RESUMO
A 55-year-old man presented with dyspnea, edema, and appetite loss. He had undergone coronary artery bypass grafting 8 years previously. He had jugular venous distention and Kussmaul's sign. Contrast-enhanced cardiac magnetic resonance imaging (CMRI) demonstrated an intrapericardial mass compressing the right ventricular (RV) cavity. T1- and T2-weighted black-blood images showed a mass with heterogeneous high signal intensity and a thick and dark rim. The mass was considered to be a chronic hematoma. After pericardiotomy with surgical removal of the hematoma, CMRI showed the marked improvement of the RV function. Late intrapericardial hematoma is rare and CMRI is useful for making a differential diagnosis.
Assuntos
Ponte de Artéria Coronária/efeitos adversos , Ventrículos do Coração/diagnóstico por imagem , Hematoma/diagnóstico por imagem , Hematoma/cirurgia , Ventrículos do Coração/patologia , Humanos , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Resultado do TratamentoRESUMO
Motilin is considered as a key factor in controlling interdigestive migrating contractions. The present electrophysiological experiments were performed in vitro to examine actions of motilin on myenteric neurons of guinea-pigs after 18-h fasting period. Superfusion of motilin depolarized both S and AH neurons; the lowest effective concentration was 10 nM, and motilin depolarization was observed in 9 of 23 S neurons and in 5 of 25 AH neurons. The motilin depolarizations were associated with an increase in neuronal input resistance. The motilin responses were preserved in Ca2+ free/high Mg2+ solution in which no Ca2+ dependent synaptic transmission occurred. The reversal potential of the motilin responses was estimated about -95 mV, close to the equilibrium potential for K+. Furthermore, muscarinic depolarizations were blocked during the motilin responses. All of these indicated that motilin directly excited myenteric neurons mainly by inactivating K+ channels. It is concluded that motilin might modulate neuronal excitability of the myenteric plexus, leading to the control of interdigestive migrating contractions.