New Zealand veterinary journal · 2012
Flow-mediated K(+) secretion in horses intoxicated with lolitrem B (perennial ryegrass staggers).
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Johnstone L K, Mayhew I G
Аннотация
AIM: To investigate the effects of lolitrem B intoxication on renal K(+) secretion in response to increased tubular flow rates.
METHODS: Results are derived from a repeated measure pilot study of seven horses fed non-perennial ryegrass feed for a week prior to exposing them to perennial ryegrass seed and hay that contained an average of 2 ppm lolitrem B. At the end of the control and treatment period frusemide (1 mg/kg I/V) was administered and serial fractional excretion of K(+)(FEK(+)) and fractional excretion of Na(+)(FENa(+)) calculated. Baseline concentration of aldosterone in plasma, serum K(+)concentration and feed K(+) concentration were also compared.
RESULTS: Key findings included a reduced change in FEK(+) from 0 to 15 minutes in response to frusemide administration (p=0.022, Wilcoxon signed-rank test) and a reduced baseline concentration of aldosterone in plasma (p=0.022, Wilcoxon signed-rank test) during the treatment period compared with the control.
CONCLUSIONS: Results suggest that lolitrem B intoxication reduced flow-mediated K(+) secretion and interfered with aldosterone production or secretion. However, further investigation is required to validate these findings and to further elucidate the underlying pathophysiology.
CLINICAL RELEVANCE: Lolitrem B intoxication in horses may cause disruption to electrolyte handling in addition to neurological deficits.
METHODS: Results are derived from a repeated measure pilot study of seven horses fed non-perennial ryegrass feed for a week prior to exposing them to perennial ryegrass seed and hay that contained an average of 2 ppm lolitrem B. At the end of the control and treatment period frusemide (1 mg/kg I/V) was administered and serial fractional excretion of K(+)(FEK(+)) and fractional excretion of Na(+)(FENa(+)) calculated. Baseline concentration of aldosterone in plasma, serum K(+)concentration and feed K(+) concentration were also compared.
RESULTS: Key findings included a reduced change in FEK(+) from 0 to 15 minutes in response to frusemide administration (p=0.022, Wilcoxon signed-rank test) and a reduced baseline concentration of aldosterone in plasma (p=0.022, Wilcoxon signed-rank test) during the treatment period compared with the control.
CONCLUSIONS: Results suggest that lolitrem B intoxication reduced flow-mediated K(+) secretion and interfered with aldosterone production or secretion. However, further investigation is required to validate these findings and to further elucidate the underlying pathophysiology.
CLINICAL RELEVANCE: Lolitrem B intoxication in horses may cause disruption to electrolyte handling in addition to neurological deficits.