The effect of the plasma glucose level on the abomasal function in dairy cows.

We have studied the effect of plasma glucose level on the abomasal outflow rate of fluid using a hyperinsulinemic glucose clamp technique in dairy cows. Four nonpregnant, nonlactating cows were subjected to one of the following treatments: hyperinsulinemic normoglycemic clamp; hyperinsulinemic hypoglycemic clamp; hyperinsulinemic hyperglycemic clamp; or, as a control, an intravenous infusion of .9% sodium chloride in a Latin square design. The cows were previously fitted with a permanent fistula in the abomasum and the outflow rate of abomasal fluid was determined using Co-EDTA as a marker assuming that the outflow followed first-order kinetics. The abomasal pH was also registered. Insulin was infused continuously through a jugular catheter at a rate of 4.8 mU. kg(-1)min(-1) for 2.5 h in the three clamp treatments. A glucose solution was infused through the catheter at a variable rate to achieve a circulating concentration, near the preinfusion glucose level (approximately 4.1 mmol/L), 2 mmol/L below the preinfusion level, and 2 mmol/L above the preinfusion level for the three hyperinsulinemic treatments, respectively. There was a significant effect of treatment on the rate of abomasal outflow (P < .001). The rate of abomasal outflow was highest for the control treatment (7.8%/min). The slowest outflow was observed in the hyperglycemic cows (3.40%/min). The hypoglycemic and normoglycemic cows showed intermediate rates (6.0%/min and 5.2%/min, respectively). The rate of outflow for the hyperglycemic cows was significantly lower than for all the other treatments (P < .01). Abomasal pH was affected by treatment (P < .05). The highest pH was observed in the hyperglycemic cows (pH 2.3). The values for the other three treatments ranged from pH 1.9 to 2.0. These results show that hyperglycemia reduced the rate of outflow and increased the pH of abomasal fluid in dairy cows. An elevated plasma glucose level thus can be considered as a potential risk factor in the pathogenesis of left-displaced abomasum.