The RV FDG accumulation corrected for the partial volume effect was significantly increased in accordance with the severity of the RV pressure overload (i.e., the RV peak-systolic wall stress) in patients with pulmonary hypertension. Furthermore, the corrected RV FDG accumulation was decreased after the treatment with epoprostenol in accordance with the degree of reduction in the pulmonary vascular resistance and RV peak-systolic wall stress.
4 There was no correlation between HI receptor occupancy by terfenadine and the plasma concentration of the active acid metabolite of terfenadine in each subject.5 PET data on human brain were essentially compatible with those on HI receptor occupancy in guinea-pig brain determined by in vivo binding techniques, although for the same HI receptor occupancy the dose was less in human subjects than in guinea-pigs.6 The PET studies demonstrated the usefulness of measuring HI receptor occupancy with classical and second-generation antihistamines in human brain to estimate their unwanted side effects such as sedation and drowsiness quantitatively.
1 Antihistamine induced cognitive decline was evaluated using positron emission tomography (PET) measurement of histamine H1 receptor (H1R) occupancy and regional cerebral blood¯ow (rCBF). 2 Cognitive performance in attention-demanding task deteriorated dose-dependently and the e ects were statistically signi®cant after the treatment of 2 mg of d-chlorpheniramine. There was no signi®cant change in subjective sleepiness in the same dose. 3 The regional blockade of H1R was observed mainly in the frontal, temporal and anterior cingulate cortices, and the intravenous administration of d-chlorpheniramine as a therapeutic dose (2 mg) blocked over 60% of H1R in the frontal cortices. 4 The results from activation study using visual discrimination tasks demonstrated that enhanced activity in the right prefrontal and anterior cingulate cortices as well as a decreased activity in the left temporal and frontal cortices and midbrain after the treatment of d-chlorpheniramine. 5 There were no changes in global CBF for the subjects treated with 2 mg d-chlorpheniramine (pre; 44.8+3.3 ml dl 71 min 71 vs post; 44.4+4.7 ml dl 71 min 71 ). 6 The results indicated that the attention system of human brain could be altered by therapeutic doses of H1R antagonists. These ®ndings provide the information as to the potential risk of antihistamines in our daily activities.
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