scholarly journals Phosphodiesterase 4 inhibition attenuates plasma volume loss and transvascular exchange in volume-expanded mice

2011 ◽  
Vol 590 (2) ◽  
pp. 309-322 ◽  
Author(s):  
Yueh-Chen Lin ◽  
Roger H. Adamson ◽  
Joyce F. Clark ◽  
Rolf K. Reed ◽  
Fitz-Roy E. Curry
2007 ◽  
Vol 57 (2) ◽  
pp. 95-99 ◽  
Author(s):  
James A. Davis ◽  
Ralph Rozenek ◽  
Derek M. DeCicco ◽  
Michael T. Carizzi ◽  
Patrick H. Pham

2012 ◽  
Vol 73 (6) ◽  
pp. 1531-1536 ◽  
Author(s):  
Peter Bansch ◽  
Cornelia Lundblad ◽  
Per-Olof Grände ◽  
Peter Bentzer

Science ◽  
1976 ◽  
Vol 191 (4229) ◽  
pp. 861-862 ◽  
Author(s):  
J. Hilton ◽  
C. Wells

1975 ◽  
Vol 49 (6) ◽  
pp. 551-555 ◽  
Author(s):  
B. Hesse ◽  
I. Nielsen ◽  
H. Lund-Jacobsen

1. Nine patients with clinically unimportant heart disease or benign essential hypertension were given frusemide intravenously during right-heart catheterization. 2. Pressures in both atria decreased rapidly and in parallel. The magnitude of the pressure decrease was clearly related to decrease in plasma volume loss. 3. Plasma renin activity increased significantly after 5 min (P < 0·01), but did not correlate with plasma volume loss. 4. Venous tone in the forearm was unchanged. 5. It is concluded that the pressure reduction was secondary to plasma volume depletion through diuresis and that increased plasma renin activity was mainly caused by intrarenal changes.


1963 ◽  
Vol 205 (2) ◽  
pp. 225-229 ◽  
Author(s):  
W. W. Swingle ◽  
A. J. Swingle

Metrazol-shocked nonadrenalectomized dogs exhibit a drastic though evanescent decline in plasma volume. A similar fall in plasma volume in the adrenalectomized dog persists and culminates in circulatory collapse unless C11 oxysteroids are administered. Loss of circulating fluid volume seems not to be due to shift of water into cells since the modest increase in hematocrit is insufficient to account for the volume change, nor can the volume decline be attributed to loss of vascular fluid into the extracellular compartment; this space decreased along with the plasma volume. The plasma volume loss of Metrazol-shocked dogs without adrenals seems due to intense, unrelieved vasoconstriction initiated by massive stimulation of the central nervous system by the drug, apparently resulting in closure of much of the vascular periphery, sequestration, and trapping of fluid and cells. Glucocorticoids somehow relieve the vasoconstriction and re-establish free blood flow at the periphery of the vascular tree. The fleeting elevation of plasma Na characteristic of Metrazol shock is independent of plasma volume changes and probably neurogenic in origin.


2020 ◽  
pp. 1-8
Author(s):  
A. Kashef ◽  
A. Sadeghi Nikoo

The purpose of this study was to investigate the cardiac biomarkers like cardiac troponin T (cTnT), cardiac troponin I, and creatine kinase-MB (CK-MB) and the cell damage biomarkers including creatine phosphokinase (CPK), C-reactive protein (CRP), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) in response to a short-duration high-intensity competition with correction of the post-exercise raw data with the plasma volume loss in trained athletes. Thirty-two male athletes (age, 26.9±4.7 years) competed in 8 min high-intensity competition. The competition items included: running for 400 meters; three-stage deadlifting; bar pulling up; and 30 kg kettlebell swinging. Venous blood samples were obtained before and immediately after the competition and biomarkers analysed. Plasma volume changes were estimated from haemoglobin and haematocrit readings before and after the competition. A significant increase was shown immediately after the competition compared to resting in cTnT, AST, ALT, CPK, and CRP (P<0/001). CK-MB showed no significant difference. When raw data were corrected for plasma volume loss, CPK showed a significant increase (P<0.001), and LDH and CK-MB a significant decrease (P<0.001), however cTnT, AST, ALT and CRP showed no significant difference. The plasma volume loss can affect the response of cardiac and cellular damage biomarkers to exercise. High-intensity competition for 8 min did not elevate the cardiac biomarkers, but elevated the muscle biomarkers.


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