Ovid Technologies (Wolters Kluwer Health)
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* Dữ liệu chỉ mang tính chất tham khảo
We studied the effects of afterload reduction in chronic severe aortic insufficiency by measuring the hemodynamic response to oral hydralazine in 10 consecutive patients. Hemodynamics were also measured during maximal exercise in eight of these patients. At rest, hydralazine reduced pulmonary artery wedge pressure from 14 to 9 mm Hg (p less than 0.01), and increased cardiac index by 70% and stroke volume index by 35% (both p less than 0.001). Before hydralazine, pulmonary artery wedge pressure exceeded 20 mm Hg in five patients during maximal exercise; with hydralazine, at identical levels of exercise, pulmonary artery wedge pressure remained below 20 mm Hg in all patients. For the group, hydralazine reduced pulmonary artery wedge pressure from 21 to 12 mm Hg (p less than 0.05) and increased cardiac index by 31% (p less than 0.05) during exercise; changes in stroke volume index were more variable and there was no significant increase for the group, although several patients increased stroke volume substantially and the overall increase was 34%. These data show that afterload reduction has beneficial effects on cardiac performance in chronic severe aortic insufficiency both at rest and during exercise. Hydralazine may be of use in such patients either in preparation for valve replacement or as interim therapy.
It has been shown that the development of coxsackievirus B3 (CB3) myocarditis is regulated by T cells and not by B cells. Interleukin-2 (IL-2) is a T-cell-derived cytokine that stimulates the growth of T cells. This study was carried out to determine the effects of IL-2 on CB3-infected BALB/c mice.
In two separate experiments, recombinant human IL-2 (5 x 10(4) U) was administered subcutaneously to 30 mice early (days 0 to 7) and 30 mice late (days 7 to 14) after infection with CB3. Each experiment had a control group of infected animals that did not receive IL-2. On days 7 and 10, splenic natural killer (NK) cell activity determined by 51Cr release assay and the distribution of myocardial lymphocyte subsets were compared in the treated and untreated groups. In the early treatment experiment, survival at 7 days was higher in treated compared with control animals, myocardial virus titers were lower, inflammatory cell infiltration was less (as was the severity of necrosis at the time the mice were killed), and NK cell activity was higher. However, in the late treatment experiment, survival at 14 days was lower in treated compared with control animals, and there was more infiltration, more severe necrosis, and more T-cell infiltration, but the NK cell activity did not differ significantly. In a third experiment similar to the late experiment described above but involving infected athymic nude mice, we confirmed the lack of effect of late in vivo administration of IL-2 on outcome.
IL-2 has the capacity to limit CB3 myocarditis by enhancing NK cell activity in the acute viremic stage, resulting in a reduction of cardiac pathology. However, in the subacute aviremic stage, in contrast, IL-2 exacerbates the course and severity of the disease by increasing the number of T cells infiltrating the myocardium. That is, IL-2 has differential effects on acute CB3 myocarditis. IL-2 is beneficial if treatment is given early but later in murine CB3 myocarditis.
In this presentation stress has been laid upon the concept that the treatment, as well as the prognosis of chronic cor pulmonale depend upon the underlying pulmonary disease. It has long been known that the chief causes of chronic cor pulmonale are chronic obstructive pulmonary emphysema and various forms of fibrosis, particularly the pneumoconioses. An understanding of the difference between these diseases, both as to their pulmonary dysfunction and their circulatory complications, is crucial to success in therapy. Management of the patient with chronic pulmonary emphysema and (or pulmoniale is quite different from that of the subject with fibrosis and right heart involxemenit.
Unfortuniately, little as yet is known about the circulation in the pulmonary fibroses. In patients with pulmonary fibrosis as well as those with granulomas of the lung it would appear that the anatomic pulmonary lesion is chiefly responsible for the pulmonary hypertension, in contradistinction to the patients with emphysema. Inasmuch as the anatomic lesions are for the most part irreversible, so is the pulmonary hypertension. This has limited our therapeutic approach in this form of chronic cor pulmonale to rigorous restriction of physical activity directed at minimizing exacerbations of pulmonary hypertension.
While emphasis has been placed upon the difference in management of the patient with emphysema or fibrosis and cor pulmonale, nonetheless it should be remembered that in any individual patient these two conditions may coexist. In that event, intensive therapy directed at the sequellae of emphysema may be very rewarding.
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