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J C Gabel

Publications and source records attributed to J C Gabel.

At least 55 records · Page 3Linked to original sources
PubMed1986

Effect of systemic venous pressure elevation on lymph flow and lung edema formation.

Pulmonary lymph drains into the thoracic duct and then into the systemic venous circulation. Since systemic venous pressure (SVP) must be overcome before pulmonary lymph can flow, variations in SVP may affect lymph flow rate and therefore the rate of fluid accumulation within the lung. The importance of this issue is evident when one considers the variety of clinical interventions that increase SVP and promote pulmonary edema formation, such as volume infusion, positive-pressure ventilation, and various vasoactive drug therapies. We recorded pulmonary arterial pressure (PAP), left atrial pressure (LAP), and SVP in chronic unanesthetized sheep. Occlusion balloons were placed in the left atrium and superior vena cava to control their respective pressures. The superior vena caval occluder was placed above the azygos vein so that bronchial venous pressure would not be elevated when the balloon was inflated. Three-hour experiments were carried out at various LAP levels with and without SVP being elevated to 20 mmHg. The amount of fluid present in the lung was determined by the wet-to-dry weight ratio method. At control LAP levels, no significant difference in lung fluid accumulation could be shown between animals with control and elevated SVP levels. When LAP was elevated above control a significantly greater amount of pulmonary fluid accumulated in animals with elevated SVP levels compared with those with control SVP levels. We conclude that significant excess pulmonary edema formation will occur when SVP is elevated at pulmonary microvascular pressures not normally associated with rapid fluid accumulation.

Animals↗
PubMed1986

Sheep lung lymph shunting.

The caudal mediastinal lymph node (CMN) has several efferent lymph vessels in most sheep. When investigators cannulate one of the CMN efferent vessels in order to collect lung lymph, it is possible that lymph may be shunted between the cannulated vessel and other vessels which drain from the CMN into the systemic veins. If shunting does occur then an increase in venous pressure could cause lymph to be shunted to the cannulated lymph vessel. This would increase the flow of lymph from the cannula and could falsely indicate that lung lymph flow had increased. To test this possibility we cannulated CMN efferent vessels in 7 sheep and then used a balloon to raise the pressure in the superior vena cava. Because uncannulated CMN efferent vessels ultimately drain into the superior vena cava, an increase in pressure may cause lymph to be shunted through the lymph cannula. We found, however, that lymph flow increased in only one of seven sheep and conclude that lymph shunting is uncommon when operative preparation includes meticulous ligation of collateral common efferent lymph vessels.

Animals↗
PubMed1985

Effect of cardiac output on extravascular lung water estimates made with the Edwards lung water computer.

The Edwards lung water computer system uses the thermal-dye indicator technique to estimate the lung extravascular fluid volume (EVLW). The authors tested the effect of changes in cardiac output (CO) on EVLW estimates made with the lung water computer in six dogs anesthetized with halothane. Baseline CO was 2.5 +/- 1.3 l/min (mean +/- SD); CO subsequently was increased either by 220% or decreased by 70% by either giving 0.5 mg/kg of isoproterenol or increasing the inspired halothane (1-4%), respectively. There was a significant correlation between the estimated EVLW and CO in each animal (P less than 0.05) such that a 50% decrease in CO from baseline caused an approximately 40% increase in estimated EVLW. Postmortem examination showed that the lungs were not edematous, even though the lung water computer data indicated that severe pulmonary edema had developed at reduced COs. At increased COs, estimated EVLW decreased. The authors conclude that the Edwards lung water computer overestimates lung water, possibly because the thermal indicator diffuses into nonpulmonary as well as pulmonary tissue. The overestimate is greatest at low cardiac outputs.

Animals↗
PubMed1984

Effect of endotoxin on lung fluid balance in unanesthetized sheep.

We used a gravimetric technique to test for increased pulmonary capillary permeability after Escherichia coli endotoxin infusion in unanesthetized sheep. The sheep were chronically prepared with cannulas placed into the left atrium and pulmonary artery 1-2 wk before the experiments. We estimated pulmonary capillary pressure (Pc) as the average of pulmonary arterial and left atrial pressures, and used the modified method of Pierce to estimate the ratio of extravascular fluid weight (EVF) to blood-free dry weight. In 15 sheep we inflated a left atrial balloon to raise Pc to -10.7, 5, 10, or 15 mmHg above plasma oncotic pressure (IIc) for 3 h, then measured EVF. EVF averaged 4.0 +/- 0.2 (base line), 4.3 +/- 0.1, 4.5 +/- 0.1, and 5.1 +/- 0.5 (SD), respectively, for the four levels of Pc - IIc. We gave seven additional sheep 1 microgram/kg of E. coli endotoxin (0127:B8) and measured EVF after 3 h of stable Pc. Endotoxin increased Pc in each sheep. EVF was higher than control for the endotoxin sheep with Pc - IIc greater than -1. This finding is consistent with an increase in pulmonary capillary permeability caused by endotoxin. However, EVF was not elevated in the endotoxin sheep with Pc - IIc less than 1 mmHg. This shows that the increased permeability was insufficient to cause edema unless Pc was elevated. Thus endotoxin may cause edema by two mechanisms, 1) an increase in capillary permeability, and 2) an increase in Pc.

Animals↗
PubMed1984

Effect of lymphatic cannula outflow height on lung microvascular permeability estimations.

Estimates of the pulmonary microvascular membrane reflection coefficient (sigma) and permeability-surface area product (PS) are frequently made with the assumption that a percent change in transmicrovascular fluid flux (Jv) will be represented by an equal percent change in the lymph flow rate (QL) from a single cannulated lung lymph vessel. To test this, we measured QL in seven anesthetized dogs with the outflow end of the lymph cannula set at several heights (H) above and below the lung hilus. The left atrial pressure was then elevated to increase Jv, and QL was again measured at several H's. The percent increase in QL at elevated left atrial pressure depended on H. We used the QL data and lymph and plasma protein concentrations to estimate sigma and PS with a modified form of the Kedem and Katchalsky equations. The calculated values varied considerably with H. Our results indicate that changes in Jv are not represented by equal changes in QL. Therefore, techniques for estimating permeability that depend upon QL as an estimate of Jv may lead to erroneous estimates of sigma and PS.

Animals↗
PubMed1983

Dog lymph flow in increased capillary permeability states.

The lung lymph flow rate (QL) is increased in edema caused by an increase in lung microvascular permeability. This increase in QL could be caused by either a decrease in the effective resistance of the lymph vessels (RL), or by an increase in the effective lymph driving pressure (PL), or by a change in both RL and PL. We estimated PL and RL from the linear relationship between QL and the pressure at the outflow end (PO) of five cannulated dog lung lymph vessels (RL = - delta Po/delta QL and PL = the PO at which QL = 0). We increased lung microvascular permeability by giving the dogs 100 mg/kg of alloxan and found that QL increased from 24.5 +/- 8.9 microliters/min to 112 +/- 41 microliters/min (mean +/- SD). RL decreased from 0.35 +/- 0.12 to 0.11 +/- 0.04 cm H2O min/microliters and PL increased from 8.5 +/- 1.5 to 15.9 +/- 2.7 cm H2O. We then increased the capillary pressures from 18.3 +/- 3.8 to 41.3 +/- 7.3 cm H2O and QL increased to 169.9 +/- 47.8 microliters/min. PL increased by an additional 6.3 cm H2O but RL decreased by only an additional 0.02 cm H2O min/microliters. These results show that the QL vs PO relationship is changed in edema secondary to an increase in microvascular permeability, and that this change can be represented as changes in RL and PL. In terms of these parameters, QL increased in edema as a result of a decrease in RL and an increase in PL.

Alloxan↗
PubMed1983

Effect of Escherichia coli endotoxin on dog lung fluid balance.

Endotoxin may cause an increase in pulmonary capillary permeability and thus promote edema formation. We used a gravimetric technique to estimate the pulmonary capillary filtration coefficient (KF) and the maximum capillary pressure at which the lung could maintain a constant weight (Pccritical) in dogs after intravenous administration of Escherichia coli (E. coli) endotoxin. KF should be increased and Pccritical should be decreased by an increase in permeability. Four groups of three to four dogs were given 1, 10, 1,000, or 3,000 micrograms/kg of endotoxin. A fifth group of five dogs, which served as controls, was given no endotoxin. KF was significantly (P less than 0.05) greater than control [0.049 +/- 0.031 (SD) ml . min-1 . mmHg-1] in only the 1-micrograms/kg group (0.100 +/- 0.027), indicating a possible increase in permeability. However, changes in capillary surface area may have affected KF. Pccritical was not significantly different from control (20.7 +/- 2.4 mmHg) in any of the E. coli groups. We conclude from these results that E. coli endotoxin may have caused a slight increase in permeability; however, the lung retained its ability to resist edema formation.

Animals↗
PubMed1983

Relationship between weight gain and lymph flow in dog lungs.

Lung weight is a useful indicator of increases in lung extravascular volume. In addition, the lung lymph flow rate (QL) is an important factor in lung fluid balance. We have studied the weight and QL responses to elevations in capillary pressure (Pc) in intact dog lung lower left lobes. We measured lobe weight continuously. We also measured QL from small lymph vessels from the same lobes. The base-line QL was 1.7 +/- 1.5 microliter/min, and the weight was constant. After we increased Pc by 8-20 cmH2O, both weight and QL increased transiently. In most lungs the weight reached a new steady state. When we increased Pc further, weight increased continuously; however, QL reached a plateau. The continuous weight gain was due to edema. These results show that weight and QL respond similarly in nonedematous lungs; however, the weight and QL responses in edematous lungs may be different.

Animals↗
PubMed1983

Pulmonary microvascular permeability after coronary arterial ligation in dogs.

Recent studies have indicated that pulmonary microvascular permeability may be increased after coronary arterial ligation. We tested this by estimating the pulmonary microvascular reflection coefficient (delta) in six anesthetized control dogs and in six dogs in which we ligated the left anterior descending coronary artery. We cannulated lung lymph vessels and measured the lymph and plasma protein concentrations (CL and CP, respectively). The left atrial pressure was increased to decrease CL to a minimum. We used the minimum CL to estimate delta as 1 -CL/CP. delta for the control [0.70 +/- 0.03 (SD)] and coronary artery ligated groups (0.70 +/- 0.04) were almost identical. This data indicates that coronary artery ligation does not increase pulmonary microvascular permeability.

Animals↗
PubMed1982

A feedback system to control blood flow in dog lung lobes.

We have developed an electromechanical feedback system to control blood flow to the lower left lung lobe of dogs. Blood flow is measured with an electromagnetic flowmeter. The feedback system compares the blood flow signal to an adjustable reference voltage and causes a motor to turn. The direction of motor rotation depends on the relative magnitude of the flow signal and the reference. The motor pushes the plunger of a syringe that is attached to a balloon in the right pulmonary artery. Inflation of the balloon causes increased blood flow to the lower left lobe. We have used the system to control lobe blood flow in three dogs.

Animals↗
PubMed1982

Effect of outflow pressure upon lymph flow from dog lungs.

The pulmonary lymph flow rate (QL) should be a function of the lymph vessels' resistance and the pressure gradient along the vessels. We attempted to study how these factors affect lymph flow. We assumed that the lymph system could be represented by a single pressure generated within the lung (PL) and a single resistance (RL). Thus, QL should be a function of the lymph vessel outflow pressure (Po): QL = (PL - Po)/RL. We cannulated tracheobronchial lymph vessels in eight anesthetized dogs and varied Po by raising the outflow end of the cannula. QL decreased linearly when we increased Po. We estimated RL as - delta Po/ delta QL and PL as the extrapolated Po at which QL = 0. At baseline PL = 7.7 +/- 2.7 (SD) cm H2O and RL = 0.36 +/- 0.25 cm H2O. min/microliters. After we increased capillary pressure to produce edema, PL and RL averaged 22.8 +/- 8.8 and 0.14 +/- 0.12, respectively. After we reduced the capillary pressure to baseline in the edematous lungs, PL and RL averaged 11.6 +/- 2.8 and 0.08 +/- 0.09, respectively. All changes in PL and RL were significant (P less than 0.05). These results show that (1) lymph flow rate depends upon lymph vessel outflow pressure, and (2) the QL vs. Po relationship is changed by edema. PL may be equal to the pressure causing lymph to flow and RL may equal the lymph vessel resistance.

Animals↗
PubMed1980

Effect of histamine and alloxan on canine pulmonary vascular permeability.

We estimated the pulmonary capillary membrane filtration coefficient (Kf) and the maximum capillary pressure (PCcritical) at which the lung could maintain a constant weight in 1) 5 control experiments in anesthetized open-chested dogs, 2) 7 experiments in which the dogs were given 3.6-8.3 microgram . kg-1 . min-1 of histamine phosphate, and 3) in 6 experiments after 75-100 mg/kg of alloxan. In additional experiments, pulmonary lymph flow (QL) and protein concentration (CL) were measured during the infusion of histamine and alloxan. After histamine, Kf averaged 0.045 +/- 0,008 ml . min-1mmHg-1 (SE) and PCcritical was 22.1 +/- 1.1 mmHg. These values were not significantly different from the control Kf and PCcritical (0.036 +/- 0.006 and 22.5 +/- 2.3, respectively). After alloxan, Kf (1.43 +/- 0.69) was larger and PCcritical (12.4 +/- 1.3) was significantly less than control (P less than 0.05). Histamine caused no significant change in QL or CL; however, both were increased after alloxan. These results show that Kf, PCcritical, QL, and CL are all changed by an increase in capillary membrane permeability caused by alloxan. Because none of these factors as significantly affected by histamine, dog lung capillary membrane permeability may not be affected by histamine.

Alloxan↗
PubMed1980

Errors in calculated oncotic pressure of dog plasma.

Several equations to calculate plasma oncotic pressure (pi) from the total protein concentration (C) have been previously described. These equations were derived empirically from samples with a wide range of C obtained by diluting or concentrating normal plasma samples. To test these equations over a range of naturally occurring C, we measured C and pi of plasma samples from 40 dogs. C ranged from 5.3 to 8.7 g/dl and averaged 6.5 +/- 0.1 (mean +/- SE) and pi averaged 17.9 +/- 0.3 mmHg. The regression equation was pi = 78.14 + 1.67 C (r = 0.74). pi increased with C much less than predicted with the commonly used equations. The albumin-to-globulin concentration ratios (A/G), determined in 27 of the dogs, decreased with increasing C (A/G = 1.56-0.128 C, r = 0.62). The lower A/G at the higher C's could cause the lower than predicted increase in pi with C, because the equations were developed from data in which A/G was constant.

Animals↗
PubMed1980

Comparison of microvascular filtration characteristics in isolated and intact lungs.

To determine whether the microvascular membrane of isolated perfused dog lungs is damaged by the isolation procedure, we compared the filtration coefficient (Kf,c) and minimum capillary pressure (Pcc) required to cause continuous edema formation in 10 intact and 8 isolated dog lower left lobes. We used the same gravimetric technique to measure Kf,c and Pcc in both preparations. The Kf,c averaged 0.09 +/- 0.03 (SD) ml . min-1 . Torr-1 . 100 g-1 in the intact and 0.30 +/- 0.16 in the isolated lobes; Pcc averaged 20.1 +/- 4.7 and 1.7 +/- 3.6 Torr in the intact and isolated lobes, respectively. Both Pcc and Kf,c were significantly different in the two preparations (P less than 0.01). These data indicate that the increased tendency of isolated lungs to become edematous at lower pressures may be caused by damage to the microvascular membranes.

Animals↗