Increase In QL Research Articles

The effectiveness of two different sub-bandage pressure values on healing and quality of life outcomes for patients with venous leg ulcers.

Venous ulcers account for over 80% of chronic wounds in the lower extremities. Venous ulcers lead to a significant decrease in the patients' quality of life. To compare the effectiveness of two different sub-bandage pressure values on healing and quality of life outcomes. The study included 116 outpatients with venous leg ulcers (VLUs), one group with a moderate compression pressure of 35-40 mm Hg and the second with a high pressure > 45 mm Hg. The Kaplan-Meier curve and log rank test were used to estimate healing by type of compression. Quality of life measures included: Quality of Life Index (QL), Numeric Pain Rating Scale (NPRS) and Geriatric Depression Scale (GDS). Patients were followed for 24 weeks. Kaplan-Maier analysis showed that a high pressure leads to a higher proportion of healed VLUs, compared to the moderate pressure (p = 0.011). QL, GDS and NPRS at the beginning were equalized between the groups. In patients with a high compression, there was a statistically significant increase in QL (p = 0.005), decrease in GDS (p = 0.040) and NPRS (p = 0.002) during 24 weeks. In patients with moderate compressions there was a statistically significant increase in QL (p = 0.013). Patients who received high pressure, healed faster. When a high pressure was applied, there was a statistically significant increase in QL, decrease in GDS and NPRS compared to the group of patients to whom the moderate pressure was applied.

Leg microvascular function remain robust throughout the female menstrual cycle

BACKGROUNDThe female menstrual cycle (MC) is characterized by fluctuating concentrations of estrogen and progesterone. While the impact of these vasoactive sex hormones on macrovascular function has received considerable attention, little is known about their influence on the microvasculature. Since the microvasculature ultimately determines skeletal muscle perfusion, a thorough understanding of the influence sex hormones have on microvascular function is needed. It was therefore the purpose of this study to investigate microvascular function, as assessed via the passive leg movement technique (PLM), of eumenorrheic females at three unique gonadal hormone profiles.METHODSSix healthy females (age: 22 ± 2 years; height: 168 ± 2 cm; weight: 59 ± 2 kg) were studied during the early follicular (EF; days 1‐4), late follicular (LF; days 8‐12), and mid luteal (ML; days 8‐10 post luteinizing hormone peak) phases of their MC. Venous blood was collected and analyzed for estrogen and progesterone concentrations. For each visit, subjects arrived at the laboratory in a fasted, rested state and at the same time of day. Passive leg movement (1 Hz for one minute; 90‐degree range of motion at the knee) was performed in a seated position. At rest and during PLM, leg blood flow (femoral artery; QL) was measured with Doppler ultrasound, while heart rate (HR), cardiac output (CO), and mean arterial pressure (MAP) were continuously measured via Finapress.RESULTSAll females presented traditional patterns of hormonal variation throughout the MC. Estrogen (EF: 144 pg/mL, LF: 239 pg/mL, ML: 359 pg/mL) was different at each phase (p < 0.05), while progesterone was similar during EF and ML (~0.2 ng/mL; p = 0.2), but significantly higher during ML (~6.8 ng/mL, p = 0.02). The area under the curve (AUC) for QL (~170 mL, p = 0.7) during the 1 min PLM, and the increase in QL from rest to the peak response to PLM (QLΔpeak; ~540 mL/min, p = 0.3) were not different at any phase of the MC. Furthermore, MAP AUC (~1.0 mL), MAPΔpeak (~6 mmHg), and therefore leg vascular conductance (VC) AUC (~1.9 mL/mmHg) and VCΔpeak (~6.5 mL/min/mmHg), did not change throughout the MC (p > 0.3). Finally, COΔpeak (~0.6 L/min) and HRΔpeak (~7 bpm) remained similar throughout the MC (p > 0.4).SUMMARY & CONCLUSIONDespite significant differences in venous estrogen and progesterone concentrations during EF, LF, and ML, the hyperemic response to PLM was unchanged at each phase, indicating that microvascular function remain consistent throughout the MC. In addition, both the MAP and the central hemodynamic response to PLM was similar at each stage of the MC. These findings suggest that a tight control of the MC may no longer be considered critical for studies focusing on microvascular function. These new insights might, ultimately, facilitate the involvement of females in future investigations.

Performance of a polypropylene membrane contactor for the recovery of dissolved methane from anaerobic effluents: Mass transfer evaluation, long-term operation and cleaning strategies

A polypropylene membrane contactor was used for the recovery of dissolved methane from an anaerobic reactor effluent. Effect of operational parameters, operation mode and fouling on long-term operation was studied using vacuum pressure or N2 as sweep gas. Results were analyzed based on the mass transfer estimations. Lower performance was observed in the shell-side mode due to the lower liquid velocity and the probable channeling. Membrane pore wetting was observed with the increase in QL in the vacuum-pressure mode. This was confirmed with mass transfer resistance analysis, resulting in an estimated wetted pore fraction of between 0.25 and 0.53. The highest removal efficiencies were obtained with the liquid flowing in the lumen side and sweep-gas operation (between 98% and 67% for QL between 4.1 and 27.2 L h–1), with negligible effect of the N2 flow rate. In the long-term operation, the impact of membrane fouling was less intense in the lumen side, with longer operation time and more reversible fouling. A complete characterization of the fouling based on water sample analysis concluded that both inorganic and organic foulants were present, probably with higher biofouling presence. A combination of water and chemical cleanings resulted in a recommended protocol based on daily water cleaning.

Enhancing recovery of ammonia from rare earth wastewater by air stripping combination of microwave heating and high gravity technology

Currently, a larger amount of NH3-N wastewater is generated in the rare earth manufacture process. Air stripping is one of the effective technologies for ammonia removal, but low separation efficiency and huge stripping tower rendering the process techno-economically inefficient. Hence, microwave heating and high gravity separation are employed to intensify air stripping process. Microwave dielectric characteristics for this solution indicate strong absorption, which can reduce the heating time rapidly. The effect of main operating parameters such as the rotational speed (ω), liquid flow rate (QL), gas flow rate (Qg), and stripping temperature (T)) on the volumetric liquid mass transfer coefficient (KLa) and stripping efficiency (η) are assessed. Results show that KLa increase significantly with increasing gas flow rate, followed by rotating speed and liquid flow rate. However, the η decrease with increase in QL due to reduction in the liquid hydraulic retention time. Under the optimal conditions, KLa and η could reach 0.0061 s−1 and 99.3%, respectively. Dimensionless empirical correlations are developed relating process parameters with the KLa and η, which shows a good agreement of the model equation with the experimental data. In addition, high gravity air stripping and conventional technologies are compared.

Ammonia removal from ammonia-rich wastewater by air stripping using a rotating packed bed

Air stripping of ammonia from an ammonia-rich stream (1000mg/L) was performed in a continuous-flow rotating packed bed (RPB) at temperatures from 25 to 40°C. The effects of the major operating variables (rotational speed (ω), liquid flow rate (QL), gas flow rate (QG), and stripping temperature (T)) on the volumetric liquid mass-transfer coefficient (KLa) and stripping efficiency (η) were elucidated. The results indicate that the RPB exhibits higher mass-transfer performance (12.3–18.41/h) compared with those of stripping tanks, packed towers, and other advanced gas–liquid contactors (0.42–1.21/h). At QL=0.05L/min, QG/QL=1600, and ω=1200rpm, η values for the RPB at 30 and 40°C respectively reached 69% and 81% within 13.3s. In contrast, conventional ammonia stripping processes with liquid recirculation in larger towers usually take hours to achieve the same values. The proposed dimensionless models describe the relationship between KLa and the major parameters for ammonia stripping in the RPB. KLa showed the greatest increase with increasing QG followed by the increase in QL, ω, and T. However, the operating conditions that would make the technology economically viable and the optimal conditions for efficient ammonia removal must be further studied.

Group III/IV Mediated Muscle Reflexes Restrain Vascular Conductance During Exercise In Patients With Hypertension

PURPOSE: We investigated the role of group III/IV-mediated muscle reflexes (i.e. the exercise pressor reflex) in determining the circulatory response to physical activity in patients with essential hypertension. METHODS: Five patients with stage 1–2 hypertension (HT; systolic: 155 ± 5 mmHg; diastolic: 90 ± 2 mmHg; 64 ± 3 years) and eight age-matched normotensive control subjects (NT; systolic: 120 ± 6 mmHg; diastolic: 80 ± 6 mmHg) performed single-leg knee extensor exercise (7, 15, 20 and 30 W) under control conditions and with lumbar intrathecal fentanyl impairing feedback from μ-opioid receptor-sensitive lower limb muscle afferents. Cardiac output (Q; photoplethysmography), leg perfusion pressure (PP = arterial pressure - venous pressure; femoral arterial and venous catheters), and femoral blood flow (QL; Doppler ultrasound) were measured continuously during exercise. Leg vascular conductance (LVC) was calculated as QL/PP. RESULTS: Hypertension had a significant main effect on PP (∼22% higher in HT vs. NT), LVC (∼30% lower in HT vs. NT), and QL (∼13% lower in HT vs. NT) during exercise in control conditions (P < 0.05). Following fentanyl blockade, which had no measurable effects at rest, Q during exercise in HT was, secondary to a small reduction in heart rate (P = 0.08) and a significant decrease in stroke volume, about ∼20% lower compared to control conditions (P < 0.05). In contrast, fentanyl blockade had no effect on Q during exercise in NT (P = 0.4). Additionally, in the face of a similar 8-10% reduction in PP during exercise with fentanyl blockade in NT and HT, there was ∼20% increase in QL during exercise with fentanyl blockade in patients with HT (P < 0.05), contrasting with the unaltered QL response in NT individuals. The net outcome of these changes was a significantly elevated LVC in both groups, but the increase was nearly three-fold greater in HT compared to NT (26 ± 3% vs. 10 ± 2%; P < 0.05). CONCLUSION: Although the exercise pressor reflex plays a critical role in facilitating central hemodynamics (i.e. Q) in HT, it also impairs QL and LVC in these patients. The excessive muscle reflex-mediated sympatho-excitation in HT contributed to the deficit in QL and LVC during exercise under normal conditions and might therefore be a substantial contributor to the exercise intolerance which characterizes this population.

Acclimation of Tobacco Leaves to High Light Intensity Drives the Plastoquinone Oxidation System—Relationship Among the Fraction of Open PSII Centers, Non-Photochemical Quenching of Chl Fluorescence and the Maximum Quantum Yield of PSII in the Dark

Responses of the reduction-oxidation level of plastoquinone (PQ) in the photosynthetic electron transport (PET) system of chloroplasts to growth light intensity were evaluated in tobacco plants. Plants grown in low light (150 micromol photons m-2 s-1) (LL plants) were exposed to a high light intensity (1,100 micromol photons m-2 s-1) for 1 d. Subsequently, the plants exposed to high light (LH plants) were returned back again to the low light condition: these plants were designated as LHL plants. Both LH and LHL plants showed higher values of non-photochemical quenching of Chl fluorescence (NPQ) and the fraction of open PSII centers (qL), and lower values of the maximum quantum yield of PSII in the dark (Fv/Fm), compared with LL plants. The dependence of qL on the quantum yield of PSII [Phi(PSII)] in LH and LHL plants was higher than that in LL plants. To evaluate the effect of an increase in NPQ and decrease in Fv/Fm on qL, we derived an equation expressing qL in relation to both NPQ and Fv/Fm, according to the lake model of photoexcitation of the PSII reaction center. As a result, the heat dissipation process, shown as NPQ, did not contribute greatly to the increase in qL. On the other hand, decreased Fv/Fm did contribute to the increase in qL, i.e. the enhanced oxidation of PQ under photosynthesis-limited conditions. Thylakoid membranes isolated from LH plants, having high qL, showed a higher tolerance against photoinhibition of PSII, compared with those from LL plants. We propose a 'plastoquinone oxidation system (POS)', which keeps PQ in an oxidized state by suppressing the accumulation of electrons in the PET system in such a way as to regulate the maximum quantum yield of PSII.

Effects of pentafraction and hetastarch plasma expansion on lung and soft tissue transvascular fluid filtration

Hetastarch and pentafraction are high molecular weight starch solutions designed to augment plasma oncotic pressure. Although clinical utilization of hetastarch has been limited by reported coagulation abnormalities, pentafraction is a newer derivative that appears to have few adverse hemostatic effects. We examined the ability of pentafraction to modulate lung and soft tissue transvascular fluid filtration under hypoproteinemic conditions compared with hetastarch and Ringer's lactate (LR). Awake, protein-depleted sheep (n = 19) were prepared with lung and soft tissue lymph fistulas, and comparable infusions of 5% pentafraction (n = 6), 6% hetastarch (n = 6), or LR (n = 7) were administered. Plasma and lymph samples were collected during 24-hour period to determine changes in protein concentrations, plasma-to-lymph oncotic gradients, and lung (QL) and soft tissue (QS) lymph flows. QL and QS rose nearly twofold after protein depletion alone. LR infusion increased QL and QS to 8.7 +/- 1.7 and 3.1 +/- 0.6 times normoproteinemic baseline, respectively (p < 0.05). In contrast, hetastarch and pentafraction infusion limited the increase in QL to 4.2 +/- 1.1 and 4.0 +/- 0.8 times normoproteinemic baseline, respectively (p < 0.05 versus LR) and did not significantly increase QS. Hetastarch and pentafraction infusions increase plasma oncotic pressure by nearly 6 mm Hg, which significantly widened the plasma-to-lymph oncotic pressure gradients above preinfusion baseline by 4.7 +/- 0.7 and 3.4 +/- 0.4 mm Hg in lung and 4.6 +/- 0.7 and 3.2 +/- 0.4 mm Hg in soft tissue, respectively (p < 0.05). Both hetastarch and pentafraction limit transvascular fluid filtration under hypoproteinemic conditions by augmenting plasma oncotic pressure and the plasma-to-lymph oncotic pressure gradient. Because of fewer adverse hemostatic effects pentafraction may be an improvement over current therapies in critical care fluid management.

Delayed elevation of ED1-cellular fibronectin in plasma following postsurgical bacteremia.

Fibronectin (Fn) exists in both a soluble form in plasma and lymph as well as an insoluble form in the extracellular matrix. Matrix-localized cellular fibronectin (cFn) contains extra domains (ED1 and/or ED2) not found in plasma Fn (pFn). Very little (< 1-2%) ED1-containing cFn exists in normal blood, and its rapid release into plasma and/or lymph is believed to reflect acute vascular injury. We used a polyclonal antibody to sheep pFn and a monoclonal antibody to ED1 domain of cFn to measure both pFn and ED1-cFn in relationship to lung lymph flow (QL), lung lymph-to-plasma (L/P) total protein concentration ratio, and lung protein clearance (LPC). Unanesthetized sheep (n = 7) were injected intravenously with Pseudomonas aeruginosa (5 x 10(8)) at both 2 and 7 days following surgical preparation of a lung lymph fistula. After both bacterial challenges, we observed an early increase in QL and a small decline in the L/P ratio (0-2 h), reflecting increased fluid filtration in the presence of an intact vascular barrier. This was followed by a further increase (P < 0.05) in QL; an elevation in the L/P ratio; and a marked (P < 0.05) increase in LPC over 3-6 h, indicative of an increase in lung endothelial protein permeability. Before the first bacterial infusion, ED1-cFn in plasma was 9.97 micrograms/ml or approximately 2% of the total Fn antigen in plasma; whereas ED1-cFn in lung lymph was 6-8% of total lymph Fn.(ABSTRACT TRUNCATED AT 250 WORDS)

Alpha-Trinositol decreases lung edema formation after smoke inhalation in an ovine model.

Inhalation injury is a dominant cause of mortality in thermally injured individuals. After acute lung injury induced by smoke inhalation, lung lymph flow (QL) increased and pulmonary microvascular reflection coefficient to protein (sigma) decreased. alpha-Trinositol (PP56, 1D-myo-inositol 1,2,6-trisphosphate) can decrease edema formation after thermal injury. We therefore tested the hypothesis that alpha-trinositol could decrease the pulmonary edema noted with inhalation injury. Seven days after surgical preparation, sheep were insufflated with smoke from burning cotton towels. The alpha-trinositol group (n = 8) were treated with alpha-trinositol (2 mg/kg + 3.5 mg.kg-1 x h-1). The sham group (n = 7) received an equal volume of 0.9% NaCl. The sham group showed a large increase in QL (9.3 +/- 1.7 to 54.1 +/- 8.8 ml/h) and a decrease in sigma (0.79 +/- 0.03 to 0.48 +/- 0.03) 24 h after smoke inhalation. alpha-Trinositol attenuated the increase in QL (8.1 +/- 1.2 to 25.6 +/- 6.9 ml/h) and the decrease in sigma (0.76 +/- 0.03 to 0.60 +/- 0.03) noted with smoke inhalation. alpha-Trinositol thus decreased the changes in pulmonary microvascular permeability and transvascular fluid flux noted with inhalation injury.

Hindlimb and lung lymph flows during prolonged exercise

We performed experiments to determine the effect of 2h of exercise on hindlimb lymph flow (QL) and protein concentration in sheep. We compared these results with the lung QL response to long-term exercise. Eleven sheep with catheters in an efferent duct of a prefemoral lymph node and 12 sheep with chronic lung lymph catheters exercised at 2.5-3.0 km/h for up to 2h (lung lymph: range 45-120 min, mean 80 min;hindlimb lymph: range 75-120 min, mean 110.5 min). Cardiac output approximately doubled. Pulmonary vascular resistance decreased by 42%, and systemic vascular resistance decreased by 35%. There were small increases in calculated pulmonary microvascular and arterial pressures. During steady-state exercise, lung QL doubled and the lung lymph-to-plasma protein concentration ratio decreased by 16%. There was an immediate fivefold increase in hindlimb QL, and the hindlimb lymph-to-plasma protein concentration ratio decreased by 26%. Hindlimb QL decreased to a constant 130% above baseline during the last 30 min of exercise. We conclude that the marked increase in hindlimb QL early in exercise is secondary to a massaging effect in working muscles. The steady-state increases in QL toward the end of the exercise period in both lung and hindlimb are secondary to both increased surface area and pressure in the pulmonary and systemic microvascular circulations. Our data suggest that in the lung the major factor determining QL is increased vascular surface area.

Effects of hypertonic saline and dextran 70 resuscitation on microvascular permeability after burn.

Administration of hyperosmolar fluids to burn patients has been proposed as a means of decreasing resuscitative fluid volume and, subsequently, wound edema accumulation. To test this hypothesis, canine hindpaw lymph flow (QL) and lymph (CL) and plasma (CP) total protein concentrations were measured, and capillary filtration coefficient (Kf) was calculated before and for 6 h after a 5-s 100 degrees C footpaw scald. Scald was followed 30 min later by bolus infusion (4 ml/kg) of 7% saline or 6% Dextran 70 or the two in combination. Before scald, venous pressure was elevated until a minimal CL/CP was reached. The reflection coefficient (sigma d) was calculated by the formula: 1-minimal CL/CP. Scald increased QL, CL/CP, and Kf, but sigma d was decreased (P less than 0.05). Compared with burn alone, 7% saline exacerbated burn-induced increases in QL and Kf. In contrast, infusion of Dextran 70 did not exacerbate these changes in QL or Kf. Perhaps more importantly, Dextran 70 may have attenuated the increase in CL/CP and reduced edema formation in the burned hindpaw. However, the addition of 7% saline to the dextran eliminated these beneficial effects.

Lung edema formation following inhalation injury: role of the bronchial blood flow

We investigated the contribution of the bronchial blood flow to the lung lymph flow (QL) and lung edema formation after inhalation injury in sheep (n = 18). The animals were equally divided into three groups and chronically prepared by implantation of cardiopulmonary catheters and a flow probe on the common bronchial artery. Groups 1 and 2 sheep were insufflated with 48 breaths of cotton smoke while group 3 received only room air. Just before injury, the bronchial artery of group 2 animals was occluded. The occlusion was maintained for the duration of the 24-h study period. At the end of the investigation, samples of lung were taken for determination of blood-free wet weight-to-dry weight ratio (W/D). Inhalation injury induced a sevenfold increase in QL in group 1 (7 +/- 1 to 50 +/- 9 ml/h; P less than 0.05) but only a threefold increase in group 2 (10 +/- 2 to 28 +/- 7 ml/h; P less than 0.05). The mean W/D value of group 1 animals was 23% higher than that of group 2 (5.1 +/- 0.4 vs. 3.9 +/- 0.2; P less than 0.05). Our data suggest that the bronchial circulation contributes to edema formation in the lung that is often seen after the acute lung injury with smoke inhalation.

Thromboxane A2 mediates increased pulmonary microvascular permeability following limb ischemia.

Lower torso ischemia and reperfusion lead to respiratory dysfunction characterized by pulmonary hypertension and increased lung microvascular permeability. This is associated with lung leukosequestration and thromboxane (TX) generation. This study tests the role of elevated TX levels following muscle ischemia in mediating remote lung injury. Anesthetized sheep prepared with chronic lung lymph fistulae underwent 2 hours of bilateral hind limb tourniquet ischemia. In untreated controls (n = 7), 1 minute after reperfusion there was a transient increase in plasma immunoreactive (i)-TXB2 levels from 211 to 735 pg/ml (p less than 0.05), and at 30 minutes, lung lymph i-TXB2 levels rose from 400 to 1,005 pg/ml (p less than 0.05). At 1 minute, the mean pulmonary arterial pressure (MPAP) increased from 13 to 38 mm Hg (p less than 0.05) and pulmonary microvascular pressure (Pmv) from 7 to 18 mm Hg (p less than 0.05). Lung lymph flow (QL) rose from 4.3 to 8.3 ml/30 min (p less than 0.05), the lymph/plasma (L/P) protein ratio was unchanged from 0.6, and the lymph protein clearance increased from 2.6 to 4.6 ml/30 min (p less than 0.05). Two hours after reperfusion, neutrophils were observed sequestered in lung capillaries and proteinaceous exudates were found in alveoli in contrast to sham-operated animals (n = 3). To maximize lung vascular surface area and achieve a pressure independent L/P protein ratio a left atrial balloon was inflated during one group of ischemia-reperfusion experiments (n = 5). This resulted in a baseline rise in MPAP to 20 mm Hg (p less than 0.05); a 4.3-fold increase in QL (p less than 0.05), a decrease in the L/P ratio from 0.70 to 0.28 (p less than 0.05) and a protein reflection coefficient (sigma d) of 0.72. During reperfusion the L/P ratio rose to 0.49 (p less than 0.05) and the sigma d decreased to 0.51 (p less than 0.05), documenting an increase in lung microvascular permeability. In contrast to untreated ischemic controls, inhibition of TX synthetase with OKY 046 (n = 6) reduced plasma i-TXB2 levels to 85 pg/ml (p less than 0.05) but also increased i-6-keto-PGF1 alpha levels to 78 pg/ml relative to 15 pg/ml in untreated controls (p less than 0.05). OKY 046 prevented the increase in MPAP, Pmv, QL, and lymph protein clearance (p less than 0.05). Lung histology was normal in distinction to the leukosequestration in untreated ischemic controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Pulmonary vascular resistance after cessation of positive end-expiratory pressure.

This report describes the pulmonary vascular response of infant lamb lung to abrupt cessation of positive end-expiratory pressure (PEEP) during volume-regulated continuous positive-pressure breathing (CPPB). In an intact, endobronchially ventilated preparation, the increase in left lung blood flow (QL) after abrupt cessation of 11 Torr left lung PEEP was found to be gradual, although peak airway pressure (Pmax) fell promptly from 36 to 14 Torr; 49% of the increase in QL occurred greater than 10 s after cessation of PEEP. Recruitment of zone I vasculature that had been created by balloon occlusion of the left pulmonary artery was found to occur promptly after balloon deflation. Isolated neonatal lamb lungs, perfused at constant flow rate, showed similar persistent elevation of pulmonary vascular resistance after cessation of 15 Torr PEEP, although Pmax fell abruptly from 39 to 12 Torr. This hysteresis was eliminated by calcium channel blockade with verapamil, and the magnitude of the change in pulmonary arterial pressure after either application or cessation of PEEP was reduced (25 and 26%, respectively). These observations suggest that, during CPPB, lung stretch alters neonatal pulmonary vascular tone or, by causing calcium channel-dependent lung volume hysteresis, modulates pulmonary vascular resistance. This interaction exaggerates the effect of airway pressure changes on pulmonary vascular resistance during mechanical ventilation.

Limb ischemia-induced increase in permeability is mediated by leukocytes and leukotrienes.

This study tests the role of white blood cells (WBC) and leukotrienes in mediating the increased microvascular permeability following ischemia and reperfusion. Anesthetized dogs (n = 23) underwent 2 hours of hind limb ischemia induced by tourniquet inflation to 300 mmHg. In untreated animals (n = 7), tourniquet release led after 5 minutes to a rise in plasma thromboxane (Tx) B2 levels from 360 to 1702 pg/ml (p less than 0.05); after 2 hours, lymph TxB2 concentration had risen from 412 to 1598 pg/ml (p less than 0.05). There were decreases in circulating WBC from 11,766 to 6550/mm3 and platelets from 230 to 155 x 10(3)/mm3. During reperfusion, popliteal lymph flow (QL) increased from 0.07 to 0.24 ml/hour (p less than 0.05), while the lymph/plasma (L/P) protein ratio was unchanged from 0.39, changes consistent with increased microvascular permeability. WBC depletion (n = 7) to 302/mm3 by hydroxyurea or nitrogen mustard attentuated (p less than 0.05) the reperfusion induced rise in plasma TxB2 from 91 to 248 pg/ml and prevented the increase in lymph TxB2 concentration. Within 5 minutes of tourniquet release WBC counts further decreased to 191/mm3 (p less than 0.05) and platelets declined from 175 to 93 x 10(3)/mm3 (p less than 0.05). QL increased from 0.07 to 0.12 ml/hour (p less than 0.05), lower than untreated animals (p less than 0.05), and the L/P protein ratio declined from 0.49 to 0.37 (p less than 0.05), dilutional changes consistent with increased filtration pressure but not permeability to protein. Pretreatment with the lipoxygenase inhibitor diethylcarbamazine (DEC) (n = 8) prevented the reperfusion-induced increase in plasma and lymph TxB2 levels (p less than 0.05) and the fall in WBC counts (p less than 0.05), while platelet counts declined from 381 to 210 x 10(3)/mm3 (p less than 0.05). QL rose from 0.09 to 0.23 ml/hour (p less than 0.05) during reperfusion, and the L/P protein ratio of 0.3 remained unchanged, a value lower than in untreated dogs (p less than 0.05). In two animals of each group, vascular recruitment was induced by tourniquet inflation to 50 mmHg. This led to a high QL of 0.25 ml/hour and a low L/P ratio of 0.18. In untreated animals during reperfusion, QL further increased to 1.3 ml/hour, and L/P ratio rose to 0.44, documenting increased vascular permeability. In contrast, reperfusion in leukopenic or diethylcarbamazine (DEC)-treated dogs with vascular recruitment, was not associated with increases in QL or the L/P protein ratio.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of platelet-activating factor antagonist SRI 63-441 on endotoxemia in sheep.

We investigated whether platelet-activating factor (PAF) mediates endotoxin-induced systemic and pulmonary vascular derangements by studying the effects of a selective PAF receptor antagonist, SRI 63-441, during endotoxemia in sheep. Endotoxin infusion (1.3 micrograms/kg over 0.5 h) caused a rapid, transient rise in pulmonary arterial pressure (Ppa) from 16 +/- 3 to 36 +/- 10 mmHg (P less than 0.001) and pulmonary vascular resistance (PVR) from 187 +/- 84 to 682 +/- 340 dyn.s.cm-5 (P less than 0.05) at 0.5 h, followed by a persistent elevation in Ppa to 22 +/- 3 mmHg and in PVR to 522 +/- 285 dyn.s.cm-5 at 5 h in anesthetized sheep. Arterial PO2 (PaO2) decreased from 341 +/- 79 to 198 +/- 97 (P less than 0.01) and 202 +/- 161 Torr at 0.5 and 5 h, respectively (inspired O2 fraction = 1.0). SRI 63-441, 20 mg.kg-1.h-1 infused for 5 h, blocked the early rise in Ppa and PVR and fall in PaO2, but had no effect on the late phase pulmonary hypertension or hypoxemia. Endotoxin caused a gradual decrease in mean aortic pressure, which was unaffected by SRI 63-441. Infusion of SRI 63-441 alone caused no hemodynamic alterations. In follow-up studies, endotoxin caused an increase in lung lymph flow (QL) from 3.8 +/- 1.1 to 14.1 +/- 8.0 (P less than 0.05) and 12.7 +/- 8.6 ml/h at 1 and 4 h, respectively. SRI 63-441 abolished the early and attenuated the late increase in QL.(ABSTRACT TRUNCATED AT 250 WORDS)

Lymph flow during increases in pulmonary blood flow and microvascular pressure in dogs.

We studied the effects of an increase in pulmonary blood flow (PBF) on steady-state lung lymph flow (QL) and protein transport in anesthetized dogs (n = 7) to estimate the effect of vascular recruitment in zone 3 on transvascular filtration. At the end of each experiment, we increased left atrial pressure to 25-30 mmHg using a balloon catheter and obtained a washdown of the lymph protein concentration. PBF was increased with an extracorporeal circuit, which pumped blood from the left to the right atrium, and increases in pulmonary capillary pressure (Pc) were minimized by lowering left atrial pressure. PBF was measured by thermodilution, and Pc was measured by transient analysis of arterial occlusion pressure with a Swan-Ganz catheter. PBF increases averaged 78% with increases ranging from 36 to 118%. Pc increases ranged from 0.5 to 6.3 mmHg, and QL increases averaged 31% with changes ranging from -2 to +138%. We observed a 16% increase in QL for each 1-mmHg increase in Pc during increased PBF, which was comparable to the relationship previously observed after an increased left atrial pressure. Lymph-to-plasma total protein concentration ratios (CL/CP) decreased from 0.71 +/- 0.04 to 0.625 +/- 0.06 during increased PBF. The relationship between CL/CP, QL, and Pc for both increased blood flow and increased left atrial pressure were within the expected range for increased pressure alone. These data suggest that there was minimal vascular recruitment for transvascular filtration in zone 3 when pulmonary blood flow was increased. Microvascular filtration pressure was the main determinant of fluid and protein transvascular filtration under these conditions.

Pulmonary embolism: analysis of endothelial pore sizes in canine lung

The effect of glass-bead microemboli (diameter 100 micron, range 77-125 micron) in the absence of fibrinolysis inhibition on pulmonary hemodynamics and microvascular permeability was determined in anesthetized, microfilaria-free dogs acutely prepared for the collection of lung lymph. Pulmonary vascular resistance, pulmonary capillary pressure (Pc), lymph flow (QL), and the ratio of lymph (CL) to plasma (Cp) protein concentrations were measured after 0.2 (n = 4), 0.4 (n = 6), or 0.6 (n = 3) g/kg beads. In all cases, emboli increased resistance and QL severalfold (P less than 0.05), while CL/Cp remained unchanged. In part, the increase in QL could be attributed to an increase in Pc compared with control (12.4 +/- 2.2 vs. 6.7 +/- 0.6 mmHg, P less than 0.05). Furthermore, since the solvent-drag reflection coefficient (sigma f) for total proteins approaches the osmotic reflection coefficient (sigma d) at high QL, sigma d was estimated under these conditions with sigma f approximately equal to sigma d approximately equal to 1 - (CL/Cp)min. The sigma d was decreased (P less than 0.05) after 0.4 and 0.6 g/kg beads to 0.55 +/- 0.03 and 0.50 +/- 0.07, respectively, when compared with that in control lungs (sigma d = 0.62 +/- 0.02; Parker et al., Circ. Res. 48: 549-561, 1981). A pore-stripping analysis demonstrated that after emboli the pulmonary endothelial barrier could be described by a population of small (80 A) and large (350 A) pores. However, the number of large to small pores was 1:1,195, compared with 1:195 in control lungs, suggesting an increased contribution of extra-alveolar vessels upstream of the emboli.(ABSTRACT TRUNCATED AT 250 WORDS)

Ibuprofen reduces the progression of permeability edema in an animal model of hyperdynamic sepsis.

Since severity of acute lung injury (ALI) is reduced by pretreatment with non-steroidal agents, we hypothesized that ibuprofen would ameliorate ALI when administered after the onset of septic lung injury. Twenty-four hours after cecal ligation and perforation (CLP) in 23 sheep during a 4 h study period (period S), pulmonary lymph flow (QL) increased 16.2 +/- 12.1 ml/min (P less than 0.01) from base line, whereas lymph-to-plasma total protein concentration ratios ([L/P]TP) remained unchanged. During the subsequent 24 h of study (period D), 10 sheep received parenteral ibuprofen, 12.5 mg/kg every 6 h, and 13 sheep served as untreated septic controls. Throughout period D, a progressive increase in QL (16.2 +/- 16.3 ml/60 min) from period S was greater in the untreated than in the ibuprofen (2.5 +/- 9.0 ml/60 min, P less than 0.02) group. Between base line and period D, increase in lung wet-to-dry weight ratios was greater in the untreated group than in the ibuprofen group (P less than 0.05). Concurrently mean pulmonary arterial pressure increased 4.7 +/- 7.3 mmHg in the untreated group (P less than 0.05) during period D vs. 0.0 +/- 5.2 mmHg in the ibuprofen group (NS). When administered after septic ALI had been established by CLP, ibuprofen reduced an otherwise progressive increase in both fluid flux and extravascular lung water.