Anesthetic management for emergency cesarean section in a patient with severe valvular disease and preeclampsia.

Wider selection of young patients for prosthetic valve replacement for valvular heart disease has resulted in an increase in number of women with heart disease reaching childbearing age. Such patients presenting in labor for emergency cesarean section require special consideration. We present a report of a parturient who presented at 36 weeks of gestation with severe aortic and mitral stenosis, pulmonary edema and severe preeclampsia. The goals of our anesthetic management included (1) careful airway management (2) maintaining stable hemodynamics (3) optimizing fluid status, and (4) preventing seizures. Issues related to management of patients with severe valvular disease, prosthetic valves and complications due to anticoagulant therapy during pregnancy are discussed.

Liver cell calcium homeostasis in carbon tetrachloride liver cell injury: new data with fura2.

The calcium fluorescent probe fura2 was used to measure concentration of free calcium in the cytosol of isolated rat hepatocytes in suspension. The resting level in untreated hepatocytes was 121 nM. On addition of CCl4 at a concentration of 0.5 mM, cytosolic free calcium rose sharply and reached a statistically significant (P less than 0.05) steady plateau level of about 190 nM within five minutes. With a concentration of 1.0 mM CCl4, cytosolic free calcium rose within ten minutes to a plateau level of about 200 nM. Use of fura2, along with the capacity of Mn2+ ions to effectively quench fura2 fluorescence, provided the basis for a simple and decisive method to determine whether the added CCl4 was permeabilizing the hepatocyte plasma membrane by direct solvent action. It was found that up to a concentration of 1.0 mM, CCl4 did not permeabilize the plasma membrane, but direct attack on the plasma membrane was unequivocally demonstrated for concentrations of 2 mM CCl4 and above. Finally, an hypothesis is presented for resolution of the puzzling dilemma that emerged from the observation, reported from two laboratories, that CCl4 can rapidly mobilize liver mitochondrial calcium despite the well-known relative resistance of these organelles to the damaging effects of this toxic agent.

Potentiation of carbon tetrachloride hepatotoxicity by chlordecone: dose-response relationships and increased covalent binding in vivo.

Chlordecone greatly potentiates carbon tetrachloride (CCl4) hepatotoxicity. In order to quantitate the degree of this potentiation, the effects of a range of doses of CCl4 on two microsomal enzymatic functions and liver enzyme release were examined in chlordecone-treated and control rats. Male Sprague-Dawley rats were pretreated with 15 mg chlordecone per kilogram body weight (BW) intragastrically or with vehicle. After 48 hours, 0 to 250 microliters CCl4 per 100 g body weight were given intraperitoneally (IP), and the rats were killed 24 hours later. Chlordecone treatment produced approximately a 17-fold potentiation of the CCl4-dependent loss of cytochrome P-450 and glucose-6-phosphatase activity, so that a dose of 6 microliters CCl4 per 100 g body weight in the chlordecone-treated animals resulted in a similar amount of damage as observed with 100 microliters CCl4 per 100 g body weight in controls. A similar potentiation by chlordecone was seen with CCl4 induced increases in serum glutamic-oxaloacetic transaminase (SGOT) levels. Chlordecone treatment also increased hepatic cytochrome P-450 levels by 67% and resulted in an increase in the covalent binding of [14-C]-CCl4-derived metabolites to microsomal protein and lipid in vivo.

Chlordecone does not interfere with hepatic repair after carbon tetrachloride or partial hepatectomy.

The effect of chlordecone (CD) on hepatic repair, measured either as recovery of microsomal enzymatic functions or as the induction of cytosolic thymidine kinase (TK) activity, was evaluated in rats given carbon tetrachloride (CCl4). Carbon tetrachloride was administered to CD-potentiated and control animals using doses of this hepatotoxin which produce similar degrees of damage at 24 hours in both groups of animals (6 and 100 microliters CCl4 per 100 g body weight, respectively). Chlordecone had no significant effect on the time course of recovery of microsomal cytochrome P-450 content or glucose-6-phosphatase activity following CCl4 administration. Hepatic TK activity was measured 48 hours after CCl4 administration as a biochemical index of the hepatic regenerative response. Thymidine kinase activity was increased eightfold in CD-treated rats receiving 6 microliters CCl4 per 100 g body weight, whereas in controls a similar induction of TK activity was produced by 100 microliters CCl4 per 100 g body weight. Therefore, the TK response in CD-treated rats receiving CCl4 is appropriate for the amount of damage produced, suggesting that CD does not inhibit the hepatic regenerative response to CCl4-induced injury. The effect of CD on hepatic repair was also examined in rats receiving a two-thirds partial hepatectomy. Pretreatment of animals with CD had no significant effect on the increase in TK activity produced 24 hours after partial hepatectomy. These results offer no support for the idea that CD impairs hepatic repair after either partial hepatectomy or CCl4 administration.