Apparent inconsistencies in the results of previous studies led us to reexamine the process by which fluid leaves the lungs of newborn rabbits after birth. We measured pulmonary blood volume, extravascular lung water, and the size of perivascular cuffs of fluid in frozen sections of lung obtained from 166 full-term rabbits (31 days gestation) born vaginally or by cesarean section. We killed the rabbits by giving them barbiturate intraperitoneally and immersing them in liquid nitrogen before they breathed or at randomly predetermined intervals from 5 min to 24 h after birth. We found that a) pulmonary blood volume of both groups of rabbits increased soon after birth, b) extravascular lung water per gram of dry lung tissue was greater at birth in rabbits born by cesarean section than in those born vaginally, c) extravascular lung water did not begin to decrease in either group of animals until 30-60 min postnatally, after which it decreased progressively for 24 h, and d) the rate of fluid clearance and pattern of puddling around pulmonary vessels was similar in both groups of rabbits, with maximal perivascular cuffs 30 min after birth, followed by diminution of cuff size as the lungs shed water.

To study lung fluid balance before and after birth, we measured lung lymph flow and concentrations of protein in lymph and plasma of 22 unanesthetized fetal lambs and compared results with previous studies done on 26 newborn lambs, 1-2 wk old. Lymph flow, relative to lung mass, was less in fetuses than in newborns; lymph protein clearance was not significantly different. Less lymph flow before birth probably reflects less available surface area for fluid exchange in microcirculation of fetal lungs, compared with newborn lungs, with no difference in endothelial permeability to protein. Extravascular lung water, measured gravimetrically for 24 fetuses (10 without labor, nine in labor, five 6 h after vaginal birth), decreased by 45% (15 +/- 2 g/kg body wt) before birth and by an additional 38% (6 +/- 1 g/kg) after birth. In five lambs killed after birth, we measured lung lymph flow before and during labor and for 6 h after breathing began. Lymph flow was unaffected by labor but increased transiently after birth, accounting for 11% of the liquid removed from lungs postnatally. Liquid clearance studies performed in eight anesthetized 3-wk-old lambs confirmed the observation that lung lymphatics drain only a small fraction of liquid in potential air spaces. Most of that liquid probably leaves the lungs directly through pulmonary circulation.

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We investigated the physiologic effects of normal saline versus 5% albuminated saline fluid resuscitation on 10-12-day-old piglets infected with group B streptococci for four hours. After intravenously receiving 1 x 10" bacteria/kg over 45 minutes, one group was untreated while the two fluid-treated groups received enough intravenous fluid to maintain the baseline cardiac output. An increase in the resistance to venous blood return was the major limitation to cardiac output. The resistance nearly quadrupled in the untreated piglets as shown by a 50% decrease in cardiac output with a nearly doubling of the driving pressure for venous return (mean circulatory pressure was normal and atrial pressures decreased by 70%). In both fluid-treated groups, resistance doubled as shown by an unchanged cardiac output with a doubling of the driving pressure (mean circulatory pressure increased by 50%) and atrial pressures remained at baseline). Blood volume was 9% below control in the untreated group and 13% above control in both fluid-treated groups. Much more crystalloid (155 ml/kg) than colloid (58 ml/kg) was necessary to maintain baseline cardiac output; this resulted in a 36% decrease in the plasma protein oncotic pressure of the former group and a 15% increase in the oncotic pressure of the latter group. Organ edema formation (ileum, pancreas, kidney, adrenal gland, lung) occurred only in the saline-treated animals. We conclude that increased resistance to venous return was the primary cause of shock in our model and that this can be effectively treated by giving enough intravenous fluid to elevate the mean circulatory pressure. However, if the plasma protein oncotic pressure is also lowered (saline group), organ edema results. Since fluid resuscitation is basic to the treatment of septic shock, we wished to see if crystalloid versus colloid fluid therapy might differentially affect cardiovascular function or organ edema. To assess these two processes, we treated 10-12-day-old piglets, infected with GBS for 4 hours, with enough normal saline or 5% albuminated saline to maintain baseline cardiac output. As opposed to most clinicians, who focus on cardiac factors as the only determinants in shock, 5 we found that the major factor limiting cardiac output in all infected animals was an increased resistance to venous blood return. Cardiac output, which fell markedly in the untreated piglets, could be brought back to normal and organ blood flow improved with either type of fluid therapy if enough fluid was given to elevate the blood volume and the upstream driving pressure for venous return (mean circulatory pressure). There has long been a controversy over the differential effects of crystalloid versus colloid fluids on organ edema, especially pulmonary edema, in septic shock. 6 We found organ edema (ileum, pancreas, kidney, adrenal gland, lung) only in the crystalloidtreated animals, possibly due to a significant decrease of plasma protein oncotic pressure in association with the elevation of mean circulatory pressure. Mater...