الفهرس 
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Abstract
Pulmonary hypertension (PHT) way occur in patients with parenchymal lung disease such as chronic obstructive pulmonary disease (COPD) (Naeije, 2005) and idiopathiec pulmonary fibrosis (IPF) (Shaprio, 2003). Potential mechanism for this include vasconstriction as a consequence of hypoxia in the pulmonary circulation, smooth muscle proliferation and vascular remodelling and destruction of alveolar capillary units by the underlying disease. More recently, attention has focused on the vascular changes in the pulmonary circulation which can accompany parenchymal lung disease, and therapies which improve right ventricular perforomance by favourably modulating pulmonary vascular resistance .one such therapy is sildenafil a selective phosphodresterase 5 inhibitor phosphodieserase in activate cyclic guanotine monophosphate (c GMP) the second messenger of prostacyclin and nitric oxide (NO). Sildenfil potentiate the effect of pulmonary (GMP) and enhance the vasodilatory effects of this pathway.
The current study was conducted at Benha university hospital during the period from October 2009 to May 2010. It include 20 patients of long standing (COPD) who received standard medical therapy for chronic Obstructive pulmonary disease.
These patients were divided into two groups:-I- the control group which include 10 patients and had received the standard medical theary.
II- the second group was the active group and include 10 patients who received standard medical treatment and sildenafil 50mg three times dialy for 8 weeks and were followed up for clinical status, PASP, and right ventricular function and pulmonary function tests. The age of patients in current study ranged from 48 to 65 with mean age (56 ± 8) years.
Regarding the follow up to 8 week in the current study the mean PASP before giving sildenafil was 62.4 ± 3mmHg which significantly reduced to 43,1 ± 1mmHg after 8 weeks of regular sildenafil intake, so there was reduction in PASP 19,3 ± 2mmHg (Average 30%) (P value < 0.05), and Basic PASP in active group 8 patient (80%) had moderate pulmonary hypertension, 2 patients (20%) had severe pulmonary hypertension change to 6 patient (60%) had mild pulmonary hypertension, 3 patient (30%) had moderate pulmonary hypertension, (10%) had severe pulmonary hypertension. In the control group 8 patient (80%) hade moderate pulmonary hypertension change to 7 patient (70%) and, 2 patient (20%) had severe pulmonary hypertension change to 3 (30%) post 8 weeks, where there was no significant changes in the control group (P value>0.05). As regard in our study the six minute walk test in the active group increased from 145.5 ± 44 to 157.5 ± 41 after 8 weeks (P value < 0.05) it increase to 12 meter. In the control group change from 132.5 ± 40 to 132 ± 44 no significance difference .In the current study the right ventricular function assessed by echocardiography in active group, TAPSE changed from 1.87 ± .29 to 2 ± .19 (p value 0.05) while RVDD and FWT wasnot no significant changed. In current study spirometry test to the active group which assess change in FEV, FVC, and FEV/FVC no significant change.In the current study some patient reported side effects from sildenafil in form of flashing 2 patients (20%), headach 20 patients (20%) and diarrhea (patients (10%), however these side effects didnot interrupt treatment, and no mortality cases in two groups. no cardiac event are reported as decompansated heart faliure or arrhythmia.