The intravenous injection into rats of dextran (average MW 70,000) 10 mg/100 gcaused marked hypotension after a delay of about 5 minutes. Blood samples collected by cardiac puncture at this time were tested for the amounts of prekallikrein activator (PKA) and kallikrein after acetone-and then kaolin activation of the plasminogen-free plasma. PKA was assayed by measuring the initial rate of release of benzoyl arginine esterase (BAEe) activity in a preparation of partially purified human prekallikrein, and kallikrein was assayed by measuring the BAEe esterase activity. Significant reductions of both parameters were registered, and the amount of high molecular weight kininogen (HMWK) present in the plasma was also reduced. Pretreatment of the rats with E-aminocaproic acid intraperitoneally (20Cb300 mg/100 g) abolished the dextran-caused decreases in the plasma levels of the above mentioned factors, and reduced the fall in blood pressure. The addition of purified human HMWK to the plasma before the acetone activation procedure was started, increased the yield of PKA activity in the final enzyme preparation. When PKA was assayed after kaolin activation of plasma at 0" using the method developed by Laake & Vennererd (1973a & b) for the determination of PKA (activated factor XII) in human plasma, no differences were registered between plasma from rats treated with dextran and plasma obtained from control rats. It is suggested that the low PKA activity of the acetone activated enzyme preparation from plasma of rats treated with dextran was due to the loss of HMWK or a fraction of HMWK.

The increases in the absorption of ouabain, phenolsulphonphthalein and pralidoxime caused by 17 mM sodium lauryl sulphate (SLS) from jejunal loops of anaesthetized rats were significantly reduced if sodium and chloride (Briseid et al., 1974) or chloride and bicarbonate were replaced by other ions in the loop fluid. Separate substitutions of sodium, chloride of bicarbonate did not significantly alter the SLS-caused absorption, except that the substitution of choline for sodium reduced the absorption of pralidoxime, both in the presence and in the absence of SLS. The increases in the absorption of phenolsulphonphthalein and pralidoxime caused by SLS were potentiated by theophylline (25 mM) and reduced by imidazole (25 mM). The addition of dibutyryl cyclic AMP (2.5 mM) to the loop fluid increased this absorption of the test substances. This effect was reduced by imidazole, but under the experimental conditions it was not potentiated by theophylline. Determinations of cyclic AMP in the rat intestinal mucosa showed that the level of this substance was significantly higher in the presence than in the absence of SLS. The experimental conditions were as described for the absorption experiments. It is concluded that the data obtained support the idea of an increased level of cyclic AMP as the main basis for the effect of SLS on the absorption.

Normal levels of factor XI1 and of high and low molecular weight kininogens (HMWK and LMWK) were registered in plasma specimens from 5 individuals who had developed anaphylactoid reactions upon injection of dextran during surgery (dextran reactors, DR). Factor XI1 was assayed as prekallikrein activator (PKA) activated with kaolin at 0 ' . and kininogen fractions were estimated through the release of kinin caused by plasma kallikrein or hog pancreas kallikrein (HPK). Subnormal levels of factor XI1 apparently present in plasma from one DR, and after affinity chromatography on a lysine-Sepharose column also in plasma from another DR, were normalized by addition of plasma deficient in factor XI1 or by addition of purified HMWK.Treatment of plasma from DR with acetone ( 2 5 % v/v) induced a conversion of HMWK into a state which was non-functional as a cofactor in the surface-dependent activation of factor XII, and the passage of plasma from DR through a lysine-Sepharose column altered the HMWK present to a substance that released kinin only very slowly by incubation with HPK. It is concluded that the treatments mentioned will favour the activation in plasma from DR of a factor that will cause the conversion of HMWK. Previous experiments with rat plasma demonstrated that plasmin and also a plasmin-like factor without affinity for lysine-Sepharose were able to destroy the capacity of HMWK to function as a cofactor in the surface-dependent activation of factor XII, without a corresponding release of kinin.

The intravenous injection into rats of dextran with a molecular weight of 1,000 (LMr dextran) in doses 200 mg/kg induced rapid, but transient falls in blood pressure. Pretreatment of the rats with LMr dextran 200 mg/kg caused a partial inhibition of the profound blood pressure fall induced by the injection of clinical dextran with a molecular weight of 70,000 (HMr dextran), 40 mg/kg. In accordance with previous works (Briseid & Berstad 1981; Berstad & Briseid 1982; Berstad 1982) it was found that the intravenous injection of HMr dextran lowered the plasma levels of plasminogen proactivator (pro‐PGA) and functionally active high molecular weight kininogen (HMrK). Also LMr dextran, 200 mg/kg, induced significant reductions in the mentioned parameters, but less extensive than those obtained by HMr dextran, 40 mg/kg, and pretreatment of the rats with LMr dextran inhibited the subsequent effects of HMr dextran. It is suggested that a dextran‐activated plasminogen activator might be an early link in the mechanism underlying the dextran‐induced state of shock in the rat.

The level of cyclic AMP in the jejunal mucosa from tied loops of anaesthetized rats was found to be significantly increased (27-50%) when sodium lauryl sulphate (SLS) was added to the loop fluid (2-27 mM). Imidazole (25 mM) did not significantly alter the resting level of cyclic AMP, but reduced the increase caused by SLS (17 mM). Theophylline (25 mM) significantly increased the intestinal level of cyclic AMP, and potentiated the increase caused by SLS. Ouabain (2.5 mM) did not alter the level of cyclic AMP in the presence or in the absence of SLS. The results of previous experiments on the increases in intestinal absorption caused by SLS or by dibutyryl cyclic AMP (Briseid et al., 1974, 1976) are discussed in light of the present data. It is concluded that the SLS-effect on absorption can only partly by ascribed to its effect on the intestinal level of cyclic AMP.