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Tight junctions are located at the luminal aspect of adjacent epithelial cells and form a barrier that limits the paracellular diffusion of hydrophilic solutes. In recent years, evidence has accumulated to indicate that tight-junction permeability is regulated by the absorption of various nutrients. In this review, we present the physiological basis and importance of tight-junction regulation in intestinal epithelium. The molecular structure of tight junctions and their interactions with the cell cytoskeleton as well as the physical and chemical forces that influence tight junction permeability are described. Much of this review addresses the controversial Pappenheimer hypothesis, which states that a major portion of intestinal glucose absorption occurs through tight junctions and not by saturable transcellular active transport. The absorption of a significant portion of glucose through tight junctions requires increased junctional permeability, a very high intralumenal glucose concentration, and a sufficient osmotic gradient to promote volume flow.

Although the number of cardiovascular deaths associated with environmental tobacco smoke cannot be predicted with absolute certainty, the available evidence indicates that environmental tobacco smoke increases the risk of heart disease. The effects of environmental tobacco smoke on cardiovascular function, platelet function, neutrophil function, and plaque formation are the probable mechanisms leading to heart disease. The risk of death due to heart disease is increased by about 30% among those exposed to environmental tobacco smoke at home and could be much higher in those exposed at the workplace, where higher levels of environmental tobacco smoke may be present. Even though considerable uncertainty is a part of any analysis on the health affects of environmental tobacco smoke because of the difficulty of conducting long-term studies and selecting sample populations, an estimated 35,000-40,000 cardiovascular disease-related deaths and 3,000-5,000 lung cancer deaths due to environmental tobacco smoke exposure have been predicted to occur each year. The AHA's Council on Cardiopulmonary and Critical Care has concluded that environmental tobacco smoke is a major preventable cause of cardiovascular disease and death. The council strongly supports efforts to eliminate all exposure of nonsmokers to environmental tobacco smoke. This requires that environmental tobacco smoke be treated as an environmental toxin, and ways to protect workers and the public from this health hazard should be developed. According to a 1989 Gallup survey commissioned by the American Lung Association, 86% of nonsmokers think that environmental tobacco smoke is harmful and 77% believe that smokers should abstain in the presence of nonsmokers.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of peak airway pressure (Paw) on vascular permeability and the "safety factor" against edema formation was determined in isolated blood-perfused lower lobes of dog lungs. Microvascular permeability was evaluated using the measured filtration coefficient (Kf,C), isogravimetric capillary pressure (Pc,i), and critical capillary pressure (Pcrit) for exhaustion of tissue safety factors. Airway pressure was maintained constant at -3 cmH2O except for the test period of 20 min when the lungs were ventilated at 6/min with sufficient volume to generate a peak inflation pressure ranging from 5 to 60 cmH2O. Mean Kf,C (in ml X min-1 X cmH2O X 100 g-1) were measured before and immediately after the period of peak airway pressures. Kf,C was significantly increased in all lungs where Paw exceeded 42 cmH2O, but in only two experiments at a lower Paw. Mean Pc,i was significantly reduced from control in the 45-55 and 55-65 cmH2O Paw groups, and both Pc,i and Pcrit were found to be inversely related to Kf,C measured after Paw ventilation. These data indicate that ventilation with Paw above 42 cmH2O (30.9 Torr) and in some cases lower pressures for 20 min significantly increased capillary hydraulic conductivity, reduced the effective osmotic effect of plasma proteins at the capillary wall, and reduced the total tissue safety factor against edema formation.