A H Foster — Page 2 | Search PubMed

PubMed1980

Myotoxicity of local anesthetics and regeneration of the damaged muscle fibers.

In view of the documented myotoxic effects of the local anesthetic, bupivacaine, a survey of myotoxic effects of seven local anesthetics was conducted. In 70 rats, 200 microliters of an anesthetic solution was injected into one tibialis anterior muscle and a control solution was injected into the contralateral muscle. The anesthetics fell into two groups in their effects upon muscle. One group, including 1% procaine, 0.2% tetracaine, 0.5% lidocaine, and 0.75% bupivacaine, produced effects that were confined principally to the muscle fiber. The other group (2% chloroprocaine, 0.25% dibucaine, 0.5% lidocaine with 1:200,000 epinephrine and 2% piperocaine) produced toxic effects on other tissue components of the muscles in addition to affecting muscle fibers. With all anesthetics, the initial damage to and breakdown on muscle fibers was restored by regeneration and 30-day muscles showed relatively few long-term effects of the damage.

Anesthetics, Local↗

PubMedDate not supplied

Heat shock protects cardiomyocytes from hypoxia-mediated apoptosis by attenuation of nitric oxide.

BACKGROUND: Considerable data exists on the beneficial effect of Heat Shock (HS) on myocardial necrosis. However, the effect of HS on apoptosis or programmed cell death, the other mode of cell death in the heart, is unknown. Hypoxia leads to apoptosis and increased nitric oxide (NO) production in myocardium. NO has also been shown to cause apoptosis. We sought to investigate if HS could protect cardiomyocytes (CM) from hypoxia-induced apoptosis and if this protection was NO-mediated. MATERIALS AND METHODS: CM were isolated from 1-2 day old rats and incubated at 37 degrees C or exposed to HS at 42 degrees C for 90 minutes before overnight incubation. CM were then subjected to hypoxic incubation in an argon/CO2 chamber (O2 concentration between 0.8-1.3 parts per million) for 90 minutes, followed by reoxygenation for 24 hours. Apoptosis was measured at 48 hours by TUNEL assay for in-situ DNA fragmentation and by immunohistochemical detection of c-myc protein, a proto-oncogene upregulated with apoptosis (grade 0 = no stain; +++ = most dense stain). NO was detected using the Griess reaction (nM +/- SEM). N > 5 for each group, performed in triplicate. RESULTS: CM viability demonstrated by spontaneously beating cells in culture and trypan blue staining was > 85%. (*, # = p < 0.01, ANOVA).

Animals↗