Effect of lacto-N-neotetraose, asialoganglioside-GM1 and neuraminidase on adherence of otitis media-associated serotypes of Streptococcus pneumoniae to chinchilla tracheal epithelium.

The adherence of Streptococcus pneumoniae (Spn) otitis media-associated serotypes 3, 6A and 14 to ciliated chinchilla respiratory epithelium was investigated using a whole organ perfusion technique. We demonstrated that Spn adhere to chinchilla tracheal epithelium within 30 min and exhibit saturation kinetics indicating that the effect being observed is receptor mediated. Inhibition of adherence was achieved by prior incubation of Spn with lacto-N-neotetraose (LNnT) or asialoIganglioside GM1 (aGM1), recognized by glycoconjugate analogs of known Spn receptors. NeurIaminidase treatment of the tracheae increased Spn adherence in vitro and reversed the inhibition effect of LNnT suggesting that neuraminidase treatment resulted in an increase in the number of available receptors for Spn. The chinchilla trachea organ perfusion culture system used in this study imitates eustachian tube conditions more closely than isolated cell culture systems and is a useful model for investigating the role of Spn adherence in vitro in the pathogenesis of OM.

Whole blood viscosity in preeclampsia.

Whole blood viscosity was measured in 41 patients with preeclampsia and in 51 normotensive control subjects. The mean viscosity in the preeclamptic group had a highly significant elevation (t = 9.752, p less than 0.001, at a shear rate of 0.1 sec-1 and t = 4.223, p less than 0.001, at a shear rate of 100 sec-1). The slower shear rate gave the better discrimination between the two groups as only four patients with preeclampsia had a value within 1 SD of the mean of the control group. It is suggested that the measurement of whole blood viscosity may be clinically useful in the management of patients with preeclampsia.

The pathogenesis of hypertensive vascular changes in the rat: microscopic and ultrastructural correlation in vivo.

1. This study describes the changes observed in the rat microcirculation in vivo in the transparent tissue chamber of the rat back, during the florid hypertension produced by ligation of the rat aorta between both renal arteries. 2. Besides providing a new model for analysis of the action of therapeutic agents in hypertension, direct evidence of the variation in blood flow in hypertension is discussed. Fixation of the chamber tissues allows direct ultrastructural correlation with the altered function of particular vessels observed and recorded cinemicroscopically in vivo.

The mechanism of glycerol-induced acute renal failure.

Ten rabbits with transparent ear chambers were grafted with small pieces of kidney. The resulting vessel anastomosis and restoration of renal blood flow allowed continuous microscopic observations of functioning renal tissue in vivo. When the grafts were well established, acute renal failure was induced in the rabbit by glycerol injection. All cases showed similar changes. Within minutes the brisk blood flow within the renal grafts became progressively more sluggish until complete stasis was established. The initial change was a blanching of intertubular and glomerular capillaries with progressive dilation and stasis of renal veins. Only after almost complete cessation of blood flow in most graft vessels, generally after a further 10 minutes, was any change in arteries or arterioles observed. The afferent arterioles and then larger arteries showed constriction followed by complete stasis. The ear chamber vessels (nonrenal) continued to flow normally. Blood flow was slowly re-established in the grafts and by the next day was normal in the surviving rabbits. These studies provided visual in vivo evidence that the mechanism of glycerol-induced acute renal failure is mediated by a reversible renal ischemia and that the factors responsible act particularly on renal vasculature. However, the mechanism whereby blood flow ceases is obscure and it cannot be attributed to arterial or arteriolar constriction.