YERSINIA-ENTEROCOLITICA ENTERITIS AFFECTS RABBIT INTESTINAL LONGITUDINAL SMOOTH-MUSCLE FUNCTION

To determine whether Yersinia enterocolitica (YE) enteritis has an effect on the biomechanical properties of intestinal smooth muscle, New Zealand White rabbits (600-900 g) were divided into an infected group (n = 9) and sham-infected animals fed ad libitum (n = 9), or pair fed with the infected group (n = 9). Animals were inoculated with 10(10) organisms of YE in 10 ml NaHCO3 (infected group) or 10 ml NaHCO3 (sham-infected control and pair-fed groups) at time 0. Daily food intake, weight gain, and YE excretion were noted. Six days later animals were killed and longitudinal smooth muscle strips prepared from proximal (P), medial (M), and distal (D) segments of intestine in each treatment group. Isometric tension was recorded in tissue baths perfused with oxygenated Krebs solution and 10(-6) M tetrodotoxin. Basal and active (the response to 10(-5) M carbachol) length-tension curves were generated. Then, with the muscle strips stretched to their optimum length for tension development, the dose response to carbachol and to graded depolarization with KCl was determined. Infected animals had a significantly reduced food intake and weight gain compared with controls. The development of basal tension with stretch was not significantly different in infected compared with control or pair-fed tissues from the same site. The dose-response curves for tissues exposed to carbachol showed that even though the doses at which the contractile response is half-maximal were not significantly different, the response of infected tissues was significantly impaired compared with that of the pair-fed group, whereas the responsiveness of pair-fed tissues was significantly greater than the response of infected or control tissues at any specific site. Graded depolarization with KCl reproduced this pattern of response. Thus longitudinal smooth muscle of infected animals (that are also undernourished because of reduced food intake) exhibits a significantly reduced ability to develop tension in response to carbachol compared with pair-fed animals; whereas pair-fed tissues (from animals that are only undernourished) exhibit a significantly increased response to carbachol compared with control or infected animals. The mechanism is unknown, but because the response can be reproduced with KCl depolarization, it probably reflects receptor-independent changes in smooth muscle function.