UTS2 FARMAKOKIMIA Nama : Ardhanareswari NIM : 118114049 Milrinone

1. Brand Name Milrinone IV [5].

2. Indication(s) : Indicated for the treatment of congestive heart failure [2]. Mechanism : Milrinone lowered Pulmonary Vascular Resistance (PVR) by decreasing Pulmonary Artery Pressure (PAM) and increasing Cardiac Output (CO) significantly. In addition, Pulmonary Capillary Wedge Pressure (PCWP) was significantly lowered [1]. 3. Side Effect(s) : hypotension [4]. Mechanism : adverse effects are inextricably linked to their inotropic mechanism of action [6]. The inotropic response to milrinone was modified by changes in the rate of stimulation and the concentration of extracellular Ca++ and by depolarization with high K+ or pretreatment with a calcium-channel blocker. Reduction of the extracellular Na+ concentration of 75% of normal potentiated the inotropic response of papillary muscles to low concentrations of milrinone, suggesting possible activation of the Na+-Ca++ exchange mechanism. These results suggest that milrinone may stimulate hypotension [7]. 4. Metabolism : Milrinone is metabolized into N-acetyl derivative [3].

REFERENCES : 1. http://www.ncbi.nlm.nih.gov/pubmed/10226902 - Pamboukian SV., et al., J Heart Lung Transplant., 1999 Apr, 18(4):367-71. 2. http://www.ncbi.nlm.nih.gov/pubmed/8241010 - Sherry KM., et al., Cardiovasc Drugs Ther., 1993 Aug, 7(4):671-5. 3. http://www.ncbi.nlm.nih.gov/pubmed/3304772 - Rocci Jr,., et al., Clin Pharmacokinet., 1987 Aug, 13(2):91-109. 4. http://www.ncbi.nlm.nih.gov/pubmed/12148128 - Saab G.,et al., Am J Kidney Dis., 2002 Aug, 40(2):E7.

5. 6. 7.

http://www.ncbi.nlm.nih.gov/pubmed/10416916 - Heinz G., et al., Intensive Care Med., 1999 Jun, 25(6):620-4. http://www.ncbi.nlm.nih.gov/pubmed/19234787 - Teerlink JR., Heart Fail Rev., 2009 Dec, 14(4):289-98 http://www.ncbi.nlm.nih.gov/pubmed/2417744 - Alousi AA., Circulation., 1986 Mar, 73 (3 Pt 2):III10-24.