RESUMEN
We tested the precision and accuracy of the AccuLevel Phenobarbital Test, which reports whole-blood (fingerstick) results in plasma equivalent values, and compared these values with plasma results obtained using established methods. We conclude that the assay is precise, reliable, accurate for single tests, and is appropriate for use in offices, outpatient settings, and emergency rooms.
Asunto(s)
Cromatografía , Técnicas Inmunológicas , Fenobarbital/sangre , Epilepsia/sangre , Epilepsia/tratamiento farmacológico , Humanos , Fenobarbital/uso terapéuticoRESUMEN
Whether steroids lead to thinner scars and larger aneurysms by delaying collagen deposition or worsening infarct expansion before significant collagen deposition begins is unknown. Rats underwent either transmural infarction by left coronary ligation or sham operation. Both infarct and sham rats were randomized to methylprednisolone 50 mg/kg i.p. X 4 or saline treatment within 24 h after operation. Sacrifice occurred before (3 d) or after (7 d) collagen deposition typically begins. Despite similar infarct size, infarct wall thickness was 1.35 +/- 0.08 mm in the saline and 0.99 +/- 0.12 mm in the methylprednisolone group (P less than 0.001) at 3 d. This decrease in wall thickness was explained by a decrease in the number of myocytes across the infarct wall (r = 0.99; P less than 0.001), suggesting that steroids promote myocyte slippage. Furthermore, methylprednisolone caused no further infarct thinning or cavity dilatation beyond 3 d. Thus, high-dose methylprednisolone given within 24 h after transmural infarction worsens infarct expansion before collagen is laid down by promoting the slippage of necrotic myocytes.
Asunto(s)
Metilprednisolona/uso terapéutico , Infarto del Miocardio/tratamiento farmacológico , Animales , Colágeno/metabolismo , Vasos Coronarios , Femenino , Ligadura , Ratas , Ratas Endogámicas , Factores de TiempoRESUMEN
The Syrian cardiomyopathic hamster has a hereditary disease in which a progressive myocardial necrosis mimics human forms of cardiac hypertrophy. Lesions are associated with calcium overload and can be prevented with the calcium antagonist verapamil. Numbers of receptor binding sites for calcium antagonists in heart, brain, skeletal muscle, and smooth muscle were markedly increased in cardiomyopathic hamsters. The uptake of calcium-45 into brain synaptosomes was also increased in cardiomyopathic hamsters. The increase in calcium antagonist receptors and related voltage-sensitive calcium channels may be involved in the pathogenesis of this cardiomyopathy.