Kinins, beta-adrenergic receptors and functional vasodilatation in the submaxillary gland of the cat

1. The close arterial infusion of bradykinin into the submaxillary gland of the cat produced a pronounced hyperaemia that could be blocked by simultaneous perfusion of the gland with blood containing carboxypeptidase B. Carboxypeptidase B, however, failed to reduce the vasodilatation of chorda tympani nerve stimulation suggesting that the kinins are not involved in the regulation of submaxillary gland blood flow.2. Isoproterenol injections produced pronounced salivary gland vasodilatation. Beta-adrenergic blocking drugs reduced or abolished the hyperaemia of isoproterenol and reduced that of chorda tympani nerve stimulation. The combination of beta-blocking drugs and atropine could abolish or reduce further this nerve induced hyperaemia.3. The above results suggest that stimulation of cholinergic and beta-adrenergic receptors could account for the chorda tympani induced hyperaemia. Conclusive proof of this possibility remains to be determined.     

THE INITIAL LESION IN EXPERIMENTAL ALLERGIC NEURITIS : A PHASE AND ELECTRON MICROSCOPIC STUDY

Experimental allergic neuritis (EAN) was produced in rats by the intradermal injection of an emulsion of peripheral nerve in Freund's adjuvant. Early lesions in perfused sciatic nerves were studied by phase, light, and electron microscopy at intervals up to 15 days following immunization. Circulating lymphocytes attached focally to the inner surface of blood vessels, primarily venules, to initiate parenchymal lesion formation. Attached cells had the hand mirror configuration typical of the motile lymphocyte. They subsequently flattened against the endothelial surface and then traversed the vascular wall by sinking into and passing through the cytoplasm of endothelial cells. The transgressor and transgressed cell membranes were intact and both cells retained their integrity. Lymphocytes began to transform and divide intravascularly; these events accelerated extravascularly. Although the migrating cells became larger and more pleomorphic in the perivascular regions, their essential character was in keeping with an origin from circulating lymphocytes. In many lesions, there was fluid with protein, possibly produced by the transformed extravascular cells. The described cellular events precede tissue damage and are likely instrumental in the myelin destruction which follows     

Waldenström's macroglobulinemia in a patient with a chronic biologic false-positive serologic test for syphilis

Acute and chronic biologic false-positive serologie reactions for syphilis (VDRL) have been associated with a variety of diseases. Several investigators emphasize that false-positive VDRL titers are usually very low. This report describes a 73 year old man with Waldenström's macroglobulinemia. The biologic false-positive serologic test for syphilis was recognized 33 years before the diagnosis of Waldenström's macroglobulinemia was made. VDRL titers were as high as 1:8192 and 1:32,000 during exacerbations of the macroglobulinemia. A biologic false-positive serologic test for syphilis is frequently associated with an elevated immunoglobulin M (IgM) level. It would be interesting to search for a relation between biologic false-positive serologic tests for syphilis and diseases characterized by monoclonal gammopathies.     

The effect of dichloromethylene diphosphonate,a pyrophosphate analog,on bone and bone cell structure in the growing rat

Dichloromethylene diphosphonate (Cl₂MDP) is a synthetic compound related in structure to inorganic pyrophosphate but is resistant to enzymatic and chemical degradation and is known to be a potent inhibitor of bone resorption. The administration of 20 mg/kg/day of Cl₂MDP for ten days to growing rats results in marked increases in metaphyseal mineralized tissue mass due to slowed bone resorption. There was an increase in resorption areas covering anorganic bone viewed by scanning electron microscopy (SEM), however, the resorption pits, or Howship's lacunae, in these resorption areas were smaller and less defined than those encountered in controls. The appearance of these large areas of poorly delineated resorption pits is likely due to an inhibition of bone resorption coupled with slowed bone formation. Administration of Cl₂MDP to growing rats also results in an increase in the numbers and size of osteoclasts. Because this would appear to be a histological paradox, in view of the ability of Cl₂MDP to slow bone resorption, the osteoclasts were examined by transmission electron microscopy (TEM). The ruffled borders and associated cytoplasmic vacuoles were generally less extensive in the Cl₂MDP-treated osteoclasts than in controls, even though clear zones were frequently seen. Examination of undecalcified light microscope sections reveal that the area of bone being degraded by adjacent osteoclasts was generally much smaller in the Cl₂MDP-treated animals than in controls. Thus the collaborating TEM observations of smaller ruffled borders, with the SEM observations of smaller, less-de-fined resorption pits, with the light microscope observations of smaller bone areas being degraded by individual osteoclasts provide a morphological basis for the observed decreases in bone resorption following Cl₂MDP administration.