***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Cilostazol , an antiplatelet drug that increases the cyclic adenosine monophosphate ( AMP ) levels in platelets via inhibition of cyclic AMP phosphodiesterase , has been used in chronic arterial occlusive disease . The purpose of the present study was to examine the effects of cilostazol on the recurrence of cerebral infa rct ion using a multicenter , r and omized , placebo-controlled , double-blind clinical trial method . Patients who suffered from cerebral infa rct ion at 1 to 6 months before the trial were enrolled between April 1992 and March 1996 . Oral administration of cilostazol ( 100 mg twice daily ) or placebo was r and omly assigned to the patients and continued until February 1997 . The primary endpoint was the recurrence of cerebral infa rct ion . In total , 1,095 patients were enrolled . An analysis based on 1,052 eligible patients ( 526 given cilostazol  and 526 given  placebo )  showed that the cilostazol treatment achieved a significant relative-risk reduction ( 41.7 % ; confidence interval [ CI ] , 9.2 % to 62.5 % ) in the recurrence of cerebral infa rct ion as compared with the placebo treatment ( P=.0150 ) . Intention-to-treat analysis of 1,067 patients also showed a significant relative-risk reduction ( 42.3 % ; CI , 10.3 % to 62.9 % , P=.0127 ) . No clinical ly significant adverse drug reactions of cilostazol were encountered . Long-term administration of cilostazol was effective and safe in the secondary prevention of cerebral infa rct ion Pneumonia is a common complication with the highest attributable proportion of deaths in patients with stroke .  Cilostazol is a potent type III phosphodiesterase inhibitor , approved as an anti-platelet aggregation agent . The present study was design ed to determine the protective mechanism of cilostazol against post-stroke pneumonia using a rat chronic cerebral hypoperfusion model . Rats were subjected to bilateral common carotid artery ligation ( LBCCA ) and divided r and omly into the vehicle  group ( n=72 ) and cilostazol  group ( n=72 ) . Rats of each group were sacrificed at baseline and at days 14 , 28 and 42 after LBCCA . Cilostazol significantly improved the swallowing reflex by shortening the latency to elicited swallowing and increasing the numbers of swallows ( P<0.05 ) at 14 days of hypoperfusion . It also decreased the numbers of bacterial colonies grown in cultures from homogenized lungs . Cilostazol markedly upregulated cyclic AMP responsive element binding protein ( CREB ) phosphorylation , increased tyrosine hydroxylase ( TH ) expression in the substantial nigra , and maintained dopamine ( 84.7+/-2.3 vs. 79.2+/-4.1 % control ; P=0.0512 ) and substance P levels ( 86.6+/-7.9 vs. 73.9+/-6.5 % control ; P<0.05 ) in the striatum , compared with the vehicle group . Our results indicate that cilostazol improves the swallowing reflex by enhancing the expression of TH through the CREB phosphorylation signaling pathway , and suggest that cilostazol could be useful in preventing pneumonia in the chronic stage of stroke 
    Output:
    
Moreover , in the two trials , cilostazol could have reduced the incidence of pneumonia via a reduction of the recurrence of cerebral infa rct ion , which suggests that other antiplatelets could also have the same effects .