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. Author manuscript; available in PMC: 2010 Apr 22.
Published in final edited form as: Circ Cardiovasc Genet. 2010 Feb 2;3(2):169–178. doi: 10.1161/CIRCGENETICS.109.908905

Figure 6. The appearance of LPL and HL in the plasma after heparin.

Figure 6

A–B. LPL in the plasma after an intravenous bolus of heparin in the subject homozygous for a C65Y mutation in GPIHBP1, his heterozygous parents, and four normolipidemic controls. LPL activity (A) and mass (B) in postheparin plasma were measured during an 18-min sampling period after an intravenous injection of heparin (50 U/kg body weight). Proband (▲); father (○) mother (◇); and controls (■). For the controls, data are expressed as mean ± SEM.

C–D. LPL in the plasma after an intravenous bolus of heparin in the subject homozygous for a Q115P mutation in GPIHBP1 and normolipidemic controls. LPL activity (C) and mass (D) in postheparin plasma was measured during an 18-min sampling period after an intravenous injection of heparin (50 U/kg body weight). Proband (▲); and controls (■). For the controls (n = 4), data are expressed as mean ± SEM.

E–F. HL in the plasma after an intravenous bolus of heparin in the subject homozygous for a C65Y mutation in GPIHBP1, his heterozygous parents, and four normolipidemic controls. HL activity (E) and mass (F) in postheparin plasma were measured during an 18-min sampling period after an intravenous injection of heparin (50 U/kg body weight). Proband (▲); father (○); mother (◇); and controls (■). For the controls, data are expressed as mean ± SEM.

G–H. HL in the plasma after an intravenous bolus of heparin in the subject homozygous for a Q115P mutation in GPIHBP1, and normolipidemic controls. HL activity (G) and mass (H) in postheparin plasma was measured during an 18-min sampling period after an intravenous injection of heparin (50 U/kg body weight). Proband (▲); and controls (■). For the (n = 4), data are expressed as mean ± SEM.