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Featured researches published by Arthur W. Lindsey.


Circulation Research | 1959

Effect of Elevated Left Atrial Pressure and Decreased Plasma Protein Concentration on the Development of Pulmonary Edema

Arthur C. Guyton; Arthur W. Lindsey; Johnnie O. Howell; W Williams John; A Franklin Malcolm

In 97 dogs left atrial pressure was elevated to various levels up to 50 mm. Hg by partial constriction of the aorta. The effect of these pressures for from 30 min. to 3 hours on the accumulation of lung edema was then studied. Edema was estimated by determining the ratio of the weight of the wet lung to the weight of the same lung after drying. In animals with normal plasma protein concentrations fluid began to transude into the lungs when the left atrial pressure rose above an average of 24 mm. Hg. In another series of animals the plasma protein concentrations were reduced by plasmapheresis at the beginning of each experiment until the plasma protein concentration averaged 47 per cent of the control value. In these animals fluid began to transude into the lungs when the left atrial pressure rose above a critical value of 11 mm Hg. Furthermore, the rate at which fluid accumulated in the lungs, in all series of experiments, was directly proportional to the rise in left atrial pressure above the critical pressure at which fluid began to collect in the lungs.


Circulation Research | 1954

The Limits of Right Ventricular Compensation Following Acute Increase in Pulmonary Circulatory Resistance

Arthur C. Guyton; Arthur W. Lindsey; John J. Gilluly

The ability of the right ventricle to compensate as the pulmonary artery is constricted appears to be determined by four major factors: (1) there occurs the well-known increased force of contraction as the right heart becomes distended; (2) the adequacy of the coronary circulation determines to a great extent the Degrees of pulmonary arterial constriction which can occur before failure occurs; (3) the circulatory reflexes apparently aid the compensation to a moderate extent; and (4) the greater the blood volume, the greater is the limit of compensation before right ventricular failure occurs.


American Journal of Physiology | 1957

Mechanism of the Increased Venous Return and Cardiac Output Caused by Epinephrine

Arthur C. Guyton; Arthur W. Lindsey; Berry Abernathy; Jimmy B. Langston

The effect of epinephrine on venous return has been measured in 11 dogs under total spinal anesthesia. The mechanism by which epinephrine increases venous return seems to be to increase the tone of...


American Journal of Physiology | 1957

Venous Return at Various Right Atrial Pressures and the Normal Venous Return Curve

Arthur C. Guyton; Arthur W. Lindsey; Berry Abernathy; Travis Q. Richardson


American Journal of Physiology | 1955

Effect of Mean Circulatory Filling Pressure and Other Peripheral Circulatory Factors on Cardiac Output

Arthur C. Guyton; Arthur W. Lindsey; Berwind N. Kaufmann


American Journal of Physiology | 1958

Effect of blood transfusion and hemorrhage on cardiac output and on the venous return curve.

Arthur C. Guyton; Arthur W. Lindsey; Berwind N. Kaufmann; Joseph B. Abernathy


American Journal of Physiology | 1957

Pulmonary blood volume of the dog and its changes in acute heart failure.

Arthur W. Lindsey; Benjamin F. Banahan; Russell H. Cannon; Arthur C. Guyton


American Journal of Physiology | 1959

Continuous recording of pulmonary blood volume: pulmonary pressure and volume changes

Arthur W. Lindsey; Arthur C. Guyton


The American Journal of Medicine | 1954

Relationship of the mean circulatory filling pressure to cardiac output

Arthur C. Guyton; Dimitri Polizo; Arthur W. Lindsey


Archive | 2010

Concentration on the Development of Pulmonary Edema Effect of Elevated Left Atrial Pressure and Decreased Plasma Protein

Arthur C. Guyton; Arthur W. Lindsey

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Arthur C. Guyton

University of Mississippi Medical Center

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John J. Gilluly

University of Mississippi

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Jimmy B. Langston

University of Mississippi Medical Center

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W Williams John

University of Mississippi

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