MECHANISMS OF HEMOCONCENTRATION IN THE DOG DURING ACUTE ENDRIN INSECTICIDE POISONING

1965 ◽  
Vol 43 (5) ◽  
pp. 793-800 ◽  
Author(s):  
Thomas E. Emerson Jr.
Keyword(s):  
Pulmonary Artery ◽  
Venous Return ◽  
Venous Pressure ◽  
Lung Weight ◽  
Vascular Volume ◽  
Isolated Perfused Lung ◽  
Blood Ph ◽  
Early Increase ◽  
Perfused Lung ◽  
Low Levels

Hemoconcentration following intravenous administration of the chlorinated hydrocarbon insecticide endrin was investigated in sham-operated, splenectomized, and abdominal-eviscerated dogs. Isolated perfused lung preparations and those in which total venous return to the heart was monitored were also utilized. By 30 minutes after endrin the hematocrit had increased 14% in sham-operated animals but only 8% in splenectomized and eviscerated dogs. Blood pH fell to low levels in all groups. Pulmonary artery pressure increased in the constant flow perfused lungs after endrin; an early increase preceded a loss of lung weight. Pulmonary vascular resistance and left atrial and pulmonary artery pressures increased after endrin in the venous return studies. Hemoconcentration appears to result in part from addition of cell-rich blood from the spleen, and an increase in mean corpuscular volume secondary to the severe acidemia as observed in several experiments may also be involved. Loss of plasma fluid in the hepatosplanchnic area does not seem to occur, but pulmonary venous pressure was elevated, and loss of vascular volume from the lungs cannot be excluded.

Effect of small doses of 5-hydroxytryptamine (serotonin) on pulmonary circulation in the closed-chest dog

1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Veins ◽  
Pulmonary Vessels ◽  
Isolated Perfused Lung ◽  
Small Doses ◽  
Perfused Lung ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
The Difference

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.

Adrenomedullin activity in chronically hypoxic rat lungs

1996 ◽  
Vol 271 (2) ◽  
pp. H622-H629 ◽  
Author(s):  
L. Zhao ◽  
L. A. Brown ◽  
A. A. Owji ◽  
D. J. Nunez ◽  
D. M. Smith ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Mrna Levels ◽  
Rat Lung ◽  
Artery Pressure ◽  
Isolated Perfused Lung ◽  
Calcitonin Gene ◽  
Perfused Lung ◽  
Hypotensive Response

Adrenomedullin (AM) is a novel vasodilator with structural similarities to calcitonin gene-related peptide (CGRP). This study investigated AM activity in the rat lung during hypoxia-induced pulmonary hypertension. Both rat AM (0.2-10 nmol) and alpha-CGRP (0.2-2 nmol) produced dose-related reductions in pulmonary artery pressure in the isolated perfused lung ventilated with 2% O2. Pretreatment with alpha-CGRP, which demonstrated tachyphylaxis, or its antagonist, CGRP-(8–37), reduced the hypotensive response to AM, suggesting that part of the response to AM is mediated by CGRP receptors. 125I-labeled AM and 125I-labeled CGRP binding was significantly increased in lung membranes from 7-day hypoxic animals (AM from 1.94 +/- 0.3 to 3.36 +/- 0.4 and CGRP from 0.06 +/- 0.01 to 0.12 +/- 0.02 pmol/mg protein), with no change in dissociation constant. Moreover, the hypotensive response to both peptides was increased in the lungs of 7-day hypoxic rats. There was no significant change in lung immunoreactive AM concentrations (hypoxic 5.04 +/- 0.48 vs. control 6.28 +/- 0.76 pmol/g wet wt of tissue) or steady-state AM mRNA levels in 7-day hypoxic rats. Nonetheless, AM may be useful for the acute pharmacological manipulation of pulmonary artery pressure in hypoxia-induced pulmonary hypertension.

Protein metabolism in lung: use of isolated perfused lung to study protein degradation

1979 ◽  
Vol 47 (1) ◽  
pp. 72-78 ◽  
Author(s):  
M. J. Chiang ◽  
P. Whitney ◽  
D. Massaro
Keyword(s):  
Protein Degradation ◽  
Protein Metabolism ◽  
Lung Weight ◽  
Isolated Perfused Lung ◽  
Constant Rate ◽  
Perfused Lung

This study investigates the use of the isolated perfused lung to study protein degradation. Proteins were labeled in vivo for 10 min or for 5 h using L-[U-14C]phenylalanine. When prelabeled lungs were perfused in vitro virtually all of the acid-soluble and acid-insoluble radioactivity in the tissue and perfusate remained as phenylalanine. Protein degradation was measured as the accumulation of free [14C]phenylalanine in ther perfusate; during the time this accumulated the amount of intracellular free phenylalanine and the free phenylalanine space remained constant. Proteins labeled during 10 min had a constant rate of degradation between 45 and 90 min of perfusion (about 11%.h-1); those labeled during 5 h had a constant rate of degradation for 90 (about 3%.h-1). The percent dry lung weight did not change during the perfusion. We conclude that measurable rates of proteolysis of “rapid” and “slowly” turning over proteins can be obtained while the lung is virtually free of edema. This system should allow studies on the modulation of proteolysis in intact lung under defined conditions.

A comparative study of the hemodynamic actions of histamine and endotoxin

1962 ◽  
Vol 203 (4) ◽  
pp. 600-606 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Thomas E. Emerson ◽  
P. F. Iampietro ◽  
Charles M. Brake
Keyword(s):  
Venous Return ◽  
Venous Pressure ◽  
Underlying Mechanism ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Relative Role ◽  
Small Vein ◽  
Early Increase ◽  
Logical Extension

The present study is a logical extension of earlier work with the aim of evaluating the relative role of histamine in endotoxin shock. A variety of experiments on 91 dogs were carried out in which the hemodynamic actions of histamine, a histamine releaser (48/80), and endotoxin were compared. Results indicate definite similarities of action in a number of vascular parameters: a) an early increase in portal venous pressure coincident with a decrease in venous return, pooling, and a rapid decrease in systemic arterial pressure and b) eventual increases in foreleg resistance, foreleg small vein pressure, leg weight, and circulating hematocrit. The early responses to endotoxin are greatly altered when 48/80 is administered prior to endotoxin which suggests a common underlying mechanism for the action of each agent. Histamine appears to serve as a triggering device for the sustained release of adrenergic-like agents which superimpose their effects on those of histamine. These findings offer additional evidence for the early release of histamine in endotoxin shock.

Solute conductance of blood-gas barrier in hamsters exposed to hyperoxia

1986 ◽  
Vol 60 (6) ◽  
pp. 1908-1916 ◽  
Author(s):  
D. Wangensteen ◽  
R. Piper ◽  
J. A. Johnson ◽  
A. A. Sinha ◽  
D. Niewoehner
Keyword(s):  
Bovine Serum Albumin ◽  
Alveolar Epithelium ◽  
Capillary Endothelium ◽  
Blood Gas ◽  
Lung Weight ◽  
Gas Barrier ◽  
Functional Changes ◽  
Isolated Perfused Lung ◽  
Perfused Lung ◽  
Wet Weight

Hamsters were exposed to greater than 95% O2 continuously for up to 5 days to determine longitudinal changes in the diffusive conductance of the alveolar epithelium and capillary endothelium as a result of hyperoxia. Permeability X surface area (PS, cm3/s X 10(-4)) was measured by isolated, perfused lung techniques. Alveolar epithelium PS for [14C]sucrose and 125I-bovine serum albumin (BSA) were determined at seven exposure times. Control PS (sucrose) and PS(BSA) averaged 1.00 and 0.022, respectively. Values were unchanged until 4.5 days, when significant increases in both, but especially PS(BSA), occurred. After 5 days, PS values were 4.69 and 0.691, respectively. Capillary endothelium PS for 125I-BSA and fluoresceinisothiocyanate dextran-150 (D-150) were measured at four exposure times. Control endothelium PS(BSA) and PS(D-150) averaged 0.232 and 0.048, respectively. These values were also unchanged after 4 days but increased to 0.440 and 0.131 after 5 days. Wet lung weight significantly increased after only 4 days. Hyperoxia thus increased both endothelium and epithelium PS, but epithelium changes were much greater. These functional changes do not occur for several days, occur simultaneously, and follow increases in lung wet weight.

Pulmonary diffusion in the dog lung

1962 ◽  
Vol 17 (6) ◽  
pp. 885-892 ◽  
Author(s):  
Albert H. Niden ◽  
Charles Mittman ◽  
Benjamin Burrows
Keyword(s):  
Carbon Monoxide ◽  
Pulmonary Artery ◽  
Experimental Animal ◽  
Venous Blood ◽  
Whole Body ◽  
Mixed Venous Blood ◽  
Pulmonary Diffusion ◽  
Perfused Lung ◽  
Pulmonary Arterial ◽  
Mixed Venous

Methods have been presented for assessing pulmonary diffusion by the “equilibration technique” in the experimental intact dog and perfused lung while controlling ventilation with a whole body respirator. No significant change in diffusion of carbon monoxide was noted between open and closed chest anesthetized animals, with duration of anesthesia in the intact dog, or with duration of perfusion of the isolated dog's lung. There was no demonstrable difference in diffusion when arterialized blood was used as the perfusate in place of mixed venous blood in the lung perfusions suggesting that within the range studied the Po2, Pco2, and pH of pulmonary artery blood does not directly affect the diffusion of carbon monoxide. Retrograde perfusions of dogs' lungs did not significantly alter diffusion, suggesting that pulmonary venous resistance was not significantly lower than pulmonary arterial resistance in the perfused dog lung at the flows and pressures studied. The equilibration technique for measuring pulmonary diffusion and assessing the uniformity of diffusion was well suited to the study of pulmonary diffusing characteristics in the experimental animal. Submitted on January 8, 1962

scholarly journals Repair of total anomalous pulmonary venous return (TAPVR) with pulmonary artery (PA) Stenosis in adult

2015 ◽  
Vol 10 (S1) ◽  
Author(s):  
Fuad Z Abdullayev ◽  
Imadaddin M Bagirov ◽  
Nigar J Kazimzade ◽  
Larisa S Shikhiyeva
Keyword(s):  
Pulmonary Artery ◽  
Venous Return ◽  
Anomalous Pulmonary Venous Return

Computer simulation of experiments in responses to intravenous and inhaled CO2

1981 ◽  
Vol 50 (4) ◽  
pp. 835-843 ◽  
Author(s):  
W. S. Yamamoto
Keyword(s):  
Venous Return ◽  
Neural Signal ◽  
Set Point ◽  
Ventilatory Responses ◽  
Operating Level ◽  
Excitatory State ◽  
Co2 Level ◽  
Neural Excitation ◽  
Low Levels ◽  
Hypercapnic Response

A simulation of ventilatory responses to infused and inhaled CO2 at controlled cardiac output and high and low levels of neural excitation mimics comparable experiments in animals. The model suggests that at low levels of endogenous and exogenous CO2 load the alert quiescent animal will show hyperpnea to both test states associated with hypercapnia. The nonalert quiescent animal simulated will show an isocapnic response to endogenous load and hypercapnic response to exogenous load. The explanation of this behavior lies in the model formulation, which allows the neural signal from metabolically active sources to drive the proportional component of the controller below an operating level established by its set point. By this reasoning the excited but metabolically inactive animal should be paradoxically less sensitive to small changes in CO2, whether exogenous or endogenous, than the quiescent animal. The model demonstrates further that a neural "exercise" signal in proportion to venous return better simulates observations in which CO2 load and venous return are dissociated than one in which the neural signal is computed from metabolism. The use of delta V/delta P slopes as estimates of sensitivity go awry in experiment and simulation when blood flow, CO2 level, and neural excitatory state are dissociated. This is particularly true when the organism is operating at and below the hypothesized set point.

Alterations in Systemic Vascular Volume of the Dog in Response to Hexamethonium and Norepinephrine

1957 ◽  
Vol 191 (2) ◽  
pp. 283-286 ◽  
Author(s):  
John C. Rose ◽  
Edward D. Freis
Keyword(s):  
Cardiac Output ◽  
Venous Return ◽  
Cardiac Activity ◽  
Left Ventricular ◽  
Vascular Volume ◽  
Vasomotor Activity ◽  
Constant Output ◽  
Arteriolar Tone ◽  
Integrated Responses

A diaphragm pump of controlled constant output was substituted for the left ventricle in dogs. Left auricular blood was conducted to a reservoir, from which it was pumped into the thoracic aorta. Left ventricular by-pass was complete. Alterations in total vascular volume were continually monitored by observation of the pump reservoir level. Sympathetic blockade (hexamethonium) increased total vascular volume (mean 15%). This resulted in decreased venous return and decreased right ventricular output. Norepinephrine constricted the total vasculature and decreased vascular volume (mean 12%). This resulted in increased venous return and cardiac output. These experiments demonstrated the complex integrated responses of the total circulation to sympathetic vasomotor activity. The role of the sympathetic nervous system not only in the regulation of arteriolar tone and cardiac activity but also in adjusting total vascular volume and venous return was emphasized. Venous return, and hence cardiac output alterations accompanying systemic vasomotor activity can only be detected by continuous methods of flow measurement.

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