Some workers in the Danish furniture industry are specific IgE sensitized against pine wood dust. Pine-specific IgE probably explains a minor part of the respiratory symptoms in workers exposed to pine wood dust.

Vasoactive intestinal polypeptide (VIP) is a neuropeptide that causes neurone excitation in the brain cortex. VIP receptors were studied in subcellular fractions isolated from rat cerebral cortex. The receptor binding of 125I‐VIP was greatest in the synaptosomal fraction at membrane protein concentrations of 50–100 μg/ml, a temperature of 37°C, and a pH from 7.4 to 7.7. Under these conditions the concomitant proteolytic degradation of 125I‐VIP was approximately 10% after 60 min of incubation. The binding of 60 pmoI/L 125I‐VIP reached steady‐state after 60 min and was maintained up to 240 min. At steady‐state, the receptor‐bound 125I‐VIP was displaced by unlabelled VIP with half‐maximal inhibition (IC50) at a concentration of approximately 3 nmol/L. The binding of 125I‐VIP in the concentration range of 10 pmol/L to 6 nmol/L was superimposable on the VIP displacement curve. The Scatchard plot was curvilinear with upward concavity, which can be interpreted to represent two classes of receptors with KD of 2.5 and 125 nmol/L, one class of receptors with negative cooperative interactions, or heterogeneity of the 125I‐ VIP preparation. The total amount of receptors was 9.5 pmol/mg of membrane protein. Secretin displaced receptor‐bound 125I‐VIP with an IC50 of 0.3 μmol/L, whereas glucagon snowed no inhibition up to 1 μmol/L. The dissociation of receptor‐bound 125I‐VIP was biexponential with rate constants (k2) of 4.1 – 10−3 and 0.18 min−1 corresponding to half‐times of approximately 170 and 4 min, respectively. The size of the two components was dependent on the duration of the 125I‐VIP association period. Initially, both components increased; at steady‐state, the rapid component declined, whereas the slow component increased to approximately 70% after 120 min. The association rate constants (k1) were estimated from the initial velocities as 106 and 4. 106 L. mol−1. min−1, and a calculation of the KD as k2/k1 gave values of 4.1 and 45 nmol/L, respectively. In conclusion, the presence of receptors for VIP on synaptosomes from the cerebral cortex supports the role of VIP as a neurotransmitter in the brain. The receptor binding was heterogeneous, suggesting the presence of two classes of receptors. The binding kinetics showed a time‐dependent transition of VIP receptors from a low‐ to a high‐affinity state, which may be interpreted as desensitisation of synapses to the action of VIP.

The concentration of vasoactive intestinal polypeptide (VIP) was determined in peripheral venous plasma from 136 patients with liver cirrhosis without gastrointestinal bleeding or coma and from 112 controls. In eight patients (cirrhosis, six; fibrosis, one; steatosis, one) arteriovenous extraction or release of VIP was measured during catheterization at four locations: brain, lower limb, intestine-liver, and kidney. The mean concentration of VIP in peripheral venous plasma from patients with cirrhosis was 9.4 pmol/l (median, 7.0; range, 0-86), which was significantly higher than that of the controls, who had a mean of 6.2 pmol/l (median, 6.0; range, 0-20, P less than 0.01). No significant extraction or release of VIP could be detected across the vascular bed in brain or lower limb. A significant arterio-hepatovenous VIP extraction ratio (mean, 0.43; range, 0.05-0.87) confirmed at net splanchnic elimination of VIP from extra-splanchnic areas and from porto-systemic shunting of VIP in cirrhosis. The net splanchnic elimination rate of VIP was estimated to be about 3 pmol/min. The concentration of VIP in ascitic fluid was on the average three times that of arterial plasma. In conclusion, VIP is significantly elevated in peripheral plasma from patients with cirrhosis, probably due to porto-systemic shunting and/or compromised hepatic elimination. Hepatic elimination is still likely to account for the inactivation of most of the VIP escaping from the neurosynapses throughout the body in patients with cirrhosis without coma.