RESUMO
Idiopathic sudden sensorineural hearing loss (ISSHL) is the newest indication approved by the Undersea and Hyperbaric Medical Society's Hyperbaric Oxygen Therapy Committee. Idiopathic sudden sensorineural hearing loss appears to be characterized by hypoxia in the perilymph and therefore the scala tympani and the organ of Corti. A review of the literature reveals more than 100 publications evaluating the use of hyperbaric oxygen (HBO2) for the treatment of ISSHL, including eight randomized controlled trials. The best and most consistent results are obtained when HBO2 is initiated within two weeks of symptom onset and combined with corticosteroid treatment. The average hearing gain is 19.3 dB for moderate hearing loss and 37.7 dB for severe cases. This improvement brings hearing deficits from the moderate/severe range into the slight/no impairment range. This is a significant gain that can markedly improve a patient's quality of life, both clinically and functionally.
Assuntos
Perda Auditiva Neurossensorial/terapia , Perda Auditiva Súbita/terapia , Oxigenoterapia Hiperbárica/métodos , Corticosteroides/uso terapêutico , Animais , Terapia Combinada/métodos , Perda Auditiva Neurossensorial/etiologia , Perda Auditiva Súbita/etiologia , Humanos , Guias de Prática Clínica como Assunto , Estudos Prospectivos , Ensaios Clínicos Controlados Aleatórios como Assunto , Estudos RetrospectivosRESUMO
A novel peptide found in human blood, adrenomedullin (ADM), has been shown to have systemic vasodepressor activity in the rat. However, the direct effects of ADM on cardiac function are unknown. Results of the present study demonstrate that ADM13-52 possesses marked systemic vasodepressor activity in the anesthetized rat. Although ADM13-52 modestly decreased peak systolic pressure (PSP) indicating mild negative inotropic activity, the present data suggest that bolus administration of ADM decreases systemic arterial pressure by dilating the systemic vasculature. The present data also suggest that only a portion of the ADM molecule is necessary to produce systemic vasodilation.
Assuntos
Anti-Hipertensivos/farmacologia , Coração/efeitos dos fármacos , Peptídeos/farmacologia , Adrenomedulina , Anestesia , Animais , Pressão Sanguínea/efeitos dos fármacos , Feminino , Coração/fisiologia , Técnicas In Vitro , Masculino , Perfusão , RatosRESUMO
Testosterone analogs have been used as performance enhancers by athletes for more than 40 yr. We asked whether the anabolic steroid 17 alpha-methyl-4-androstene-17-ol-3-one (17 alpha-MT) would affect intrinsic contractile function of the heart. Male Sprague-Dawley rats, 125-150 g, were treated with 17 alpha-MT either parenterally or orally for up to 8 wk. Intrinsic contractile function of the hearts was assessed utilizing both the isolated working heart and isovolumic perfused heart preparations. Isolated working hearts from 17 alpha-MT-treated rats had a 45% decrease in heart work attributable largely to a similarly decreased stroke volume. Isovolumic perfused hearts from treated animals had elevated left ventricular systolic and diastolic pressures at similar interventricular volumes compared to controls. Rates of ventricular pressure development (+dP/dT) or relaxation (-dP/dT) were unchanged as a result of the treatment. However, static elastance was reduced in potassium-arrested hearts from the 17 alpha-MT treatment (63% increase in interventricular pressure), consistent with a limitation being imposed on stroke volume by a decreased myocardial compliance. Hydroxyproline content of the hearts was not altered by 17 alpha-MT treatment suggesting that increased stiffness was not a consequence of collagen proliferation. Treatment of the steroid rats with beta-aminopropionitrile, a compound that inhibits lysyl oxidase, restored the left ventricular volume-pressure relationship (elastance curve) to that of control hearts. Thus, chronic treatment with anabolic steroids appears to reduce left ventricular compliance, possibly related to an enhanced activity of lysyl oxidase, and results in increased crosslink formation between collagen strands in the extracellular matrix.