RESUMEN
Context: Pulmonary hypertension (PH) is a serious and sometimes life-threatening event that occurs as a complication of various cardiopulmonary disorders, of which rheumatic heart disease (RHD) is an important example in our country. The pathogenesis of PH is a complex, multistep process in which "pulmonary endothelial dysfunction" (PED) is widely regarded as the central pathogenetic event. PED is, in turn, influenced by several local and systemic factors, of which nitric oxide synthase 3 (NOS3) and endothelin 1 (ET1) are 2 prime candidates, and are the subject of our study. Aims: Our aim was to study the immunoreactivity of NOS3 and ET1 in the pulmonary vasculature of PH patients of various etiologies, with emphasis on RHD cases. Settings and Design: A retrospective, autopsy-based study. Subjects and Methods: A total of 49 autopsy cases (39 patients and 10 controls) were chosen for our study. Of the 39 patients, 20 had PH secondary to RHD, whereas the remaining 19 patients had non-RHD etiologies as the basis of their PH. Lung sections taken from all the 49 cases were subjected to routine H and E, elastic van Gieson, and immunohistochemical staining (with NOS3 and ET1 separately). The intensity of immunostaining in all the cases and controls were then graded as focal/diffuse and weak/strong. Results: Controls showed positivity for both NOS3 (bronchiolar epithelium) and ET1 (endothelium of pulmonary arteries). Characteristic changes of PH on H and E were seen in 14 out of 19 non-RHD cases, which matched with the number of ET1 positivity cases. Similarly, for the RHD cases, 14 out of 20 cases showed changes of PH on H and E, but only 2 cases showed mild, focal positivity for ET1. Surprisingly, NOS3 positivity was largely absent in both the non-RHD and RHD cases. Conclusions: Our study showed NOS3 negativity and ET1 positivity in the lung vasculature of patients with PH, a conclusion more or less in line with the predominant view of the other investigators in this field. But at the same time, our study could not conclude an unequivocal role of NOS3 in PH, whereas it could, in the case of ET1.
RESUMEN
Objective To study the effect of cistanche deserticola on lactate dehydrogenase(LDH) isoenzyme,glycogen and nitric oxide synthase 3(NOS3) of liver in the mice burden swimming and explore relevant molecular mechanisms of anti-sports fatigue.Methods The mice were devided into the normal control group,the sport control group and the cistanche deserticola experimental group.Each mice of the normal control group and the sport control group was given saline 0.2 mL per day.Each mice of the cistanche deserticola experimental group was given water decoction of cistanche deserticola 0.2 mL(3 g/kg) per day.The administrations were for 15 days.The burden swimming for 90 minutes was carried out on the mice of the sport control group and the cistanche deserticola experimental group at 1 hour after the last administration.Livers of the mice were removed after 10 hours of swimming.One part of liver was fixed in the neutral formalin liquid to prepare the paraffin sections and the others was used for measurement of LDH activity.The structure of the liver was observed by staining of HE and the liver glycogen were measured by staining of glycogen.NOS3 was examined by S-P immunohistochemical method.Results The liver structure of the sport control group was injured seriously,the isoenzyme of LDH4 and LDH5 were higher,the liver glycogen were poor,NOS3 was decreased compared with the normal control group(P