Cellular therapy for myocardial repair has been one of the most intensely investigated interventional strategies for acute myocardium infarction. Although the therapeutic potential of stem cells has been demonstrated in various studies, the underlying mechanisms for such improvement are poorly understood. In the present study, we investigated the long-term effects of stem cell therapy on both myocardial fiber organization and regional contractile function using a rat model of post-infarct remodeling. Human non-hematopoietic umbilical cord blood stem cells (nh-UCBSCs) were administered via tail vein to rats 2 days after infarct surgery. Animals were maintained without immunosuppressive therapy. In vivo and ex vivo MR imaging was performed on infarct hearts ten months after cell transplantation. Compared to the age-matched rats exposed to the identical surgery, both global and regional cardiac function of the nh-UCBSC-treated hearts, such as ejection fraction, ventricular strain and torsion, were significantly improved. More importantly, the treated hearts exhibited preserved fiber orientation and water diffusivities that were similar to those in sham-operated control hearts. These data provide the first evidence that nh-UCBSC treatment may prevent/delay untoward structural remodeling in post-infarct hearts, which supports the improved LV function observed in vivo in the absence of immunosuppression, suggesting a beneficial paracrine effect that occurred with the cellular therapy.

Elevation of the factor VIII protein to coagulant ratio previously has been reported to predict the severity of pre-eclampsia. Abnormal levels and patterns of factor VIII: von Willebrand factor (VIII/vWF) have been reported in thrombotic thrombocytopenia purpura (TTP). Severe pre-eclampsia shares many features with this syndrome. Nine primigravid patients with pre-eclampsia were evaluated by assays for factor VIII/vWF protein and coagulant activity and were compared to nine normal primigravid (controls). The patients and controls were indistinguishable by factor VIII antigen/coagulant activity ratios. Pre-eclamptic patients also had unremarkable factor VIII patterns on crossed immunoelectrophoresis. The evaluation of factor VIII/vWF multimeric patterns showed four patients with abnormal patterns in the pre-eclamptic patients and three abnormal patterns in the controls. These patterns were not analogous to the factor VIII abnormalities found in TTP.

Plasma fibronectin and prostacyclin levels have been reported to vary in preeclamptic women when compared with pregnant control women. Elevation of fibronectin and deficiency of prostacyclin have been postulated to be due to endothelial cell disruption or dysfunction. Eighteen preeclamptic women and 19 normal pregnant controls were evaluated for plasma levels of fibronectin and the prostacyclin metabolite 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). 6-keto-PGF1 alpha and fibronectin plasma levels in patients were significantly different from control patients, with preeclamptic patients exceeding control subjects. Five patients had serial samples of 6-keto-PGF1 alpha prior to, during, and after intravenous magnesium sulfate therapy and no consistent effect was noted. No correlation existed between fibronectin and 6-keto-PGF1 alpha levels or between either compound and platelet count or liver function tests. Despite an overall elevation of fibronectin in preeclamptic patients, two patients with the hemolysis, elevated liver tests, and low platelet count syndrome showed low normal fibronectin levels coinciding with thrombocytopenia, hemolysis, and liver dysfunction. The magnitude of fibronectin elevation may therefore not predict the severity of preeclampsia. The significance of these findings is discussed.

Ascites has been reported at cesarean section delivery in pregnancies complicated by preeclampsia. The frequency and composition of peritoneal fluid collections in pregnancy have not previously been described. This descriptive study evaluated presence, composition, and characteristics of ascites present in 41 women undergoing cesarean delivery for a variety of indications. Twenty-six women had sufficient quantities of peritoneal fluid to be collected immediately after opening the parietal peritoneum. The protein content of the fluid was analyzed. The presence of fluid was not related to labor preceding delivery. All preeclamptic women in this study had fluid obtainable at cesarean section. Large volume ascites was noted in five preeclamptic women whose fluid had low total protein content, consistent with a transudate. Intrahepatic portal hypertension is one possible explanation of the large volume and low protein ascites in some preeclamptic patients. Ultrasonic measurements in preeclamptic patients and normotensive pregnant women showed uniform portal vein diameters and Doppler-derived portal vein flow velocities in all patients. The physiology of peritoneal fluid production in complicated and normal pregnancy remains unexplained.

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