Permeability In Dogs Research Articles

A pathophysiological role of endogenous prostacyclin in endotoxin induced increase in lung vascular permeability in dogs

Escherichia coli endotoxin (1 mg/kg) infusion over 30 min into anesthetized artificially ventilated dogs caused a biphasic response: an early phase of pulmonary hypertension and a late phase of increased hung vascular permeability. During an early phase, PG F 2α, Tx A 2 (as Tx B 2) and prostacyclin (as 6-keto-PG F 1α) concentrations increased in plasma or right duct lymph of dogs. During a late phase, the concentrations of PG F 2α and Tx A 2 decreased to near the base-line values, while the concentration of prostacyclin remained elevated.Administrations of PG synthetase inhibitors 45 min prior to endotoxin inhibited the increase in concentration of prostacyclin following the infusion of endotoxin and potentiated the increase in lung vascular permeability at the beginning of the late phase. Continuous infusion of prostacyclin (20 ng/kg/min) starting one hour before endotoxin for 5 hour periods prevented the increase in lung vascular permeability induced by endotoxin. Based on these results, we could conclude that endogenous prostacyclin might play an important role in preserving cell integrity of lungs and counteract the deleterious effects of endotoxin.

Effect of temperature changes on intrapulpal pressure and hydraulic permeability in dogs

The purpose of this study was to examine the effect of temperature in the physiologic range (30 °–45 °C) on intrapulpal pressure and hydraulic permeability. A cylindrical channel was drilled by hand to the pulpo-dentinal junction in canine teeth of dogs. A threaded stainless steel cannula was screwed to a jam fit in the dentinal wall of the channel. A thermocouple for measuring temperature extended beyond the tip of the cannula to the pulp surface; a sidearm connected the cannula to a low compliance pressure transducer system. Nichrome heating wire, wound around the external tooth surface and held in place by acrylic coping, was used to alter tooth temperature. Before applying heat, the average initial values in the 13 teeth were: pulp pressure, 36mmHg, pulp temperature, 30.4 °C. As temperature was increased, pressure rose linearly with a slope averaging 2.5 mmHg/ °C. When temperature was returned to its original level, pressure declined at a less steep rate, averaging 1.6 mmHg/ °C. The pressure changes noted were due to temperature-induced alterations in vasomotor state rather than to thermal expansion and contraction of hard tissue, as indicated by the lack of any permanent baseline shift following microinjections. Pressure pulses whose amplitude varied directly with temperature were superimposed upon baseline pressure. Hydraulic permeability, determined by injecting small amounts of fluid from the microsyringe, was doubled by increasing the pulpal temperature from 30 ° to 40 °C, indicating a decreased resistance to fluid transport in the pulp at higher temperatures. Because of the difference in slopes upon increasing and decreasing temperature, pressure did not return to its initial value, but rose with each successive cycle throughout the experiment. Thus, the effect of temperature on pulp pressure had both reversible and irreversible components. We ascribe the reversible component to the direct effect of temperature on arteriolar dilatation, an explanation consistent with our observations on hydraulic permeability. The most likely explanation for the irreversible component is increased capillary permeability due to trauma, or sustained vasodilatation due to long-term neural or chemical influences.