Beta-adrenergic modulation of pulmonary transvascular fluid and protein exchange

1986 ◽  
Vol 60 (1) ◽  
pp. 266-274 ◽  
Author(s):  
F. L. Minnear ◽  
A. Johnson ◽  
A. B. Malik
Keyword(s):  
Control Group ◽  
Protective Effects ◽  
Beta Adrenergic ◽  
Intravascular Coagulation ◽  
Protein Clearance ◽  
Adrenergic Antagonist ◽  
Adrenergic Modulation ◽  
Pulmonary Arterial ◽  
Beta Adrenergic Agonist ◽  
Protein Exchange

We determined in anesthetized sheep whether isoproterenol, a beta-adrenergic agonist, prevents the increases in pulmonary fluid and protein exchange produced by thrombin-induced intravascular coagulation. Seven sheep were infused intravenously with 0.05 micrograms X kg-1 X min-1 isoproterenol before infusion of alpha-thrombin, and six sheep were infused with alpha-thrombin only and served as control subjects. The marked increases in pulmonary lymph flow and lymph protein clearance in the control thrombin group were attenuated (P less than 0.05) in the isoproterenol group in association with a higher pulmonary blood flow (P less than 0.05) and a lower pulmonary vascular resistance (P less than 0.05) in the isoproterenol group and with similar increases in pulmonary arterial and pulmonary arterial wedge pressures in both groups. The decreases in fluid and protein fluxes produced by isoproterenol are related to its beta-adrenergic properties because propranolol, a beta-adrenergic antagonist, blocked the protective effects of isoproterenol in a second group of sheep infused with propranolol, isoproterenol, and thrombin. Raising left atrial pressure to test for changes in vascular permeability increased protein flux to a much greater extent in the thrombin control group than in the isoproterenol group challenged with thrombin. The data suggest that isoproterenol attenuated the increase in fluid and protein fluxes produced by thrombin-induced intravascular coagulation by a permeability-decreasing mechanism.

Does ADP-Induced Platelet Aggregation Mediate Lung Vascular Injury?

1981 ◽  
Author(s):  
A B Malik ◽  
F L Minnear ◽  
M V Tahamont ◽  
D G Moon ◽  
J E Kaplan
Keyword(s):  
Platelet Aggregation ◽  
Vascular Injury ◽  
Protein Concentration ◽  
Control Group ◽  
Plasma Protein Concentration ◽  
Fluid Filtration ◽  
Lung Fluid ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Protein Exchange

We determined the effects of ADP-induced platelet aggregation on lung fluid and protein exchange to examine whether platelet aggregation mediates lung vascular injury. The studies were made in intact sheep in which pulmonary lymph was obtained, and the protein concentration of lymph was compared to that of plasma. Two groups were studied: Control sheep receiving i.v. infusion of 10 mg/kg of ADP and experimental sheep in which platelets were depleted with anti-platelet serum prior to ADP infusion. In the control group, ADP decreased the platelet count from 178,554 ± 62,750 to 103,500 ± 47,828 cells/mm3, suggesting the entrapment of platelet in the pulmonary circulation. The pulmonary arterial pressure (Ppa) increased from 13.1 ± 1.8 to 15.9 ± 1.2 mmHg. Lung lymph flow (Qlym) increased from 8.4 ± 1.8 to 11.4 ± 2.3ml/hr (p < 0.05) and transvascular protein clearance (Qlym x lymph/plasma protein concentration), a measure of protein exchange, increased from 6.7 ± 1.3 to 9.4 ± 3.0 ml/hr (p < 0.05). These increases could be explained by an increase in microvascular pressure (Pmv) and ultrafiltration since mechanically elevation of Pmv produced the same changes in Qlym and clearance. Platelet depletion prevented the ADP-induced increases in platelet aggregation does not mediate lung vascular injury, but increases fluid filtration by increasing the microvascular pressure. This effect may be mediated by release of pulmonary vasoconstrictor substances such as thromboxane A2 and serotonin after platelet aggregation.

Beta-adrenergic modulation of Na-K pump activity in young and adult canine cardiac Purkinje fibers

1996 ◽  
Vol 271 (2) ◽  
pp. H706-H712
Author(s):  
F. Charpentier ◽  
M. J. Legato ◽  
S. F. Steinberg ◽  
I. S. Cohen ◽  
M. R. Rosen
Keyword(s):  
Cell Surface ◽  
Volume Ratio ◽  
Beta Adrenergic ◽  
Purkinje Fibers ◽  
Age Related ◽  
Cardiac Purkinje Fibers ◽  
Adrenergic Modulation ◽  
Pump Activity ◽  
The Difference ◽  
Beta Adrenergic Agonist

We used standard microelectrode techniques to study the developmental changes and beta-adrenergic modulation of membrane potential and of Na-K pump activity in adult (> 1 yr of age) and neonatal (2-10 days) canine Purkinje fibers. Isoproterenol (10(-7) M) increased the rate of development and magnitude of pacing-induced hyperpolarization of adult fibers driven at a 1-s cycle length. This effect of isoproterenol was attenuated by treating dogs with pertussis toxin (PTX), (30 micrograms/kg). Other adult and neonatal fibers were superfused with a Tyrode solution containing Ba2+ 0.2 mM, Cs+ 2 mM, and 10(-6) M verapamil, thus leading to depolarization and cessation of spontaneous activity. The Na-K pump was studied by alternating solutions containing [K] at 0 mM (inhibiting the pump) and 4 mM (reactivating the pump). Although the kinetics of the Na-K pump appeared faster in neonatal fibers than in adult fibers, measurement of cell surface-to-volume ratio compensated for the difference. We therefore conclude that 1) the apparent age-related changes in Na-K pump activity in canine Purkinje fibers in fact reflect cell surface-to-volume ratio and, 2) the beta-adrenergic agonist-induced hyperpolarization in adults requires the presence of a PTX-sensitive G protein for its occurrence.

Failure of chronic beta-adrenergic blockade to inhibit overfeeding-induced thermogenesis in humans

1989 ◽  
Vol 256 (3) ◽  
pp. R653-R658 ◽  
Author(s):  
S. L. Welle ◽  
K. S. Nair ◽  
R. G. Campbell
Keyword(s):  
Weight Maintenance ◽  
Resting Metabolic Rate ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Initial Reduction ◽  
Adrenergic Antagonist ◽  
Adrenergic Activity ◽  
Propranolol Treatment ◽  
Male Subjects

The effect of the beta-adrenergic antagonist propranolol on the increase in resting metabolic rate (RMR) induced by overfeeding was examined to determine whether increased beta-adrenergic activity contributes to this response. Six male subjects who were overfed with carbohydrate (1,600 excess kcal/day) for 10 days without drug treatment (control group) had increases (compared with values after 10 days of weight maintenance) in RMR after 6 days [0.24 +/- 0.06 kcal/min (22%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. Eight male subjects were given a weight-maintenance diet for 10 days with oral propranolol treatment (40-60 mg every 6 h) over the last 7 days of this period. Five of these subjects were then overfed for 10 days, and three remained on the weight-maintenance diet; propranolol treatment continued until the end of the study. Propranolol significantly reduced RMR (mean 9%) before the onset of overfeeding but did not prevent increases in RMR after 6 days [0.18 +/- 0.05 kcal/min (16%)] and 10 days of overfeeding [0.17 +/- 0.03 kcal/min (15%)]. In the subjects who remained on the weight-maintenance diet throughout the study, there was no reversal of propranolol's initial reduction of RMR that would have falsely elevated the overfeeding effect. These data provide further evidence that the increase in RMR induced by overfeeding in humans is not mediated by increased beta-adrenergic activity.

scholarly journals The effect of β-adrenergic agonists on the membrane potential of fat-cell mitochondria in situ

1982 ◽  
Vol 206 (3) ◽  
pp. 611-618 ◽  
Author(s):  
R J Davis ◽  
B R Martin
Keyword(s):  
Membrane Potential ◽  
Fat Cells ◽  
Adrenergic Agonists ◽  
Fat Cell ◽  
Beta Adrenergic ◽  
Fatty Acid Binding ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Beta Adrenergic Agonist

1. The accumulation of [3H]methyltriphenylphosphonium by isolated fat-cells was used to estimate the membrane potential of mitochondria in situ. 2. Adrenaline caused a large decrease in the accumulation of [3H]methyltriphenylphosphonium. Mitochondria in fat-cells incubated in the presence of adrenaline had a very low calculated membrane potential. This effect was also given by isoprenaline (a beta-adrenergic agonist) and was blocked by propranolol (a beta-adrenergic antagonist). 3. The effect of isoprenaline could be partially antagonized by the use of media with high albumin concentrations. Addition of sodium oleate to saturate the fatty acid-binding sites on the albumin reversed this antagonism. 4. It is proposed that the decrease in the calculated mitochondrial membrane potential is due to the uncoupling effect of the non-esterified fatty acids released by the stimulation of lipolysis observed in the presence of beta-adrenergic agonists.

CVF-induced decomplementation: effect on lung transvascular protein flux after thrombin

1987 ◽  
Vol 62 (3) ◽  
pp. 863-869 ◽  
Author(s):  
A. Johnson ◽  
S. K. Lo ◽  
F. B. Blumenstock ◽  
A. B. Malik
Keyword(s):  
Plasma Protein Concentration ◽  
Pulmonary Hemodynamics ◽  
Mean Pulmonary Arterial Pressure ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Hemolytic Complement Activity ◽  
The Mean ◽  
Lung Lymph ◽  
Made In ◽  
Protein Exchange

We examined the effects of cobra venom factor (CVF) on the changes in pulmonary hemodynamics and transvascular fluid and protein exchange following thrombin-induced pulmonary microembolism. Studies were made in unanesthetized sheep prepared with lung lymph fistulas. The animals received tranexamic acid (100 mg) to suppress fibrinolysis and were then challenged with an intravenous infusion of alpha-thrombin (80 U/kg). Control-thrombin challenged sheep were compared with the CVF-treated sheep challenged with the same thrombin dosage. CVF treatment (187 U X kg-1 X day-1 for 4 days) decreased the total hemolytic complement activity by 45% of control. Thrombin infusion in control sheep increased the mean pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), and lymph protein clearance (pulmonary lymph flow X lymph-to-plasma protein concentration ratio, Clym). Thrombin infusion in CVF-treated sheep produced smaller increments in Ppa, PVR, and Clym. Pulmonary lymph obtained from control-thrombin and CVF-thrombin sheep induced migration of granulocytes obtained from normal unchallenged sheep. The granulocytes obtained from CVF-treated sheep responded relatively less to the migratory and O-2-generating stimuli (i.e., zymosan-treated serum, pulmonary lymph from sheep after thrombin challenge, and plasma from sheep after CVF treatment) compared with normal granulocytes. The attenuation of the thrombin-induced increases in Ppa, PVR, and lung transvascular fluid and protein exchange by CVF treatment may be the result of impaired function of granulocytes.

Effect of pulmonary arterial occlusion on lung fluid and protein exchange

1982 ◽  
Vol 53 (3) ◽  
pp. 543-548 ◽  
Author(s):  
P. S. Barie ◽  
A. B. Malik
Keyword(s):  
Protein Concentration ◽  
Arterial Occlusion ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Lung Fluid ◽  
Mean Pulmonary Arterial Pressure ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Lung Lymph ◽  
Protein Exchange

We examined the effects of left pulmonary arterial occlusion and reperfusion on pulmonary transvascular fluid and protein exchange in the sheep lung lymph fistula preparation. Pulmonary lymph flow (Qlym) increased from the base-line value of 5.0 +/- 0.8 to 10.0 +/- 2.1 ml/h after occlusion (P less than 0.05); the steady-state value of 11.9 +/- 2.2 ml/h during reperfusion was not significantly different from the value during occlusion. The lymph-to-plasma protein concentration ratio (L/P) did not change significantly during either occlusion or reperfusion. Transvascular protein clearance (Qlym X L/P) increased from 3.7 +/- 0.6 to 8.4 +/- 2.1 ml/h during occlusion (P less than 0.05) and remained elevated at 8.6 +/- 1.7 ml/h during reperfusion. The sustained increases in Qlym and protein clearance could not be explained by the 3-Torr increase in mean pulmonary arterial pressure during the occlusion period or by an increase in the interstitial protein concentration caused by a period of decreased filtration during occlusion. The increases in protein clearance that occurred with increased Qlym during occlusion and reperfusion were greater than the increases in protein clearance with comparably increased Qlym during left atrial hypertension. The results suggest that occlusion of a pulmonary artery increases vascular permeability to plasma proteins in the lung.

Developmental changes of beta-adrenergic receptor-linked adenylate cyclase of rat liver

1985 ◽  
Vol 248 (6) ◽  
pp. E712-E718 ◽  
Author(s):  
M. S. Katz ◽  
S. R. Boland ◽  
S. J. Schmidt
Keyword(s):  
Adenylate Cyclase ◽  
Rat Liver ◽  
Adrenergic Receptor ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Adrenergic Agonist ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Adrenergic Antagonist ◽  
Beta Adrenergic Agonist

beta-Adrenergic agonist-sensitive adenylate cyclase activity and binding of the beta-adrenergic antagonist(-)-[125I]iodopindolol were studied in rat liver during development of male Fischer 344 rats ages 6-60 days. In liver homogenates maximum adenylate cyclase response to beta-adrenergic agonist (10(-5) M isoproterenol or epinephrine) decreased by 73% (P less than 0.01) between 6 and 60 days, with most of the decrease (56%; P less than 0.01) occurring by 20 days. beta-adrenergic receptor density (Bmax) showed a corresponding decrease of 66% (P less than 0.01) by 20 days without subsequent change. Binding characteristics of stereospecificity, pharmacological specificity, saturability with time, and reversibility were unchanged with age. GTP-, fluoride-, forskolin-, and Mn2+-stimulated adenylate cyclase activities also decreased during development, suggesting a decrease of activity of the catalytic component and/or guanine nucleotide regulatory component of adenylate cyclase. These results indicate that the developmental decrease of beta-adrenergic agonist-sensitive adenylate cyclase activity may result from decreased numbers of beta-adrenergic receptors. Developmental alterations of nonreceptor components of the enzyme may also contribute to changes of catecholamine-sensitive adenylate cyclase.

Beta-adrenergic inhibition of Na-K-Cl cotransport in lymphocytes

1992 ◽  
Vol 263 (5) ◽  
pp. C1015-C1020 ◽  
Author(s):  
R. D. Feldman
Keyword(s):  
Physiological Role ◽  
Lymphocyte Function ◽  
Beta Adrenergic ◽  
Homogeneous Population ◽  
Beta Adrenoceptor ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Human Lymphoma ◽  
Extracellular Sodium ◽  
Beta Adrenergic Agonist

Lymphocytes contain a homogeneous population of beta 2-adrenoceptors. However, their physiological role in the regulation of lymphocyte function, especially early in the activation/proliferation process, remains unclear. To study the role of beta-adrenergic activation on the regulation of membrane transport, we examined 86Rb uptake in the Jurkat human lymphoma cell line. 86Rb uptake was predominantly accounted for by bumetanide-sensitive uptake (74 +/- 2% total 86Rb uptake) and ouabain-sensitive uptake (20 +/- 2%). Bumetanide potently inhibited 86Rb uptake (50% inhibitory concentration = 210 +/- 40 nM), and bumetanide-sensitive uptake was dependent on extracellular sodium and chloride, consistent with uptake via Na-K-Cl cotransport. The beta-adrenergic agonist isoproterenol (10 microM) mediated a 50 +/- 11% reduction in bumetanide-sensitive uptake without a significant alteration in ouabain-sensitive uptake. The effect of isoproterenol was potent (50% effective concentration = 4.42 +/- 1.70 nM), stereoselective, and was inhibited by the beta-adrenergic antagonist nadolol. The effect of isoproterenol was mimicked by permeant adenosine 3',5'-cyclic monophosphate analogues but not by pindolol. These data indicate that beta-adrenoceptor activation decreases 86Rb uptake in lymphocytes via inhibition of Na-K-Cl cotransport. Modulation of this transporter could be one mechanism by which beta-adrenergic agonists regulate lymphocyte function.

Effect of bradykinin on lung vascular permeability in sheep

1983 ◽  
Vol 55 (4) ◽  
pp. 1079-1084 ◽  
Author(s):  
F. L. Minnear ◽  
C. M. Kivlen ◽  
A. B. Malik
Keyword(s):  
Vascular Permeability ◽  
Plasma Protein Concentration ◽  
Pulmonary Hemodynamics ◽  
Beta Adrenergic ◽  
Pulmonary Vascular Permeability ◽  
Group Iii ◽  
Arterial Blood ◽  
Group I ◽  
Adrenergic Antagonist ◽  
Protein Exchange

Bradykinin (BK, 0.03-3.11 micrograms X kg-1 X min-1) was infused intravenously for 4-5.5 h to assess its effects on pulmonary transvascular fluid and protein exchange in three groups of artificially ventilated sheep prepared with lung lymph fistulas. In group I, BK was infused alone for 5.5 h. In group II, BK and captopril (SQ 14,225), an inhibitor of angiotensin-converting enzyme (ACE), were infused together because the effects of BK may be attenuated by its rapid degradation in the lung by ACE. In group III, BK was infused in the presence of propranolol, a beta-adrenergic antagonist, to prevent any permeability-decreasing effects of beta-adrenergic activation. The dosages of BK used, which decreased systemic arterial blood pressure by 10-20 mmHg, did not alter either pulmonary transvascular fluid and protein exchange or pulmonary hemodynamics at any time during infusion of BK alone or in combination with captopril or propranolol. Raising pulmonary microvascular pressure (Pmv) by inflating a left atrial balloon during the last 2 h of infusion in all three groups slightly increased pulmonary lymph flow and markedly decreased the lymph-to-plasma protein concentration ratio. These results are comparable with those obtained after increasing Pmv in normal anesthetized sheep and indicate that BK did not alter the pulmonary vascular permeability to proteins.

Effect of prostacyclin on pulmonary vascular response to thrombin in awake sheep

1986 ◽  
Vol 60 (2) ◽  
pp. 546-553 ◽  
Author(s):  
M. B. Perlman ◽  
S. K. Lo ◽  
A. B. Malik
Keyword(s):  
Platelet Aggregation ◽  
Control Group ◽  
In Vitro Tests ◽  
Neutrophil Chemotaxis ◽  
Plasma Protein Concentration ◽  
Platelet Counts ◽  
Protein Clearance ◽  
Pulmonary Arterial ◽  
Made In

We determined the effects of infusion of prostacyclin (PGI2) and 6-alpha-carba-PGI2 (6-cPGI2), a stable PGI2 analogue, on pulmonary transvascular fluid and protein fluxes after intravascular coagulation induced by thrombin. Studies were made in control awake sheep prepared with lung lymph fistulas (n = 6) and in similarly prepared awake sheep pretreated with either 6-cPGI2 (n = 5) or PGI2 (n = 5). Both prostacyclin compounds (500 ng X kg-1 X min-1) were infused intravenously. All groups were challenged with 80 U/kg thrombin. Pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), pulmonary lymph flow (Qlym), lymph protein clearance (Qlym X lymph/plasma protein concentration ratio), and neutrophil and platelet counts were determined. In vitro tests assessed sheep neutrophil chemotaxis and chemiluminescence and platelet aggregation. In both 6-cPGI2 and PGI2 groups, the increases in Qlym after thrombin were less than those in the control group. The increase in lymph protein clearance in the 6-cPGI2 group was the same as that in control, whereas the increase in clearance in the PGI2 group was reduced. PVR and Ppa increased to a greater extent in the 6-cPGI2 group than in the control group, whereas the increases in PVR and Ppa were inhibited in the PGI2 group. Neutrophil and platelet counts decreased after thrombin in PGI2 and 6-cPGI2 groups, as they did in the control group. Neither 6-cPGI2 altered neutrophil chemotaxis induced by thrombin and chemiluminescence induced by opsonized zymosan. Both prostacyclin compounds inhibited platelet aggregation induced by ADP or thrombin.(ABSTRACT TRUNCATED AT 250 WORDS)

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