Respiratory Responses to Intravenous Infusion of Sodium Lactate in Male and Female Wistar Rats
In patients with panic disorder or premenstrual dysphoria, anxiety attacks can be triggered by intravenous administration of sodium lactate. Since respiratory symptoms, such as hyperventilation and shortness of breath, are characteristic features of spontaneous as well as lactate-induced panic, an involvement of central or peripheral chemoreceptors in this reaction has been suggested. In the present study, we examined to what extent intravenous infusion of sodium lactate influences respiratory parameters in freely moving male and female Wistar rats. Prompted by clinical reports suggesting that the susceptibility to spontaneous and lactate-induced anxiety may be influenced by the menstrual cycle, we also investigated if the effect of lactate on respiration in female rats is estrus cycle-dependent. Male and ovariectomized female rats exposed to sodium lactate displayed a larger increase in respiratory rate than rats given an infusion of saline. In intact female rats, the response to lactate infusion was significantly more pronounced in the diestrus phase than in the proestrus/estrus phase of the cycle. It is concluded that sodium lactate is a respiratory stimulant in rat, and that this effect is influenced by female sex steroids.
Sodium Lactate Elicits a Rapid Increase in Blood Pressure in Wistar Rats and Spontaneously Hypertensive Rats
Effect of Pretreatment with the Antipanic Drugs Clomipramine and Alprazolam Intravenous administration of sodium lactate in concentrations (0.5 M, 2 M) previously shown to elicit panic attacks in patients with panic disorder was found to cause a prompt and short-lasting increase in blood pressure in spontaneously hypertensive (SH) rats and in normotensive Wistar rats; in contrast, only weak and nonsignificant effects of lactate were observed in rats of the Sprague-Dawley strain. The effects of lactate on heart rate in SH rats varied; thus, whereas most rats displayed a modest bradycardia during lactate infusions, in some rats the increase in blood pressure was accompanied by an increase in heart rate. After pretreatment with antipanic medication [the serotonin and noradrenaline reuptake inhibitor clomipramine (10 mg/kg/day, 3 weeks) or the triazolobenzodiazepine alprazolam (2 mg/kg/day, 3 weeks)], the blood pressure response to sodium lactate in SH rats was significantly blunted; in contrast, acute pretreatment with clomipramine (10 mg/kg) did not reduce the response. It is suggested that further studies on the cardiovascular effects of sodium lactate in SH or Wistar rats may shed further light on the mechanisms underlying the panic-provoking effect of lactate in panic disorder patients and on the mode of action of antipanic drugs.
Sodium Lactate depresses urate clearance by facilitating urate reabsorption in the mongrel
Sodium lactate was infused and urate clearance was measured under conditions of osmotic diuresis alone, as well as during simultaneous urate infusion. Urate clearance in the Dalmatian was not depressed by the administration of sodium lactate of 1.2–9.3 mEq/kg dl -sodium lactate, indicating that sodium lactate has no inhibitory effect on tubular secretion of urate. dl -Sodium lactate, 0.54–11.8 mEq/kg, was administered to four mongrel dogs in five experiments. In three experiments a significant drop of urate clearance in relation to filtration rate was observed. In two experiments in which urine flows exceeded 10 ml/min no significant decrease in urate clearance was recorded following dl -sodium lactate administration. The depression of urate clearance in the mongrel under conditions of moderate urine flow where reabsorption of solutes is more easily accomplished, and the absence of this effect in the Dalmatian as well as in the mongrel under conditions of vigorous diuresis where reabsorption of solutes is greatly diminished, lends support to the belief that sodium lactate depresses urate clearance by facilitating urate reabsorption in the mongrel.
