PubMed · 7471196
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G P Jena. 1980. Dermatofibrosarcoma protuberans.. https://pubmed.ncbi.nlm.nih.gov/7471196/
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BACKGROUND: Complications can arise from standard intrathoracic central venous pressure (CVP) measurements in critically ill, mechanically ventilated patients. We have assessed the feasibility of catheterisation by the femoral route to measure CVP in the abdomen (ACVP). We compared measurements by the standard jugular or subclavian route (TCVP) with simultaneous ACVP measurements by the femoral route. METHODS: Between June, 1994 and May, 1995, we recruited 20 critically ill adult patients with various disorders; all patients already had a TCVP line in situ. We placed a femoral catheter in the inferior vena cava close to the right atrium under electrocardiographic guidance. The catheter position was confirmed (and corrected if necessary) by chest radiography. CVP was measured from both sites hourly for 6 h. Positive end-expiratory pressure, mean airway pressure, and intra-abdominal pressure were recorded simultaneously. FINDINGS: One patient was excluded because radiography showed that the catheter position was incorrect. For 133 paired measurements of ACVP and TCVP in the remaining 19 patients, the mean difference was 0.45 mm Hg (SD 0.89: 95% Cl 0.30-0.60); the limits of agreement were -1.33 to 2.23 mm Hg (-1.63 to 2.53). We found a small tendency for the difference between ACVP and TCVP to increase as positive end-expiratory pressure and mean airway pressure increased; the difference was statistically, but not clinically, significant. INTERPRETATION: Our study showed that for clinical purposes CVP can be measured by a femoral catheter placed in the abdominal inferior vena cava near the right atrium. This approach can replace standard TCVP measurements in critically ill, mechanically ventilated patients.
Estrogen's involvement in inflammation and wound healing is poorly understood. To examine the role of estrogen in peritoneal adhesion formation, we gave ovariectomized female C57BL/6 mice time-release pellets containing placebo, 0.05 mg 17 beta-estradiol (low E2), or 5 mg 17 beta-estradiol (high E2) before i.p. injection of talc in saline or saline alone. Analyses of abdominal wall connective tissue thickness and peritoneal cell populations were performed. Talc-treated mice receiving low and high E2 replacement had a decreased amount of abdominal connective tissue deposition (29% and 65% decrease, respectively) as compared with talc-treated mice receiving placebo pellets. At high E2 replacement, the difference in connective tissue deposition was significant statistically (p less than 0.01). Immunohistochemical analysis revealed that the number of macrophages in adhesion tissue was proportionate to the amount of connective tissue present, regardless of the circulating levels of E2. Northern blot analysis of abdominal wall tissue showed that five of six talc-treated animals given placebo expressed mRNA for the murine monocyte chemoattractant protein-1 (MCP-1), JE. Conversely, only one of five talc-treated animals that received E2 replacement expressed JE/MCP-1 mRNA, suggesting that the hormone may inhibit connective tissue deposition by altering the production of chemotactic factors. Furthermore, E2 suppressed talc-induced expression of JE/MCP-1 mRNA in murine macrophages. Since macrophages play a central role in the wound healing process, these studies suggest that E2 inhibition of adhesion formation could be mediated by suppressing macrophage activation and/or recruitment to inflammatory sites.