Transpulmonary pharmacokinetics of an ACE inhibitor (perindoprilat) in man.
1. The transpulmonary pharmacokinetics of the intravenous diacid ACE inhibitor perindoprilat were studied in 10 male patients undergoing diagnostic cardiac catheterisation for the management of ischaemic heart disease. 2. Following successful completion of diagnostic cardiac catheterisation and ventriculography, subjects received a low dose (1 mg) constant rate infusion of perindoprilat over 20 min with co-infusion of the intravenous marker dye indocyanine green (0.5 mg kg-1). Simultaneous transpulmonary blood sampling was conducted for 1 h and subsequent peripheral venous blood samples were collected for 20 h. 3. No acute changes in blood pressure or heart rate were noted despite rapid and marked inhibition of central circulation plasma ACE activity persisting in peripheral venous blood for 20 h. A delayed rise in plasma renin activity was noted. 4. Transpulmonary passage during early accumulation of the drug was seen to incorporate an early delay. Concurrent ICG measurements suggested that this was entirely due to circulatory delay and not to binding of the drug. Thus, despite the suggested high concentration of tissue ACE activity in the pulmonary circulation, transpulmonary passage of perindoprilat was not measurably influenced by binding at this site under the conditions studied.[1]References
- Transpulmonary pharmacokinetics of an ACE inhibitor (perindoprilat) in man. MacFadyen, R.J., Lees, K.R., Gemmill, J.D., Hillis, W.S., Reid, J.L. British journal of clinical pharmacology. (1991) [Pubmed]
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