With the use of epicardial mapping, we investigated the electrical alternans of the ST segment during acute myocardial ischemia and studied the difference in ST alternans between dogs with resultant ventricular fibrillation and those without it. During the 7-minute occlusion of the left anterior descending coronary artery below its first diagonal branch, 60
To examine the clinical significance of ST-T isopotential maps, 87-lead body surface mapping was performed after treadmill exercise in 21 patients with efort angina pectoris, single-vessel disease, and normal ST-T waves on the resting electrocardiogram. Single-vessel disease was found in the left anterior descending artery (LAD) (nine patients), in the right coronary artery (RCA) (seven patients), and in the left circumflex artery (LCx) (five patients). At 40 msec after the J point, the isopotential maps showed the site of the minimum to be in the left anterior chest in all patients. According to the changes in the position of the minimum from the ST segment to the T wave, postexercise maps were classified into four types. Type A maps (n=8) were characterized by the persistence of the minimum in the left anterior chest until its negativity decreased and until it became less negative than another minimum that subsequently appeared in a different position. Type B maps (n =6) were characterized by the gradual movement of the minimum toward the lower thoracic surface. Type C maps (n=5)
To investigate the effect of cigarette smoke on the development of bleomycin (BLM)-induced pulmonary fibrosis in hamsters, four experimental groups were studied: a control group (C), a cigarette smoke-inhaled group (T), a BLM-administered group (B), and a cigarette smoke-inhaled plus BLM-administered group (TB). Groups T and TB were exposed to sidestream smoke of cigarettes for 30 min/day, 5 days/wk. Groups B and TB were administered 0.5 mg BLM hydrochloride per 100 g body weight endotracheally once on day 30 (Day 0) after housing start. Quantitative morphometry of the lungs revealed that Group TB showed less lung fibrotic change compared with Group B, but based on qualitative observation, the fibrotic lesions of Group TB were intermingled with slight emphysematous changes. Neutrophils in bronchoalveolar lavage fluid were remarkably increased in both the groups, with a peak on Day 1, but the increase in Group TB lasted longer. Alveolar macrophages were increased in both smoking groups (T and TB) compared to the non-smoking groups (C and B). These results suggest that cigarette smoke reduces BLM-induced lung fibrotic changes; however, it simultaneously causes derangement of alveolar architecture. The persistence of increased neutrophils in the early phase after BLM accompanied by exposure to cigarette smoke may play an important role in the mechanism by which smoke ameliorates the effect of BLM.
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