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The effect of heparin on serum esterase in arteriosclerosis
VOL. 2 (I(j57)
SIIORT
CLINIC.1 CHIMIC.1 ACT:\
CORI~IlJNlC.-\TIOS
In man, heparin increases serum esterase activity in oivo, as shown by the splitting of ethyl butyrate’, and this activity is resistant to inhibitors ?. In this work we attempted to ascertain whether the effect of heparin on serum esterase is altered in arteriosclerosis. Ethyl butyrate was again used since the rise in man is most marked and since the results obtained with tributyrin are not consistent 3r 4, j. Heparin was injected in amounts of IOO units/kg body-weight in a group of fasting subjects with proven symptoms of arteriosclerosis and in a group of controls. Blood samples were taken five minutes after the intravenous injection of heparin. Esterase activitv was determined by the titrimetric method G. It is seen from Table I
that in all 50 subjects examined there was a rise in esterase activity after administration of heparin. It was not possible to demonstrate a significant difference between the group of arteriosclerotic patients and the control group (t = 0.65; P > 0.5). Our results, therefore, are not in parallel with the decrease in the post-hcparin clearing reaction in arteriosclerotic patients, reported by 13LOCK et al.‘. It is probable that the esterase activated by heparin is not identical with the clearing factor. V’hile the clearing factor breaks down lipoproteins, esterase hydrolyses the products resulting from lipoproteins in the clearing reaction and its rcturbidihcation effect can be observed even when the clearing factor is inhibited by sodium chloride *. M’e wish to thank Professor Dr. R. PRUS~K for the interest he has shown in this work.
\.C)I*. 2 (1957)
SIIORT
CLINIC.1 CHIMIC.1 ACT:\
CORI~IlJNlC.-\TIOS
In man, heparin increases serum esterase activity in oivo, as shown by the splitting of ethyl butyrate’, and this activity is resistant to inhibitors ?. In this work we attempted to ascertain whether the effect of heparin on serum esterase is altered in arteriosclerosis. Ethyl butyrate was again used since the rise in man is most marked and since the results obtained with tributyrin are not consistent 3r 4, j. Heparin was injected in amounts of IOO units/kg body-weight in a group of fasting subjects with proven symptoms of arteriosclerosis and in a group of controls. Blood samples were taken five minutes after the intravenous injection of heparin. Esterase activitv was determined by the titrimetric method G. It is seen from Table I
that in all 50 subjects examined there was a rise in esterase activity after administration of heparin. It was not possible to demonstrate a significant difference between the group of arteriosclerotic patients and the control group (t = 0.65; P > 0.5). Our results, therefore, are not in parallel with the decrease in the post-hcparin clearing reaction in arteriosclerotic patients, reported by 13LOCK et al.‘. It is probable that the esterase activated by heparin is not identical with the clearing factor. V’hile the clearing factor breaks down lipoproteins, esterase hydrolyses the products resulting from lipoproteins in the clearing reaction and its rcturbidihcation effect can be observed even when the clearing factor is inhibited by sodium chloride *. M’e wish to thank Professor Dr. R. PRUS~K for the interest he has shown in this work.
\.C)I*. 2 (1957)