Lymph Protein Concentration Research Articles

Redistribution of regional lymph to the thoracic duct in rats during heat stress.

The protein concentration of the thoracic duct lymph and the amount of protein transported by the thoracic duct decreased during an acute heat stress in rats. The changes in regional lymph flow into the thoracic duct were calculated and the ratio of the lymph from the skin increased 13% and that from the visceral organs decreased 6% during heat stress.

Modification of lymph by lymph nodes. III. Effect of increased lymph hydrostatic pressure.

Previous studies have shown that lymph nodes function as fluid exchange chambers in which the protein concentration of lymph is changed in the direction required to establish equilibrium of the Starling forces acting across the nodal blood-lymph barrier. We examined the effect of increased lymph hydrostatic pressure on efferent lymph by use of an isolated dog popliteal node preparation in which lymph having a protein concentration averaging 27.6 +/- 1.2% (SD) of that of plasma was infused into the node at a flow rate averaging 45.6 +/- 0.2 (SD) microliter/min. We compared steady-state values of prenodal and postnodal lymph flow and protein concentration following step increases in efferent lymph pressure from 0 to over 15 mmHg. Increasing efferent lymph pressure to values less than about 8 mmHg caused the efferent lymph protein concentration to increase; however, further increases in lymph pressure caused the lymph protein concentration to decrease to values approaching those attained at very low lymph pressures. We suggest that the failure of high lymph pressure to increase lymph protein concentration might be caused by blood vessel collapse within the node, a condition believed to increase nodal blood capillary pressure and to decrease blood-lymph barrier filtration coefficient. An important finding was that increasing efferent lymph pressure caused significant amounts of lymph proteins to be lost during nodal transit. Therefore, it appears that increasing efferent lymph pressure to very high values has little effect on lymph protein concentration but has great effect on postnodal lymph protein flux.

The long-term collection of lymph from single lymph nodes of foetal lambs in utero.

Surgical techniques are described for the long-term collection of lymph from both prescapular efferent lymph ducts of foetal lambs in utero. Lymph ducts in foetal lambs 95 to 136 days post-conception were cannulated with a high rate of success. Lymph flow from the cannulas was not compromised by deliberate primary or secondary challenge of the lymph nodes with a wide variety of antigens, and often continued for long periods after the lambs were born naturally. The techniques allow cellular and humoral lymph-borne immune responses of foetal lambs to authentic primary antigenic challenge to be studied in utero, uncomplicated by any previous experience of antigens. Loss of lymphocytes from the cannulated ducts depleted the numbers of cells in the lymph, but lymph protein concentrations were unaffected by lymph drainage.

Lymph flow, lymph protein concentration, and protein output from rat small intestine.

Lymph flow (JL), lymph protein concentration (CL), and protein output (JP) from the main intestinal lymph duct were determined. The basal JL from the mesenteric pedicle alone was the same as that from the mesenteric pedicle attached with a segment of the nonabsorbing intestine, indicating that the basal JL does not originate from the intestine but is totally from the region of the mesenteric pedicle. The basal CL was 3.5-3.8 g/100 ml. When the intestine was absorbing water, JL increased and CL decreased, but JP increased above the basal JP in the initial 20 min of water absorption and then decreased progressively with time. Furthermore, it was estimated that CL in the "excess lymph" (formed during water absorption) was 1.4 +/- 0.2 g/100 ml in the initial 10 min of water absorption and was zero or nearly so in the later periods. From this and other evidence, it is concluded that under various conditions without net water absorption rat small intestine does not produce lymph and that during water absorption there is no significant increase in capillary permeability or capillary filtration. Therefore, the excess lymph could be mostly derived from the fluid absorbed from the lumen of the intestine.

1540 MECHANISM OF INCREASED LUNG FLUID FILTRATION DURING LIPID INFUSION IN LAMBS

Intravenous lipid infusion in newborn lambs causes acute pulmonary hypertension followed by a sustained increase in lung lymph flow and reduction in lymph protein concentration (Teague et al, Pediatr Res 18:313A, 1984). We found that plasma concentrations of the pulmonary vasoconstrictors thromboxane B2 and serotonin (5-HT) both increased during lipid infusion in lambs. To see if these vasoactive substances might play a role in the lung microvascular changes associated with lipid infusion, we pretreated 14 lambs with suitable inhibitors: 8 received indomethacin (1-5 mg/kg/h for 6h) and 6 received a 5-HT blocker, methysergide (0.6 mg/kg/d for 2d) before and during lipid infusion. We measured pulmonary artery (Ppa) and left atrial pressures, lung lymph flow (QL), and lymph and plasma protein concentrations during a 2-4h control period followed by 6h of constant lipid infusion, 0.25 g/kg/h. Indomethacin alone increased Ppa and QL, but lipid infusion in the presence of indomethacin caused no further increases of either Ppa or QL. Methysergide reduced steady-state QL without preventing the acute pulmonary hypertension associated with lipid infusion. In 6 lambs, intravenous infusion of 5-HT (4-6 μg/kg/min for 5h) increased QL without affecting Ppa. These results suggest that cyclooxygenase products of arachidonic acid metabolism may cause the acute pulmonary hypertension that occurs during lipid infusion, whereas 5-HT may be responsible for the steady-state increase in lung fluid filtration.

Inspiratory airway obstruction does not affect lung fluid balance in lambs.

The purpose of this study was to examine the effects of inspiratory airway obstruction on lung fluid balance in newborn lambs. We studied seven 2- to 4-wk-old lambs that were sedated with chloral hydrate and allowed to breathe 30-40% O2 spontaneously through an endotracheal tube. We measured lung lymph flow, lymph and plasma protein concentrations, pulmonary arterial and left atrial pressures, mean and phasic pleural pressures and airway pressures, and cardiac output during a 2-h base-line period and then during a 2- to 3-h period of inspiratory airway obstruction produced by partially occluding the inspiratory limb of a nonrebreathing valve attached to the endotracheal tube. During inspiratory airway obstruction, both pleural and airway pressures decreased 5 Torr, whereas pulmonary arterial and left atrial pressures each decreased 4 Torr. As a result, calculated filtration pressure remained unchanged. Inspiratory airway obstruction had no effect on steady-state lung lymph flow or the lymph protein concentration relative to that of plasma. We conclude that in the spontaneously breathing lamb, any decrease in interstitial pressure resulting from inspiratory airway obstruction is offset by a decrease in microvascular hydrostatic pressure so that net fluid filtration remains unchanged.

Oxygen-induced lung microvascular injury in neutropenic rabbits and lambs.

We did two studies to see if severe neutropenia might reduce the severity or delay development of O2-induced lung microvascular injury. First, we treated 11 rabbits with nitrogen mustard until their circulating neurophil count decreased to less than 50/microliters of blood, after which the rabbits breathed pure O2 until death; nine other rabbits received no nitrogen mustard and had normal numbers of circulating neutrophils during O2 breathing. All rabbits died of respiratory failure with pulmonary edema, and although chemotherapy decreased the number of neutrophils in the lungs by greater than 90%, it did not influence survival time or extravascular lung water content. To see if severe neutropenia might slow the development of O2-induced lung microvascular injury, we assessed the effects of sustained hyperoxia on lung fluid balance in unanesthetized lambs treated with hydroxyurea, so that their absolute neutrophil count was less than 50/microliters of blood. We measured pulmonary arterial and left atrial pressures, cardiac output, lung lymph flow, and concentrations of protein in lymph and plasma during a 2- to 4-h control period and then daily for 2 to 4 h as the lambs continuously breathed pure O2. After 3 days of hyperoxia, lymph flow doubled and the concentration of protein in lymph increased from 3.3 +/- 0.5 to 4.2 +/- 0.3 g/dl. Tracer studies with 125I-albumin before and 3 days after the start of O2 breathing confirmed the development of increased lung vascular permeability to protein. All lambs died of respiratory failure with pulmonary edema after 3-5 days in O2.(ABSTRACT TRUNCATED AT 250 WORDS)

Tubuloglomerular feedback in hypertensive rats of the Milan strain.

In rats of the Milan hypertensive strain (MHS) the disease can be transplanted with the kidney to rats of the Milan normotensive strain (MNS). It has been found that GFR, salt and volume regulation differ between MHS and MNS rats. Tubuloglomerular feedback control mechanism (TGF) is important for body volume regulation and we therefore wanted to study the TGF control in MHS and MNS rats. Whole kidney and micropuncture experiments were done before and during saline volume expansion (5% of body weight). In an initial series of experiments measurements were made of total kidney GFR, urine excretion rate of sodium and potassium and subcapsular interstitial hydrostatic pressure (psc); interstitial oncotic pressure (pi int) was estimated from hilar lymph protein concentration. In a second series, proximal tubular stop-flow pressure (psf) was determined upstream from a wax block while the distal nephron was being perfused with Ringer solution at a flow rate varying from 0 to 40 nl X min-1. In this way the maximal drop in stop-flow pressure (delta psf) and also the turning point (TP), the tubular flow rate at which 50% of this response was achieved, could be determined after saline volume expansion and after 2 h of complete ureteral occlusion. The results showed that GFR was similar in MHS and MNS rats in the control situation, but that during volume expansion it was significantly lower in the MHS group. Interstitial psc and pi int and net interstitial pressure (psc - pi int) were similar in MHS and MNS rats both under control conditions and during volume expansion.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of a body burn on the lung response to endotoxin.

Our purpose was, in general, to determine the effect of a body burn on the pulmonary response to endotoxemia and, specifically, to determine whether increased thromboxane (TxA2) production by the burn wound was responsible for the accentuated lung injury. Thirty-two unanesthetized sheep with lung and soft tissue lymph fistulae were studied. Twelve sheep were given a sublethal dose of intravenous E. coli endotoxin (2 micrograms/kg). A characteristic two-phase injury was noted as evidenced by early pulmonary hypertension and hypoxia and later increased lung permeability. TxA2 was significantly increased in lung lymph as well as aortic plasma relative to venous plasma, indicating the lung to be the source. Twelve of 12 sheep survived. Five of 13 sheep died from endotoxemia when given 3-5 days after a 25% total body surface (TBS) burn and five of seven died with endotoxin (2 micrograms/kg) and a 50% burn. Physiologic parameters were at preburn levels before endotoxin. Animals died both during the early phase from hypoxia and the later phase due, in large part, to increasing pulmonary dysfunction. Absolute levels of TxA2 were not increased in the postburn animals, nor was there a clear release of TxA2 from burn tissue to explain the accentuated response. Prostacyclin levels were, however, less elevated in postburn animals in response to endotoxin, thereby altering the TxA2/PGI2 ratio in favor of TxA2. However, a cause and effect relationship between the increased lung injury and TxA2 remains undetermined. Lymph flow or lymph protein content was not altered in burn tissue in response to endotoxin.

Effect of outflow pressure on lung lymph flow in unanesthetized sheep.

Studies in anesthetized animals have shown that the flow rate from lung lymphatics (QL) depends on the pressure at the outflow end of the vessels (Po). We tested this in unanesthetized sheep prepared with chronic lung lymph cannula. We measured QL with the lymph cannula held at various heights above the olecranon and calculated Po as the height + QL X cannula resistance. QL decreased with increases in Po (delta QL/delta Po = -8.2 +/- 6.4 microliter X min-1 X cmH2O-1, mean +/- SD). We increased QL by raising left atrial pressure or infusing Ringer solution or Escherichia coli endotoxin and found that QL was even more sensitive to Po (delta QL/delta Po = -32 +/- 22). Cannula resistance caused a 9-70% reduction in QL. Changes in QL caused by increasing Po were not associated with changes in lymph protein concentration for up to 330 min. This indicates that increases in Po shunt lymph away from cannulated vessels but do not substantially effect microvascular filtration rate. The shunted lymph may flow into other vessels or collect in the lung. We conclude that QL does not accurately represent microvascular filtration rate because it depends on the cannula resistance and position at which the investigator chooses to place the cannula.

The pathophysiology of smoke inhalation injury in a sheep model.

This study describes an experimental model of smoke inhalation injury in sheep, in which the same pathophysiologic alterations occur as with clinical inhalation in man. Both the patients and the experimental sheep develop diffuse pulmonary mucosal sloughing, pulmonary edema, and a decrease in systemic oxygen tension. The results of this study indicate that the pulmonary edema is the result of an increase in microvascular permeability, characterized by increases in lung lymph flow (Qlym), lymph-to-plasma protein concentration ratio (L/P), and transvascular protein flux (Qlym X lung lymph protein concentration), while pulmonary vascular pressures remain constant. Neutrophil degranulation may contribute to the increased microvascular permeability.

Modification of pulmonary responses to endotoxemia in awake sheep by steroidal and nonsteroidal anti-inflammatory agents.

The effects of intravenous infusions of Escherichia coli endotoxin on white blood cell counts, hemodynamics, gas exchange, body temperature, and lung lymph flow were studied in chronically instrumented unanesthetized sheep. Six sheep received endotoxin (0.5 micrograms/kg) in the presence and absence of methylprednisolone treatment. Six sheep received the same dose of endotoxin with and without meclofenamate and methylprednisolone infusion. Endotoxemia caused an early increase in pulmonary artery pressure from 15.5 +/- 1.3 (mean +/- SEM) to 52.7 +/- 2.1 cmH2O (p less than 0.05), an initial phase of high flow of protein-poor lung lymph, an elevation in core body temperature, severe leukopenia, and an early increase in the alveolar to arterial oxygen difference (AaPO2) from 7.4 +/- 2.5 mmHg to 35.9 +/- 2.5 mmHg (p less than 0.05). From 2 to 5 h after endotoxin infusion, lung lymph flow averaged 4.8 times that of the baseline measurement, although lymph protein concentration relative to plasma was not different from the baseline measurement. Peripheral leukopenia and significantly increased AaPO2 (28.8 +/- 4.5 mmHg) persisted at 2 to 5 h. Methylprednisolone attenuated the early pulmonary artery hypertension (43.0 +/- 3.4 cmH2O), but did not inhibit the initial febrile response, severe leukopenia, or the early increase in AaPO2 (29.2 +/- 1.6 mmHg) in response to endotoxemia. Methylprednisolone did prevent the late phase increase in lung lymph flow, significantly attenuated the late phase leukopenia and hypoxemia (AaPO2, 13.3 +/- 5.9 mmHg), and attenuated accumulation of granulocytes in peripheral lung tissue throughout the endotoxin reaction.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the microcirculation in ethanolinduced mucosal injury in the dog

The aim of the present study was to assess the role of the intestinal microcirculation in the mucosal injury induced by intraenteric ethanol. Mucosal injury was assessed histologically in the ileum and jejunum and quantitated in the ileum by measuring clearance of albumin (37 Å, radius) and β-lactoglobulin A (27 Å, radius). A steady-state analysis of the forces and flows governing transcapillary fluid movement was performed in autoperfused segments of jejunum and ileum. In the jejunum and ileum ethanol induced the formation of subepithelial blisters in 10%–40% of the villi. In the ileum, ethanol (5%, vol/ vol) increased the clearance of both proteins but the ratio of lactoglobulin to albumin clearance decreased, indicating that the selectivity of the mucosal membrane was diminished. In both the jejunum and ileum ethanol produced similar alterations in the forces governing transcapillary fluid exchange. Ethanol increased the filtration coefficient (35%–40%), but did not alter the osmotic reflection coefficient of intestinal capillaries, indicating that surface area increased whereas vascular permeability was not affected. Capillary pressure increased (2–3 mmHg) whereas interstitial (lymph) protein concentration decreased resulting in an increase in the transcapillary oncotic pressure gradient (1–2 mmHg). The net result of the alterations in the forces governing transcapillary movement was only a doubling of the transcapillary filtration rate (lymph flow). It is concluded that the ethanol-induced increase in mucosal permeability to macromolecules cannot be explained solely on the basis of alterations in the forces and flows governing transcapillary fluid exchange in the small intestine.

Effect of neurotensin on intestinal capillary permeability and blood flow

Experiments were performed in 10 cats of either sex to ascertain the effects of postprandial arterial plasma concentrations of neurotensin (NT) on intestinal capillary permeability and blood flow. NT was infused intra-arterially into an isolated perfused loop of terminal ileum to produce a 182 +/- 15 (SE) pM plasma NT concentration. Intestinal lymph (L) and plasma (P) protein concentrations were measured at various venous pressures under control conditions and during NT infusion. The osmotic reflection coefficient (sigma d) was estimated under all conditions assuming sigma d = 1 - L/P at high capillary filtration rates. NT infusion significantly (P less than 0.001) reduced sigma d to 0.73 +/- 0.02 (SE) from a control level of 0.91 +/- 0.01. NT infusion also significantly increased intestinal blood flow [47.0 +/- 4.3 (SE) ml X min-1 X 100 g-1] versus control (36.6 +/- 3.2 ml X min-1 X 100 g-1), a 28.4% increase. Intestinal vascular resistance was decreased from 3.21 +/- 0.31 to 2.42 +/- 0.28 mmHg X min X ml-1 X 100 g in the absence of a change in local mean arterial blood pressure. Pore-stripping analysis of lymph and plasma solute fractions during NT infusion at high lymph flows predicted two populations of pores, 330-A and 46-A radius, accounting for 31 and 67%, respectively, of the total transcapillary hydraulic flow. NT infusion preferentially increased large-pore radius as a means of increasing intestinal capillary permeability. The rates of small- to large-pore areas and numbers were 106:1 and 5,225:1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of asphyxia on lung fluid balance in baby lambs.

The purpose of this study was to assess the effects of combined hypoxia and hypercapnia and of severe asphyxia on lung water balance and protein transport in newborn lambs. We studied ten 2-4-wk-old anesthetized lambs which were mechanically ventilated first with air for 2-3 h, then with 10-12% oxygen in nitrogen for 2-4 h, and then with 10-12% oxygen and 10-12% carbon dioxide in nitrogen for 2-4 h. Next we stopped their breathing for 1-2 min to produce severe asphyxia, after which we followed their recovery in air for 2-4 h. In 5 of the 10 lambs we intravenously injected radioactive albumin and measured its turnover time between plasma and lymph during the baseline period and after recovery from asphyxia. During alveolar hypoxia alone, mean pulmonary arterial pressure increased 60% and lung lymph flow increased 74%, whereas lymph protein concentration decreased from 3.47 +/- 0.13 to 2.83 +/- 0.15 g/dl. Cardiac output, left atrial pressure, and plasma protein concentration did not change. When carbon dioxide was added to the inspired gas mixture, pulmonary arterial pressure increased 22%, cardiac output increased 13%, lung lymph flow increased 33%, and lymph protein concentration decreased from 2.83 +/- 0.15 to 2.41 +/- 0.13 g/dl. Left atrial pressure and plasma protein concentration did not change. After 60-90 s of induced asphyxia, vascular pressures and lung lymph flow rapidly returned to values the same as those obtained during the baseline period. The turnover time for radioactive albumin between plasma and lymph was the same between the baseline and recovery periods (185 +/- 16 vs. 179 +/- 12 min). The ratio of albumin to globulin in lymph relative to the same ratio in plasma did not change during any phase of these experiments. Five lambs killed after recovery from asphyxia had significantly less blood and extravascular water in their lungs than control lambs had. We conclude that in the newborn lamb both alveolar hypoxia and alveolar hypoxia with hypercapnia increase lung lymph flow by increasing filtration pressure in the microcirculation, but neither hypoxia with hypercapnia nor brief severe asphyxia alters the protein permeability of the pulmonary microcirculation.

Protein concentration of lymph and interstitial fluid in the rat tail.

Lymph was collected from tail lymphatics of anesthetized rats, subcutaneous interstitial fluid was obtained by implanting nylon wicks, and tendon interstitial fluid was obtained by centrifugation of pieces of tendon. Spontaneous lymph flow rates averaged 70 nl X min-1 X g skin-1. Protein concentrations and colloid osmotic pressures of sampled fluids differed significantly. Tail lymph had the highest protein concentration relative to plasma [lymph-to-plasma ratio 0.71 +/- 0.03 (SE) n = 10], followed by wick fluid (0.62 +/- 0.02, n = 9), with tendon fluid lowest (0.50 +/- 0.03, n = 10). Albumin and immunoglobulin G (IgG) concentrations in samples of tail skin and tendon were assayed by rocket immunoelectrophoresis. Comparison of their distribution volumes at lymph or tendon fluid concentrations, respectively, with interstitial fluid volumes measured as 2-h 51Cr-ethylenediaminetetraacetic acid space minus 5-min 125I-albumin space indicated that 50-60% of the interstitial volume in these tissues is not available for distribution of albumin or IgG. Low lymph flow and high interstitial protein content of rat tail indicate a slow turnover of interstitial protein. This suggests that interstitial washout of protein plays a role in limiting edema only after a sustained or chronic increase in fluid filtration.

Effects of experimental cirrhosis on splanchnic microvascular fluid and solute exchange in the rat

In human cirrhosis, there is evidence that there are considerable alterations in fluid and solute exchange in the hepatic and intestinal microcirculations. Experimental cirrhosis was induced in rats by using oral phenobarbitone and carbon tetrachloride inhalation over an 8-wk period. Portal venous pressure, hepatic and intestinal lymph flows, and lymph and plasma protein concentrations were measured. Liver samples were obtained for histologic examination. Portal venous pressure increased from a normal value (control animals) of 9.0 (6.3–13.1) cmH2O to 17.9 (9.0–29.0) cmH2O in cirrhotic rats. There was a strong correlation between the degree of fibrotic change on histology and portal venous pressure. Lymph flows from the intestine and liver in cirrhotic animals were increased threefold and 30-fold, respectively, over values obtained from control animals. There was a good correlation between intestinal and liver lymph flows and portal venous pressure. Analysis of lymph/plasma protein concentration ratios at various lymph flows suggests that capillary permeability in the small intestine during sustained portal hypertension is comparable to that in normal animals. However, the highly permeable blood-lymph barrier of the normal liver becomes markedly restrictive in cirrhotic animals.

The effect of intraarterial infusion of prostacyclin on the tubuloglomerular feedback control in the rat.

Effects of intraarterial prostacyclin (PGI2) infusions on interstitial hydrostatic and oncotic pressures and on the tubuloglomerular feedback (TGF) control of glomerular filtration rate (GFR) were studied in rat kidneys. The hilar lymph flow rate was used as a measure of interstitial hydrostatic pressure and the lymph protein concentration was used for interstitial oncotic pressure estimation. In the micropuncture experiments the stop-flow pressure technique was employed for determining the TGF characteristics, i.e. stop-flow pressure (PSF), maximal reduction of PSF (delta PSF) and turning point (TP), defined as the end-proximal flow rate at which 50% of delta PSF was obtained. Non-hypotensive doses of PGI2 (50 to 100 ng X kg-1 B.W. X min-1) infused in 30 min evoked an increase in urine and lymph flow rates and a decrease in lymph protein concentration, but did not affect GFR. delta PSF was reduced (9.9 +/- 1.0 mmHg versus 4.7 +/- 2.2 mmHg) and TP increased (22 +/- 2 nl/min versus 34 +/- 2 nl/min), but the PSF was unaffected. These changes were seen during the infusion period and during the immediate post-infusion control period of 30 min. Our data indicate that non-hypotensive doses of PGI2 in some way can affect the renal interstitial pressure and the TGF control system.

Lung fluid balance in hypoxic lambs.

In spontaneously breathing newborn lambs, alveolar hypoxia increases lung microvascular pressure, which causes lung lymph flow to increase and the concentration of protein in lymph to decrease. To see if this response derives from hypoxia itself rather than from the change in breathing pattern that occurs during hypoxia, we measured lung vascular pressures, pleural pressure, cardiac output, and lung lymph flow in 12 anesthetized lambs that were ventilated at a fixed rate and tidal volume, first with air, then with 10-14% O2 in nitrogen. Alveolar hypoxia did not affect pleural pressure, but pulmonary arterial pressure increased from 19 to 32 torr, lung lymph flow increased from 2.20 to 3.83 ml/h and lymph protein concentration decreased from 3.4 to 2.8 g/dl. To be certain that the increased lymph flow associated with hypoxia is not simply the result of an acute release of fluid from the lungs and to assess the effects of carbon dioxide on lymph flow during hypoxia, we next studied six unanesthetized lambs kept hypoxic for a total of 12 h. After a 2-4-h period in air the lambs breathed 9-11% O2 in nitrogen for 2-4 h, then 8-11% O2 and 3-5% CO2 in nitrogen for 8-10 h. In these lambs we injected intravenously radioactive albumin and measured its uptake in lymph to see if sustained hypoxia alters microvascular permeability to protein in the lungs. In these experiments pulmonary arterial pressure increased from 17 to 37 torr, lung lymph flow increased from 1.74 to 3.28 ml/h, and lymph protein concentration decreased from 3.8 to 3.1 g/dl during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of nitroprusside administration and sudden withdrawal on pulmonary vascular tone and lung fluid balance.

We previously reported an increase in lung lymph flow rate (QL) on cessation of nitroprusside (NP) infusion after endotoxin lung injury. Utilizing sheep with chronic lung lymph fistulas and no lung injury, we studied pulmonary transvascular fluid filtration rate and protein flux (as measured via lung lymph flow and lymph protein content, respectively) during and after NP administration. The mean aortic pressure (Ao) and pulmonary arterial pressure (PAP) were significantly reduced by NP infusion. QL rose slightly during this reduction in pressure. Sudden withdrawal of NP infusion resulted in a significant rise in QL (as seen in our previous study) and a decrease in lymph to plasma protection ratio (L/P). There were only slight changes in PAP and mean pulmonary capillary wedge pressures (WP). We suggest that withdrawal of NP increases pulmonary microvascular pressure (Pmv).