Intestinal atresia and necrotizing enterocolitis: Embryology and anatomy.

The primitive gut originates at week 3 of gestation from the endoderm, with posterior incorporation of the remaining embryo layers. Wnt, Notch and TLR4 pathways have been shown to play central roles in the correct development of the intestine. The classical hypothesis for intestinal atresia development consists of failure in bowel recanalization or a vascular accident with secondary bowel reabsorption. These have been challenged due to the high frequency of associated malformations, and furthermore, with the discovery of molecular pathways and genes involved in bowel formation and correlated defects producing atresia. Necrotizing enterocolitis (NEC) has a multifactorial pathogenesis with prematurity being the most important risk factor; therefore, bowel immaturity plays a central role in NEC. Some of the same molecular pathways involved in gut maturation have been found to correlate with the predisposition of the immature bowel to develop the pathological findings seen in NEC.

Paraquat poisoning: evidence of systemic toxicity after dermal exposure.

Exposure of the scrotal skin to a concentrated paraquat solution led to renal and respiratory failure and to hepatic damage with eventual recovery of the patient. Dermal exposure to paraquat, especially to the scrotum may produce serious systemic toxicity.

Accelerated hypertension in the rat: relation between renin, renal vascular lesions, salt intake and blood pressure.

1. Complete ligation of the aorta between the origins of the two renal arteries in the rat produces a predictable form of accelerated hypertension. Changes in the blood pressure, plasma renin activity and renal histological lesions have been studied. 2. Group 1 rats and their control group (group 2) received tap water, and group 3 and its control group (group 4) received sodium chloride solution (0-154 mol/l) in place of tap water, for 4 weeks before aortic ligation. In the experimental groups 1 and 3, complete ligation was carried out. In groups 2 and 4 the aorta and renal arteries were exposed, but not ligated. Interlobular artery lesions were studied on a blind basis and graded 0-4 according to severity. 3. Groups 1 and 3 developed severe hypertension. In group 1 the raised mean arterial pressure showed a significant correlation with increased plasma renin activity. Both mean arterial pressure and plasma renin activity also showed a significant correlation with changes in interlobular arteries. In group 3 the raised mean arterial blood pressure did not show a significant correlation with the depressed plasma renin activity, or with changes in interlobular arteries. A significant correlation was, however, found between plasma renin activity and interlobular artery lesions in group 3. 4. These results suggest that the renin-angiotensin system may influence renal vascular lesions through some mechanism independent of the blood pressure.

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.