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N Johnstone

Publications and source records attributed to N Johnstone.

2 recordsLinked to original sources

Acute respiratory alkalosis and acidosis and rabbit intestinal ion transport in vivo.

The effects of acute respiratory alkalosis and acidosis on electrolyte transport in the rabbit ileum, colon, and gallbladder were studied. During in situ perfusion, anesthetized animals were ventilated with 0, 3, or 8% CO2 gas, creating states of alkalosis (pH 7.49 +/- 0.01, PCO2 = 27.0 +/- 0.9 mmHg, HCO3 = 21.7 mM), normocapnia (pH 7.38 +/- 0.02, PCO2 = 41.3 +/- 1.1 mmHg, HCO3 = 25.9 +/- 0.4 mM), and acidosis (pH 7.21 +/- 0.01, PCO2 = 66.3 +/- 1.3 mmHg, HCO3 = 28.1 +/- 0.8 mM). In the ileum alkalosis decreased the net absorption of water (-36%), sodium (-44%), and chloride (-27%), whereas acidosis had the opposite effect on water (+69%), sodium (+98%), and chloride (+32%) absorption and reduced bicarbonate secretion. Small changes in net potassium absorption occurred in the direction of water movement. There was no effect on the ileal transmural potential difference (PD). The colon and gallbladder did not respond to the acid-base disorders with changes in electrolyte transport or PD. These results suggest that systemic pH and/or PCO2 affect an electroneutral sodium chloride absorptive process in the rabbit ileum. The simple presence of this absorptive process in the gallbladder was not a sufficient basis for this organ to respond to alterations in systemic pH.

Acidosis, Respiratory↗

Effect of cycloheximide on corticosteroid-induced changes in colonic function.

Chronic parenteral mineralocorticoid and glucocorticoid treatment increases colonic sodium and water absorption and mucosal Na-K-ATPase activity. Cycloheximide, a protein synthesis inhibitor, was utilized to compare the mechanisms of action of these corticosteroids. Rats were injected with 50 or 100 micrograms/100 g body wet cycloheximide every 12 h, 0.5 or 3 mg/100 g deoxycorticosterone (DOCA) daily, or 3 mg/100 g methylprednisolone (MP) daily, singly or in combination for 2 days. In water absorption, transmural potential difference, and the specific activity of Na-K-ATPase were measured. Cycloheximide alone did not alter colonic water, sodium, or chloride absorption or Na-K-ATPase activity but did increase transmural potential difference. DOCA-induced increases in colonic absorption and Na-K-ATPase were completely prevented by cycloheximide. Cycloheximide completely prevented the increase in Na-K-ATPase in MP-treated rats but only partially reduced the MP-induced increase in sodium and water absorption. These results suggest that this enzyme is not the primary site of glucocorticoid action. It remains to be determined whether an increase in Na-K-ATPase activity is a necessary part of the maximal colonic response to chronic glucocorticoid treatment.

Absorption↗