A 24-year-old female with idiopathic thrombocytopenic purpura (ITP) and total placenta praevia was scheduled for caesarean section. Anesthetic management during caesarean section with ITP and placenta praevia is critical because of possibility of massive intra- and postpartal bleeding. The patient received prednisolone 30 mg per day for 10 days before surgery. Bleeding time and value of platelet count returned to normal range on the operative day. Hydrocortisone 100 mg and atropine sulfate 0.3 mg were given intravenously just before the start of anesthesia. Anesthesia was induced with thiamylal 4 mg.kg-1 and SCC 1 mg.kg-1 and maintained with N2O-O2-enflurane. A baby girl was delivered after 7 min, and the Apgar score was 9 at 1 min after delivery. Intraoperative bleeding totaled 1,314 ml, but we could avoid total hysterectomy.
We have reported that there was a significant difference in the anti-endotoxic potency between dexamethasone disodium phosphate (DM-P) and dexamethasone sodium sulfate (DM-S) in mice. In this report we shall try to compare the dose-dependent anti-endotoxic effect between DM-P and DM-S in mice and show whether there is any relationship between the serum concentration of free 17-OHCS following the intravenous administration of 2 mg/kg dexamethasone and the anti-endotoxic potency or not.1) Six hundred and eighty-nine young male mice of DDN strain (20-25g b.w.) were used. 3.2, 1.6, 0.8, 0.4, 0.2, 0.1, 0.05, 0.025, 0.0125 and 0.00625mg dexamethasone (DM-P or DM-S) and 0.5mg endotoxin (E-coli 0127 B8, Difco, USA) were intraperitoneally injected. 72 hours later survival rates were counted. Survival rates in the group administered DM-P were 73.3, 60.0, 53.3, 53.3, 60.0, 49.3, 62.5, 53.3, 40.0 and 46.6% respectively. In the group administered DM-S, survival rates were 20.0, 26.6, 6.6, 18.9, 16.6, 25.0, 23.2, 26.6, 14.2 and 19.3% respectively.2) Twenty-seven elective surgical patients were investigated concerning their serum concentration of 17-OHCS following the administration of 2mg/kg dexamethasone during surgery (9 control patients, 10 patients administered DM-P, 8 patients administered DM-S). Serum 17-OHCS was measured at the control state, 30 min., 60 min., 120 min. and 180 min. after the administration of DM by the Porter-Silber method. The serum concentration of free 17-OHCS was 11.3 ± 2.0μg/ dl at the control state, and that in the control group was 5.2 ± 2.3, 17.1 ± 4.4, 10.6 ± 3.2 and 11.1 ± 4.2μg/dl respectively. In the DM-P group, it measured 208.6 ± 18.8,151.7 ± 15.3,113.7 ± 15.2 and 107.8 ± 12.1μg/dl respectively. (mean ± s.e.m.) We concluded that there was a significant difference in anti-endotoxic potency between DM-P and DM-S, that the serum concentration of free 17-OHCS was significantly elevated after administration of 2mg/kg DM-P but not after DM-S, that there was a close correlation between the anti-endotoxic potency of DM and its free form serum concentration, and finally that the biological action of glucocorticoid was greatly influenced by its side chain.
Protective action of conjugated equine estrogen (CEE) against endotoxin shock was admitted in mice. Male DDN strain mice pretreated intraperitoneally with 2 mg of CEE showed various survival rates according to the interval between administration of CEE and endotoxin injection. Survival rates of the control were 20.4%, but in the group pretreated with CEE they were 0% at 0 hour, 26.3% at 1 hour, 33.3% at 12 hours, 55.7% at 24 hours (p less than 0.001), 10.5% at 36 hours, and 31.2% at 48 hours respectively. Mice pretreated with 2 mg of CEE before 24 hours exhibited excellent resistance to 0.5 mg endotoxin. On the other hand, the hemodynamic effect of CEE was examined in six mongrel dogs, which showed little hemodynamic changes following administration of 10 mg/kg CEE for three hours observation. We speculated that the anti-shock action of CEE was due to the modification of vascular response to vasoactive substances, on the one hand it augmented the vascular contractile response to vasopressors and on the other hand it lessened the hypersensitive vasoconstriction under shock state.
