using flow cytometry by the binding of FITC-conjugated fibrinogen to vesicles in the presence of fresh frozen plasma and the suppression of this binding by heparin. Bupivacaine (1 mg/ml) increased the apoptotic cells and procoagulant vesicles. LY294002 (100 µM), that inhibits the recruiting of intracellular component of NADPH oxidase to construct the activated form of this enzyme complex, or superoxide dismutase (1500 unit/ml) suppressed bupivacaine-provoked induction of apoptosis and the increase of procoagulant vesicles. We suggest that this simple experimental system is useful to explore the molecular mechanisms of action of superoxide in the shedding of procoagulant vesicles from human monocytic cells.
