RESUMEN
A 24-year-old female patient from Sierra Leone was referred to the authors' hospital after several unclear intracerebral bleeding events and an echogenic structure on the aortic valve. The patient was receiving oral anticoagulation therapy due to paroxysmal atrial fibrillation and left ventricular noncompaction. Fluorescence in situ hybridization in combination with polymerase chain reaction and sequencing revealed infective endocarditis of the mitral and aortic valve caused by Bartonella quintana. In retrospect, the intracerebral bleeding events could be identified as septic emboli with secondary haemorrhagic transformation under anticoagulation therapy. The patient showed significant clinical improvement and no further bleeding events occurred after receiving biological mitral and aortic valve replacement and several weeks of doxycycline and gentamicin antibiotic therapy.
Asunto(s)
Bartonella quintana , Endocarditis Bacteriana , Fiebre de las Trincheras , Adulto , Válvula Aórtica , Bartonella quintana/genética , Hemorragia Cerebral/diagnóstico , Hemorragia Cerebral/diagnóstico por imagen , Femenino , Humanos , Hibridación Fluorescente in Situ , Recurrencia Local de Neoplasia , Adulto JovenAsunto(s)
Electrodos Implantados/efectos adversos , Migración de Cuerpo Extraño/cirugía , Mucosa Gástrica/lesiones , Gastroscopía , Melena/etiología , Marcapaso Artificial , Anciano , Procedimientos Quirúrgicos Cardíacos , Remoción de Dispositivos/métodos , Humanos , Enfermedad Iatrogénica , Masculino , Factores de TiempoRESUMEN
The aim of this study was to outline the consequences of a hypertonic saline-dextran-40 (HSD) infusion-induced peripheral flow stimulus on the ventricular function in closed-chest, pentobarbital-anesthetized dogs. We hypothesized that HSD-induced elevation in endothelin-1 (ET-1) and nitric oxide (NO) release can have a role in myocardial contractile responses; and that cardiac mast cells (MC) degranulation may be involved in this process. The consequences of disodium cromoglycate (a MC stabilizer) or ETR-p1/fl peptide (an endothelin-A receptor antagonist) treatment were evaluated. A 4 ml/kg iv HSD40 infusion significantly increased cardiac index and myocardial contractility, and resulted in a decreased peripheral resistance. The postinfusion period was characterized by significant plasma NO and ET-1 elevations, these hemodynamic and biochemical changes being accompanied by a decreased myocardial ET-1 content, NO synthase activity and enhanced myocardial MC degranulation. Disodium cromoglycate treatment inhibited the HSD40-induced elevations in myocardial contractility and MC degranulation, and similar hemodynamic changes were noted after treatment with ETR-p1/fl peptide, together with a normalized myocardial myocardial ET-1 content, NO synthesis and a significant reduction in MC degranulation. These results indicate that peripheral NO and ET-1 release modulates the cardiac contractility through myocardial ET-A receptor activation and MC degranulation.