FIGURE 6.

Smoking increases the severity of cerulein‐induced pancreatitis. Acute pancreatitis (AP) was induced by 10 h i.p. injections of either physiological saline (PS and control group) or 50 µg/kg cerulein after a 6‐week smoking period. (A–D) Representative haematoxylin and eosin (H&E) images of guinea pig pancreas. (A and B) PS and smoking alone caused no significant changes in pancreas histology. However, cerulein administration (C and D) induced a significant increase in pancreatic oedema (grey arrow on H&E image) (E), leukocyte infiltration scores (red arrow on H&E image) (E), necrosis (black arrow on H&E image) (E) or serum amylase activity (F). No significant differences were observed in the extent of interstitial oedema or leukocyte infiltration between the cerulein‐treated non‐smoker and smoker groups (E). However, the level of necrosis was significantly higher in the cerulein‐treated smoker group in comparison with the cerulein‐treated non‐smoking animals (E). Serum amylase activity was also significantly elevated in the cerulein‐treated smoking animals versus the cerulein‐treated non‐smoker group (F). Scale bar = 50 µm. Chronic pancreatitis (CP) was induced by repetitive i.p. injection of cerulein during the smoke‐exposed period in mice. In the last 2 weeks of the 6‐week smoking period used in previous experiments, the mice received five series of 8 hourly PS (control group) or 50 µg/bw kg cerulein injections every third day. (G–J) Representative Crossmon's trichrome staining images of mouse pancreas. Both the smoking and non‐smoking animals had normal pancreatic histology (G and H), whereas repetitive cerulein administration caused severe acinar cell atrophy, extensive fibrosis and the presence of acinar‐to‐ductal metaplasia (I and J), which was significantly worsened in the mice exposed to whole‐body smoke for 6 weeks (K). There was no significant difference was detected in pancreas weight/body weight ratio between the non‐smoker and smoker CP animals (L).