Acute gaseous peritonitis after rupture of a retroperitoneal rectal diverticulum in a dog.

An 11-year-old, entire male coton de tulear was presented on emergency with acute and severe depression, acute abdominal pain and vomiting of 24 hours duration. Historical complaints included right perineal swelling, dyschezia and tenesmus of 18 months duration. Abdominal ultrasonography and radiography suggested a pneumoperitoneum and positive-contrast colonography showed leakage of contrast medium into the caudal abdomen and the presence of a large retroperitoneal pouch. Exploratory laparotomy allowed the visualisation of faecal leakage from the retroperitoneal space into the peritoneal cavity. Using a perineal approach, a large necrotised rectal diverticulum filled with faeces was found over the retroperitoneal structures. A standard herniorrhaphy was then performed. The dog recovered uneventfully and dyschezia did not recur at the nine month follow-up. Rectal diverticulum rupture associated with peritonitis has not been described in the veterinary literature, to the authors' knowledge, and should be considered as a rare differential diagnosis in dogs being presented with gaseous peritonitis.

Chronic hypoxia delays myocardial lactate dehydrogenase maturation in young rats.

The effect of exposure to hypobaric hypoxia for 4 weeks (oxygen pressure = 106 hPa), equivalent to 5500 m in altitude) on myocardial total lactate dehydrogenase (tLDH) activity and isoform (H and M) composition was comparatively studied in growing (4.5 weeks old) and in adult (4.5 months old) male rats. The consequences of the hypoxia-induced anorexia were checked in growing rats using a pair-fed group. Exposure to hypoxia induced a significant decrease in the H/tLDH ratio in the left (LV) and right ventricle (RV) of growing and adult rats. In adult rats this alteration was mainly a consequence of the significant increase in the specific activity of the M isomer, which resulted in an increase in the overall LDH activity. In contrast, in the LV of young rats exposed to hypoxia, the specific activity of the M isomer was similar to that of normoxic animals while the H isomer activity was significantly lower than in normoxic rats, and the overall LDH activity remained unchanged. These effects were specifically due to hypoxia per se since no significant alterations were observed in pair-fed animals. In the hypertrophied RV, the alteration of H and M isomers following hypoxia was similar to that observed in adults (i.e. no change in H and an increase in M isoform). We conclude that the well-known hypoxia-induced decrease in the H/tLDH ratio is governed by different age-dependent mechanisms. In adult rats, hypoxia may induce in both ventricles a stimulating effect on M isomer expression. In the LV of growing rats this stress could inhibit the H isomer maturation without any effect on the M isomer. In the RV of growing rats this effect could have been counteracted by the growth effect of the hypertrophying process.