Dido Franceschi

The management of localized abdominal aortic dissections

Aortic dissections limited to the abdominal aorta occur infrequently. We have identified four cases of abdominal aortic dissection and have reviewed these in combination with 43 previously reported cases to identify factors that influence the prognosis and management of this disease. Abdominal aortic dissections are similar to thoracic dissections in their presentation, with acute shearing pain and systolic hypertension occurring commonly. Although the diagnosis may be made by ultrasonography or CT scanning, angiography is the definitive diagnostic study. Factors found to be associated with high mortality include presentation with acute pain (p less than 0.0003), involvement of visceral vessels (p less than 0.02), and rupture (p less than 0.000002). Chronicity appears to be protective (p less than 0.04), although chronic dissections may present acutely. Although prosthetic replacement of the involved aorta is the treatment of choice in most cases, nonoperative management with regular follow-up can be considered in asymptomatic chronic dissections.

Peripheral lymphocyte membrane fluidity after thermal injury

Serum cortisol levels are increased in patients after thermal injury. Lymphocyte function is altered in these patients, which renders them susceptible to infections. Elevated cortisol levels may contribute to this compromised state. In this study, we have demonstrated that cortisol directly affects lymphocyte membrane fluidity as measured by the polarization of fluorescence from the membrane-associated probe diphenylhexatriene in peripheral blood lymphocytes. Membrane fluidity increased in vitro with short- or long-term cortisol exposure. However, membranes of control peripheral blood lymphocytes that were previously exposed to cortisol became resistant to the fluidizing effect of cortisol, which implies membrane adaptation to long-term cortisol exposure. Cortisol effects were similar to those associated with ethanol, a known membrane-fluidizing agent, in peripheral blood lymphocytes and cytotoxic T lymphocytes. Membrane fluidity was compared in peripheral blood lymphocytes from thermally injured patients and peripheral blood lymphocytes from normal (control) subjects. Peripheral blood lymphocyte membrane fluidity increased in major thermal injury. Our data suggest that cortisol affects lymphocyte membrane fluidity in vitro in a manner similar to the membrane fluidity alterations that are observed in vivo after thermal injury. These observations reflect a direct membrane effect of cortisol, which may explain, in part, the cellular dysfunction and immunologic suppression that is observed after thermal injury.

Effects of Argon laser radiation on aortic endothelial cells: Early membrane changes and proliferative response

Membrane fluidity, transmembrane signaling responses, and proliferative characteristics of endothelial cells were studied to characterize biochemical and molecular changes after treatment with argon laser energy. Bovine aortic endothelial cells grown in monolayers were irradiated at 50, 100, and 200 J with an argon laser (wavelength, 488 and 514 nm). Proliferation, assayed by [3H]thymidine incorporation, was measured daily for 6 days. An initial lag phase was observed for irradiated cells when compared to nonirradiated controls (P less than 0.03), with eventual recovery by the third day. Membrane fluidity, determined by fluorescence anisotropy, was measured 1 hr after irradiation. A decrease in static rotational motion of 1,6-diphenyl-1,3,5-hexatriene (DPH) was noted in irradiated versus nonirradiated cells indicating a decrease in membrane fluidity (P less than 0.02). Dynamic studies of intracellular calcium and pH flux utilizing fluorescent probes demonstrated a preserved response to mitogenic stimulation. An increase in intracellular Ca2+ with a concomitant alkalinization of the intracellular milieu was observed in irradiated and non-irradiated cells in response to stimulation with endothelial cell growth factor (ECGF). These responses resemble those characterized for other mitogens. Argon laser energy applied to aortic endothelial cells decreases membrane fluidity early after irradiation. These alterations probably cause the initial lag observed in their proliferative response; however, the capacity to respond to exogenous mitogenic stimulation is maintained.