Changes in the acid-base equilibrium in hypokalemic patients during potassium infusions with various anions]

Based on the parameters of the acid-base status, the effect of different anions in potassium and magnesium substitution was studied. A mixture of chloride with the metabolisable anions acetate and malate does not cause any changes in the acid-base balance. The exclusive supply of metabolisable anions in the form of aspartate always results in a change of blood pH values towards an alkalosis.     

Selective dietary potassium depletion and acid-base equilibrium in the rat

K+ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H+, K+, Na+ and Cl- were carried out daily during weeks 1, 3 and 5. In control rats of group A (receiving K+ with sodium chloride), plasma pH (7.47) and HCO3- (25 mmol/l), as well TA (titratable acid)--HCO3- and NH+4 urinary excretion rates, were stable, while balances were nil for K+ and slightly positive for Cl-. In K+-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO3- 35.8 mmol/l by 5 weeks), and TA--HCO3- and NH+4 urinary excretion rates were not different from controls. Plasma K+ fell progressively from 4.20 to 2.20 mmol/l, with negative K+ balance. Balances for Na+ and H2O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl- balance. In control rats of group B (receiving K+ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA--HCO3- excretion rate was increased compared with control rats of group A.(ABSTRACT TRUNCATED AT 250 WORDS)     

The antihypertensive effect of dietary potassium chloride loading in rats with adrenal regeneration hypertension

Adrenal regeneration hypertension was induced in male Wistar rats by unilateral adrenal enucleation, contralateral adrenalectomy and the provision of a 1% (w/v) NaCl solution for drinking. A fivefold increase in dietary KCl content caused a significant reduction in the systolic blood pressure of hypertensive rats but not of control rats. During the increase in potassium intake there was a marked polydipsia. When 1% NaCl solution was the drinking fluid, the resultant increase in sodium intake was associated with an abolition of the antihypertensive effect of potassium loading, but when the sodium intake was held constant, the antihypertensive effect was maintained. In rats with adrenal regeneration hypertension, plasma volume was significantly higher, and packed cell volume and plasma protein concentrations were significantly lower than in control rats. These differences were abolished after 4 days of dietary KCl supplementation. Increased dietary potassium intake was associated with significantly lower serum aldosterone concentrations and significantly higher plasma potassium concentrations in adrenal enucleated rats compared with controls. The possibility that a reduction in extracellular fluid volume (due to a natriuresis) and/or a peripheral vasodilatation contributed to the antihypertensive effect of KCl loading is discussed.     

The effect of chronic hypotonic volume expansion on the renal regulation of acid-base equilibrium

Balance studies have been carried out to evaluate the influence of vasopressin-induced volume expansion on acid-base equilibrium in normal dogs and in dogs with steady-state metabolic acidosis induced by the administration of 5-7 mmoles/kg per day of hydrochloric acid.Hypotonic expansion in dogs with metabolic acidosis (mean plasma bicarbonate concentration 14 mEq/liter) produced a marked increase in renal acid excretion that restored plasma bicarbonate concentration to normal (20-21 mEq/liter) despite continued ingestion of acid. When water was restricted during the vasopressin period, and fluid retention thus prevented, no increase in acid excretion or plasma bicarbonate concentration occurred. From these findings we conclude that hypotonic expansion is a potent stimulus to renal hydrogen ion secretion and greatly facilitates the renal removal of an acid load.Normal dogs subjected to expansion demonstrated no change in net acid excretion or in plasma bicarbonate concentration even in the face of a marked diuresis of sodium and chloride and a reduction in plasma sodium concentration to approximately 110 mEq/liter. The animals did, however, regularly lose potassium, a finding that clearly indicates an acceleration of distal sodiumcation exchange. On the basis of these observations, and the findings in the expanded acidotic dogs, we suggest that in the expanded normal dogs acceleration of sodium-hydrogen exchange was responsible for preventing a bicarbonate diuresis and for stabilizing plasma bicarbonate concentration.These studies clearly demonstrate that chronic hypotonic expansion exerts a major influence on the renal regulation of acid-base equilibrium. The exact nature of the mechanism responsible for the increase in sodium-hydrogen exchange during hypotonic expansion remains to be determined.     

Urinary kallikrein excretion during potassium chloride infusion in potassium-adapted rats: effect of amiloride

1. Urinary kallikrein excretion in the anaesthetized rat was measured during intravenous KCl infusion in control and in K+-adapted rats. 2. The infusion of 0.1 mol/l KCl at 3.0 ml/h for 60 min in control rats resulted in a significant increase in urinary kallikrein excretion, associated with diuresis, natriuresis and kaliuresis. 3. When rats were offered 0.1 mol/l KCl to drink ad libitum for 14 days (K+-adaptation), the basal excretion of kallikrein was higher than in the control rats. In K+-adapted rats, intravenous infusion of 0.1 mol/l KCl resulted in significantly greater increase in urinary kallikrein excretion than in the control rats. 4. The Na+-channel blocker, amiloride (8.5 mg/kg body weight), significantly increased urinary kallikrein excretion immediately after injection in control and K+-adapted rats. However, in the subsequent 60 min, kallikrein excretion decreased markedly to values lower than those before injection of amiloride. 5. When amiloride was superimposed on a continuous 0.1 mol/l KCl infusion in K+-adapted rats, there was an immediate increase in kallikrein excretion. In the subsequent 20 min, kallikrein excretion decreased only to increase again in the next 40 min of KCl infusion. 6. Since amiloride injection reduces urinary kallikrein excretion in control and K+-adapted rats, the results suggest that urinary kallikrein excretion in the rat is through a mechanism(s) affected by amiloride. The high urinary kallikrein excretion and the greater response to KCl infusion in K+-adapted rats suggest that the K+-transport mechanism is more important than the mechanism affected by amiloride.     

The serum level of substances to be excreted in the urine and the acid-base equilibrium after parenteral feeding]

By the present study it was demonstrated that the administration of an amino acid solution containing 20 essential and non-essential amino acids (Aminoplasmal L) together with a fat emulsion (Lipofundin S) and a full electrolyte solution with 10% dextrose (Sterofundin G-10) do not give rise to an increase in creatinine, uric acid, urea and bilirubin in the serum during an observation time of 11 hours.     

The effect of epinephrine on hemodynamics, acid-base status and potassium during spontaneous circulation and cardiopulmonary resuscitation

The effect of a bolus dose of epinephrine on hemodynamics, acid-base status and potassium during spontaneous circulation and cardiopulmonary resuscitation (CPR) was investigated in 24 pigs weighing 20-25 kg over a period of 10 min. In a study of 12 pigs in a stable hemodynamic condition, at the 1- and 2-min point after injection of epinephrine or saline the mean serum potassium concentration was significantly higher in the six animals given epinephrine (6.9 +/- 0.7 and 5.4 +/- 0.6 mmol/l, respectively) than in the six control animals (3.8 +/- 0.6 and 3.9 +/- 0.4 mmol/l, respectively). At the later points of observation (3, 4, 5 and 10 min after injection of either epinephrine or saline) no significant difference was found between the groups. Following 1 min of ventricular fibrillation 12 pigs were resuscitated by closed-chest CPR. Six of these animals received 45 micrograms/kg epinephrine (epinephrine group), the other six animals were given physiological saline (control group). Mean aortic diastolic pressure during the relaxation phase was significantly higher in the epinephrine group than in the control group. There was no difference in cardiac index or acid-base status between the groups. In the epinephrine group mean arterial serum potassium concentrations reached a peak value of 6.7 +/- 1.1 mmol/l at 3 min after injection, when they were significantly (P less than 0.05) higher than in the control group (4.4 +/- 0.5 mmol/l). At 5 and 10 min, the potassium levels sank to 5.9 +/- 0.9 and 5.6 +/- 0.8 mmol/l, respectively, in the epinephrine group, and were no longer significantly different from the control group.     

雾化吸入补钾效果及钾对气道敏感性影响的动物实验研究

目的探讨雾化吸入补钾效果及钾对气道敏感性的影响,为气道补钾的可行性提供理论依据。方法用0.1%组织胺与2%乙酰胆碱的等体积溶液对实验豚鼠进行气道激发试验,测量其喘息时间基数值与窒息倒地时间基础值,窒息倒地时间基础值<100s的豚鼠入选。按吸入钾的浓度将实验动物分为A、B、C组,在吸入不同浓度氯化钾10min后,对豚鼠进行气道激发试验并与基础值作自身对照。结果入选实验组的豚鼠采用20mg速尿建立低钾动物模型,与腹腔注射速尿前的血清钾值比较,差异有统计学意义(P<0.05)。雾化吸入补钾后30min、60min、120min、240min测定血清钾值与腹腔注射速尿前比较,差异无统计学意义(P>0.05),与腹腔注射速尿30min后血清钾值比较,差异无统计学意义(P<0.05)。A、B、C三组豚鼠吸入5%、10%、20%不同浓度的氯化钾,进行气道激发实验并与基础值做自身对照无统计学意义(P>0.05)。结论雾化吸入10%、20%的氯化钾可以在短时间内达到血药浓度高峰,可作为紧急快速补钾方法,5%的氯化钾雾化吸入可以作为维持治疗的方法,不同浓度氯化钾雾化吸入均不会引起实验豚鼠气道反应性增加。     

The effect of berberine chloride on experimental colitis in rats in vivo and in vitro

Berberine is an isoquinoline alkaloid with multiple pharmacological actions, including anti-inflammatory activity. The aims of this study were to examine the effect of berberine on the mucosal healing process and to investigate whether berberine can inhibit the increased production of interleukin-8 in trinitrobenzene sulfonic acid-induced colitis in rats. Berberine was administered orally for 3 days or 1 week at a dosage of 7.5 or 15 mg/kg/day. Tissue damage scores, body weight, colon wet weight, and colon wall thickness were measured, and myeloperoxidase activity in colon tissue was also examined. Histological lesions, morphological damage, and myeloperoxidase activity were reduced after 1 week of treatment with berberine at a dosage of 15 mg/kg/day. Furthermore, 1 week after trinitrobenzene sulfonic acid treatment, the production of interleukin-8 by cultured rectal mucosa or cardiac blood mononuclear cells with or without stimulation of lipopolysaccharide for 24 h was also analyzed by enzyme-linked immunosorbent assay. Cardiac blood mononuclear cells and rectal mucosa of normal rats produced substantial amounts of interleukin-8, which increased strikingly with the stimulation of lipopolysaccharide. Cardiac blood mononuclear cells and rectal mucosa of trinitrobenzene sulfonic acid-treated rats secreted more interleukin-8 than those of normal rats. The addition of berberine with a concentration of 10(-5) M to the culture media resulted in an inhibition of interleukin-8 production of rectal mucosa.