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Biomedical subjects

J C Gabel

Publications and source records attributed to J C Gabel.

At least 37 records · Page 2Linked to original sources
PubMed1991

Abdominal lymph flow response to intraperitoneal fluid in awake sheep.

Lymphatic vessels are important in draining excess fluid from the abdominal space and preventing ascites. In sheep, diaphragmatic lymph vessels draining the abdominal space run to the caudal mediastinal lymph node and efferent vessels from the node drain into veins in the neck. To estimate the lymph flow response to excess intraperitoneal fluid in sheep, we cannulated a caudal mediastinal node efferent lymphatic in 5 sheep. After the sheep recovered from the surgery, the lymph flow (QL) was 154 +/- 161 (SD) microliters/min and the lymph protein concentration (CL) was 3.7 +/- 9 g/dl. Lymph flow decreased linearly with increases in lymphatic outflow pressure greater than 6 cmH2O. From this linear QL vs. outflow pressure relationship, we estimated the effective pressure driving lymph flow as the outflow pressure at which QL = 0. At baseline, the driving pressure was 24.7 +/- 14.0 cmH2O. After we infused Ringers solution (10% body weight) into the abdominal space, QL increased significantly to 7.0 +/- 4.1 times baseline and CL decreased significantly to 0.7 +/- 0.6 g/dl. Although the abdominal pressure increased significantly from 10.6 +/- 2.8 cmH2O to 15.8 +/- 2.1 cmH2O, we found no increase in lymphatic driving pressure.

Abdomen↗
PubMed1990

Changes in microvascular permeability with acceleration of edema in dog lungs.

Elevation of left atrial pressure to 25-40 mmHg causes continuous pulmonary edema formation in dog lungs. However, after 5-120 min, the rate of edema formation often increases (acceleration of edema). Acceleration of edema could be associated with an increase in microvascular membrane permeability because an increase in permeability would cause fluid to filter through the microvascular membrane more rapidly. To test the hypothesis that acceleration is associated with increased permeability, we used the continuous weight-gain technique to estimate the pulmonary microvascular membrane filtration coefficient (Kf) before and after acceleration of edema in 10 dogs. Acceleration occurred 36 +/- 38 (SD) min after elevation of left atrial pressure to 35.2 +/- 5.4 mmHg. Rate of weight gain increased from 0.47 +/- 0.17 g/min before acceleration to 0.88 +/- 0.26 g/min (P less than 0.05) after acceleration of pulmonary edema. Kf was increased from initial values of 0.058 +/- 0.027 to 0.075 +/- 0.029 ml.min-1.mmHg-1 (P less than 0.05) after acceleration. In five additional dogs we cannulated lung lymphatics and determined the lymph to plasma protein concentration ratio (CL/CP) before and after acceleration. CL/CP increased from base-line values of 0.37 +/- 0.07 to 0.44 +/- 0.06 (P less than 0.05) after acceleration. Both the increase in Kf and CL/CP data support the hypothesis that acceleration of edema is due, in part, to a slight increase in microvascular membrane permeability. However, the findings could also have been caused by an increase in interstitial conductance, washout of interstitial proteins, or alveolar flooding.

Animals↗
PubMed1990

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

We used lymph flow rate (QL) to lymphatic vessel outflow pressure (Po) relationships to analyze lymphatic flow in five unanesthetized sheep with liver lymphatic cannulas. The olecranon was the zero reference level for pressures. Increases in Po did not change QL until Po exceeded 19 +/- 4 (SD) cmH2O. However, for Po greater than 19 +/- 4 cmH2O, QL decreased linearly with increases in Po. We fit regression lines to the QL vs. Po data for Po greater than 19 cmH2O and estimated the effective lymphatic resistance (RL) as -delta Po/delta QL. The effective pressure driving lymph (PL) was the Po at which QL = 0. At baseline, RL = 0.18 +/- 0.10 cmH2O.min.microliter-1 and PL = 29.6 +/- 3.4 cmH2O. When we increased hepatic vein pressure by 5.7 +/- 1.7 cmH2O, QL increased to 6.2 +/- 3.2 times baseline, RL decreased to 0.050 +/- 0.015 cmH2O.min.microliter-1, and PL increased to 37.1 +/- 3.5 cmH2O (P less than 0.05). Thus 1) liver lymph flow is very sensitive to increases in hepatic vein pressure, 2) there is a substantial QL vs. Po plateau for liver lymphatics, and 3) after hepatic venous pressure elevations, liver lymph flow increases as if it were driven by a higher pressure through a lower resistance.

Animals↗
PubMed1990

The effect of anesthesia and surgery on diaphragmatic lymph vessel flow after endotoxin in sheep.

Increases in diaphragmatic lymph vessel flow (Qdi) may be important in preventing ascites because diaphragmatic lymph vessels drain the peritoneal space. However, lymphatic vessel function may be depressed in anesthetized, open chested animals. To test this hypothesis, we cannulated diaphragmatic lymph vessels in five sheep which were anesthetized with 1-2% halothane. We performed a thoracotomy and cannulated a diaphragmatic lymph vessel in each sheep. Then we infused 0.75-1.0 micrograms/kg of E. coli endotoxin intravenously and we measured Qdi and the lymph protein concentration for 2-4 hrs. The data were compared to previously reported data for five unanesthetized sheep (J. Appl. Physiol. 62:706-710, 1987). At baseline Qdi = 0.8 +/- 0.7 (SD) in the anesthetized sheep and 1.0 +/- 0.8 ml/hr in the unanesthetized sheep. After endotoxin, Qdi increased to 4.5 +/- 3.1 ml/hr in the unanesthetized sheep (p less than 0.05) but Qdi did not change in the anesthetized sheep. However, the lymph protein concentration increased similarly in each group, indicating that endotoxin caused the same degree of injury in each group. Our results indicate that diaphragmatic lymph vessel function is depressed in anesthetized, open chested sheep.

Analysis of Variance↗
PubMed1988

Lymphatic function in the liver after hepatic venous pressure elevation.

The liver lymphatic system plays an important role in removing excess fluid from the hepatic tissue. A complete analysis of the liver lymphatic system would be difficult. However, we used a simple circuit-analysis technique to represent the intrahepatic portion of the lymph system as a single pressure source (PL) pushing lymph through a single resistance (RL). Liver lymphatic vessels were cannulated in nine halothane-anesthetized dogs. The lymphatic vessel outflow pressure (PO) was varied by raising the outflow end of the cannula. Lymph flow from the cannula (QL) decreased linearly with PO, and we calculated RL as -delta PO/delta QL and PL as the extrapolated PO at which QL = 0. At base line, PL = 8.5 +/- 2.9 cmH2O, and RL = 0.05 +/- 0.03 cmH2O.min/microliter. After we increased inferior vena caval pressure from 5.8 +/- 2.7 to 15.2 +/- 2.5 cmH2O, PL increased significantly to 13.7 +/- 3.4 cmH2O, and RL decreased to 0.02 +/- 0.02 cmH2O.min/microliter (P less than 0.05). The results indicate that increases in QL occur because the effective pressure pushing lymph from the liver (PL) increases, and the effective resistance of the intrahepatic lymph vessels (RL) decreases.

Algorithms↗
PubMed1988

Superior vena caval pressure elevation causes pleural effusion formation in sheep.

The effect of superior vena caval pressure (SVCP) elevation on the formation of pleural effusions (PE) was studied in sheep. Through a right thoracotomy, a Silastic cuff was placed around the superior vena cava. Catheters for monitoring SVCP and pulmonary artery pressure (PAP) were also placed. After a 1- to 3-wk recovery period, we measured the SVCP, PAP, cardiac output, and plasma protein concentration (Cp). We then elevated the SVCP to various levels from base line [5.3 +/- 2.6 (SD) mmHg] to 33 mmHg. The cardiac output, PAP, and Cp were remeasured 1-2 h and 24 h after SVCP elevation. At the end of the 24-h period, the animals were killed. The PE volume and pleural fluid protein concentration (Cpl) were measured, and the Cpl/Cp was calculated. PE generally did not occur until the SVCP was elevated above 15 mmHg. To study the effect of the thoracotomy on the subsequent pleural effusion, we studied six additional sheep in which we did not perform a thoracotomy. In these animals, the SVCP was elevated to between 5 and 28 mmHg for 24 h by use of a 16-Fr balloon catheter placed via a left external jugular vein and a right carotid-external jugular shunt. We found that the PE volume, for a given SVCP elevation, was similar to that present in sheep that received a thoracotomy. For all sheep the volume of PE was related to SVCP by the equation PE (ml) = 0.24e0.26SVCP, r = 0.85. In the sheep without a thoracotomy, Cpl/Cp rose with increasing volume of PE. Our data demonstrate that elevation of SVCP greater than 15 mmHg for 24 h results in the formation of PE. The rise in Cpl/Cp with PE volume suggests that filtration through the pleural vessels is not the major contributor to PE formation.

Animals↗
PubMed1987

Outflow pressure reduces lymph flow rate from various tissues.

We previously reported that the very act of cannulating a lung lymph vessel could alter the unique flow characteristics that existed within the lymphatic before cannulation. We postulated that this phenomenon could hold true for lymphatics draining any organ within the body. Since it is frequently important to know the relationship between the transmicrovascular fluid flux and true lymph flow rate, it would be critical that a cannulated lymphatic vessel have the same flow characteristics as those uncannulated vessels draining the same organ. In order to test our hypothesis we cannulated lymph vessels draining the heart, liver, small intestine, kidney, and skeletal muscle. By altering the lymphatic outflow pressure (normally related to systemic venous pressure) and by using lymphatic cannulas of various resistance, we were able to demonstrate that lymph flow varied linearly with lymphatic outflow pressure in every organ. By increasing transmicrovascular fluid flux and lymph flow rate in each organ we were also able to demonstrate that effective resistance of the lymphatic vessels and the effective pressure driving lymph flow varied as a function of the physical characteristics of the organ under investigation. Characteristic effective resistances of the heart, liver, skeletal muscle, kidney, and small intestine lymphatics decreased by 83, 40, 61, 36, and 50%, respectively. Along with these changes in effective resistance, the effective lymph driving pressure in the same organs varied by 49, 0, 257, 0, and 63%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

A model of the lung interstitial-lymphatic system.

Our model of the pulmonary interstitial-lymphatic system is based on the assumption that the lung interstitial space can be divided into two compartments. The first compartment (C1) contains the terminal lymph vessels. Increases in the fluid pressure within this compartment, along with increased pressure generated by lymph vessel pumping, cause the lymph flow rate to increase. The lymph vessels run through the second compartment (C2) which we believe represents the perivascular spaces. Increases in the fluid volume of C2 cause the lymph vessels to dilate and this causes lymph vessel resistance to decrease. Normally the lymph flow rate equals the microvascular filtration rate so that lung fluid volume is constant. According to our model, increases in filtration rate cause fluid to collect in C1 and C2. The resulting increase in fluid pressure in C1, increased lymph vessel pumping, and the decrease in lymph vessel resistance in C2 cause lymph flow to increase. Eventually, the lymph flow rises to equal the filtration rate and lung fluid volume becomes constant again. The results of simulations with our model indicate that decreases in lymph vessel resistance are essential for lymph flow to increase substantially as edema develops.

Extracellular Space↗
PubMed1987

Effect of endotoxin on diaphragm lymph contamination in unanesthetized sheep.

The preparation for collecting lung lymph from sheep caudal mediastinal lymph node (CMN) efferent vessels is widely used to study the effects of endotoxin on lung microvascular permeability. However, there are nonpulmonary lymph vessels that drain into the CMN along with the afferent lymph vessels from the lung. Thus CMN lymph is a mixture of lymph from the lung and diaphragm lymph vessels as well as from other nonpulmonary lymph vessels. We studied the effect of 0.5-1.0 microgram/kg Escherichia coli endotoxin on the flow rates in diaphragm and CMN efferent lymph vessels (Qdi and QCMN, respectively) in unanesthetized sheep. For the time period between 2 and 5.5 h after endotoxin QCMN was increased from its base line of 7.2 +/- 4.4 (SD) to 17.3 +/- 10.6 ml/h and the lymph-to-plasma protein concentration ratio (L/PCMN) had increased from 0.68 +/- 0.11 to 0.81 +/- 0.06. During the same time period, Qdi was 4.5 +/- 3.1 ml/h compared with 1.0 +/- 0.8 ml/h at base line and the diaphragm lymph-to-plasma protein concentration ratio (L/Pdi) was 0.92 +/- 0.07 (base line = 0.74 +/- 0.15). The increases in flow rate and protein concentration were significant for each type of vessel (P less than 0.05). We conclude that the period of increased QCMN and L/PCMN after endotoxin is associated with an increase in Qdi and L/Pdi. Thus, it is difficult to determine how much of the CMN lymph response comes from the lungs and how much comes from diaphragm lymph vessels.

Animals↗
PubMed1987

Elevation of superior vena caval pressure increases extravascular lung water after endotoxemia.

In many sheep Escherichia coli endotoxin results in pulmonary hypertension, increased microvascular permeability, pulmonary edema, and increased central venous pressure. Since lung lymph drains into the systemic veins, increases in venous pressure may impair lymph flow sufficiently to enhance the accumulation of extravascular fluid. We tested the hypothesis that, following endotoxin, elevating the venous pressure would increase extravascular fluid. Thirteen sheep were chronically instrumented with catheters to monitor left atrial pressure (LAP), pulmonary arterial pressure (PAP), and superior vena caval pressure (SVCP) as well as balloons to elevate LAP and SVCP. These sheep received 4 micrograms/kg endotoxin, and following the pulmonary hypertensive spike the left atrial balloon was inflated so that (PAP + LAP)/2 = colloid osmotic pressure. It was necessary to control PAP + LAP in this way to minimize the sheep-to-sheep differences in the pulmonary hypertension. We elevated the SVCP to 10 or 17 mmHg or allowed it to stay low (3.2 mmHg). After a 3-h period, we killed the sheep and removed the right lungs for determination of the extravascular fluid-to-blood-free dry weight ratio (EVF). Sheep with SVCP elevated to 10 or 17 mmHg had significant increases in EVF (5.2 +/- 0.1 and 5.6 +/- 1.2) compared with the sheep in which we did not elevate SVCP (EVF = 4.5 +/- 0.4). These results indicate that sustained elevation in central venous pressure in patients contributes to the amount of pulmonary edema associated with endotoxemia.

Animals↗
PubMed1987

Lymph flow from edematous dog lungs.

We measured the flow rate (QLV) from cannulated lung lymph vessels in anesthetized dogs. Low-resistance lymph cannulas were used and the vessels were cannulated at the lung hilus. When we increased left atrial pressure to 42.9 +/- 5.7 (SD) cmH2O (base line = 6.6 +/- 4.6 cmH2O), the lungs became edematous and QLV increased from a base line of 20.4 +/- 21.5 microliters/min to 388 +/- 185 microliters/min. QLV plateaued at the higher level. We also measured the relationship between lymph flow rate and the height of the outflow end of the lymph cannula. From this relationship, determined at the end of the period of elevated left atrial pressure, we calculated the effective resistance and pressure driving lymph from the lungs. We also cannulated lymph vessels in the downstream direction and estimated the effective resistance and pressure opposing flow into the part of the lymphatic system between the lung hilus and the veins (extrapulmonary lymph vessels). We found that the effective resistance of the extrapulmonary part of the lymph system (0.042 +/- 0.030 (SD) cmH2O X min X microliter-1) was large compared with the resistance of the lymph vessels from the lungs (0.026 +/- 0.027). These data indicate that the resistance of the extrapulmonary part of the lung lymph system limits the maximum flow of lymph from edematous lungs.

Animals↗
PubMed1987

Lowered pulmonary arterial pressure prevents edema after endotoxin in sheep.

Escherichia coli endotoxin causes increased capillary membrane permeability and increased pulmonary arterial pressure (PAP) in sheep. If the pulmonary hypertension extends to the level of the microvasculature, then the increased microvascular pressure may contribute to the pulmonary edema caused by endotoxin. We tested the hypothesis that reducing the pulmonary hypertension would reduce the amount of edema caused by endotoxin. Twelve sheep were chronically instrumented with catheters to measure PAP, left atrial pressure, and central venous pressure. The sheep were divided into two groups. One group (E) of six sheep received an intravenous infusion of 4 micrograms/kg of E. coli endotoxin. The second group (E + SNP) received the same dose of endotoxin as well as a continuous infusion of sodium nitroprusside (SNP) to reduce PAP. Three hours after the endotoxin infusions, the sheep were terminated and the extravascular fluid-to-blood-free dry weight ratios of the lungs were determined (EVF). The base-line PAP was 17.5 +/- 2.7 mmHg. A two-way analysis of variance demonstrated a significant difference (P less than 0.01) in PAP between the E and E + SNP groups. Although PAP in each group varied as a function of time, the difference between the two groups did not. The mean PAP for the E + SNP group (20.9 +/- 1.5 mmHg) was lower than the E group PAP of 27.3 +/- 2.1 mmHg after the endotoxin spike. Furthermore, the E + SNP group EVF (3.9 +/- 0.2) was significantly less than the EVF of the E group (4.7 +/- 0.5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Equivalent circuit technique for lymph flow studies.

Lymph vessels branch and interconnect in a manner similar to a complex electronic circuit. Accordingly, we have applied circuit analysis techniques to the analysis of lymphatic systems. A lymph vessel is cannulated and the "equivalent circuits" are determined for the parts of the vessel upstream and downstream of the site of cannulation. Each equivalent circuit consists of a single resistor in series with a single pressure source. A diode is included to represent the lymphatic valves. The lymph flow rate may be determined by calculating the flow in the circuits when they are connected to each other. This technique can be applied to larger lymph trunks that receive lymph from many tissues.

Animals↗
PubMed1986

Lung lymph flow during volume infusions.

We investigated the effect of intravenous isotonic crystalloid solution infusion on lung lymph flow. Tracheobronchial lung lymph vessels were cannulated in 13 anesthetized dogs. The lymph flow rate was measured 1) with the lymph flowing against atmospheric pressure (QL), and 2) with the pressure at the outflow end of the lymph cannula equal to systemic venous pressure (QLV). QL and QLV were measured alternately in each lymph vessel. In one group of nine dogs, the base-line QL and QLV were 18 +/- 9 and 13 +/- 6 (SD) microliter/min, respectively (P less than 0.05). QL increased by 4.8 +/- 1.4-fold, and QLV increased by 3.5 +/- 2.1-fold during a 4-h infusion of 25 ml X kg-1 X h-1 of Ringer solution. QLV was significantly less than QL at all times. The increases in lymph flow were caused primarily by a reduction in the effective resistance of the lymph vessels with little rise in the pressure driving lymph from the lungs. Because QLV flowed against systemic venous pressure, the increase in QLV was blunted by a 3.1 +/- 2.3 cmH2O rise in venous pressure during the infusions. In the remaining four dogs, we infused Ringer solution rapidly in order to raise venous pressure to greater than 15 cmH2O. This caused QL to increase by 25 +/- 7-fold; however, QLV decreased to zero. We conclude that elevations in venous pressure which occur during volume infusions oppose lung lymph flow and lead to accumulation of excess fluid in the lungs.

Animals↗
PubMed1986

Overestimation of sheep lung lymph contamination.

We have previously reported that lymph from the chronic sheep lung lymph preparation contains 25-60% lymph from nonpulmonary sources. In subsequent studies we found that the lymph flow rate from cannulated lymph vessels depends on the resistance and position of the lymph cannula. Because we did not account for these factors in our estimate of the amount of nonpulmonary lymph in the sheep lung lymph preparation, our data were not accurate. We probably overestimated the amount of nonpulmonary lymph. However, the presence of nonpulmonary lymph remains a potentially serious problem with the sheep lung lymph preparation.

Animals↗