Journal of applied physiology
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The inherent electrical resistance of the rat vaginal wall rises markedly near the beginning of estrus and then falls again to low levels for the remainder of the ovarian cycle. Accordingly, special instruments have been developed to measure such resistances (within seconds) on simply inserting a small probe fitted with a pair of recording electrodes into the vagina (i.e., the MK-10A impedance checker and the EC40 estrus cycle monitor). As described herein, these two instruments are far more convenient for monitoring individual cycles than more laborious methods in which vaginal smears are inspected for changes in numbers of cornified (C), nucleated (N), and leukocytic (L) cells. ⋯ In rats from which vagina smears revealed cell numbers in the order of C > N > L (typical of early estrus) electrical resistances were high, 488 +/- 130 k Omega (18 rats). In rats from which vagina smears revealed all other possible cell distributions, electrical resistances (combined) were much lower (P < 0.05), 124 +/- 23 k Omega (32 rats). Thus readily accessible, inexpensive electrical meters may be useful in assessing the status of estrus in female rats, either to improve reproductive efficiencies and/or for other purposes involving experiments in which such information is desirable.
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The effects of mechanical ventilation (MV) on the surfactant system and cytokine secretion were studied in isolated septic rat lungs. At 23 h after sham surgery or induction of sepsis by cecal ligation and perforation (CLP), lungs were excised and randomized to one of three groups: 1) a nonventilated group, 2) a group subjected to 1 h of noninjurious MV (tidal volume = 10 ml/kg, positive end-expiratory pressure = 3 cmH(2)O), or 3) a group subjected to 1 h of injurious MV (tidal volume = 20 ml/kg, positive end-expiratory pressure = 0 cmH(2)O). ⋯ In these lungs, the surfactant system was similar in sham and CLP lungs; however, tumor necrosis factor-alpha and interleukin-6 levels were significantly higher in CLP lungs. We conclude that injurious ventilation altered surfactant independent of sepsis and that the CLP lungs were predisposed to the secretion of larger amounts of cytokines because of ventilation.