Search

Your search keyword '"Machado, Tiago M."' showing total 9 results
Start Over Author "Machado, Tiago M."
9 results on '"Machado, Tiago M."'

3. Interaction between the muscle metaboreflex and the arterial baroreflex in control of arterial pressure and skeletal muscle blood flow

Author

Kaur, Jasdeep, primary, Alvarez, Alberto, additional, Hanna, Hanna W., additional, Krishnan, Abhinav C., additional, Senador, Danielle, additional, Machado, Tiago M., additional, Altamimi, Yasir H., additional, Lovelace, Abe T., additional, Dombrowski, Maryetta D., additional, Spranger, Marty D., additional, and O'Leary, Donal S., additional

Published
2016
Full Text
View/download PDF

8. Integrative Cardiovascular Physiology and Pathophysiology: Exaggerated coronary vasoconstriction limits muscle metaboreflex-induced increases in ventricular performance in hypertension.

Author

Spranger, Marty D., Kaur, Jasdeep, Sala-Mercado, Javier A., Krishnan, Abhinav C., Abu-Hamdah, Rania, Alvarez, Alberto, Machado, Tiago M., Augustyniak, Robert A., and O'Leary, Donal S.

Subjects
PATHOLOGICAL physiology, HYPERTENSION
Abstract

Increases in myocardial oxygen consumption during exercise mainly occur via increases in coronary blood flow (CBF) as cardiac oxygen extraction is high even at rest. However, sympathetic coronary constrictor tone can limit increases in CBF. Increased sympathetic nerve activity (SNA) during exercise likely occurs via the action of and interaction among activation of skeletal muscle afferents, central command, and resetting of the arterial baroreflex. As SNA is heightened even at rest in subjects with hypertension (HTN), we tested whether HTN causes exaggerated coronary vasoconstriction in canines during mild treadmill exercise with muscle metaboreflex activation (MMA; elicited by reducing hindlimb blood flow by ~60%) thereby limiting increases in CBF and ventricular performance. Experiments were repeated after α1-adrenergic blockade (prazosin; 75 κg/kg) and in the same animals following induction of HTN (modified Goldblatt 2K1C model). HTN increased mean arterial pressure from 97.1 ± 2.6 to 132.1 ± 5.6 mmHg at rest and MMA-induced increases in CBF, left ventricular dP/dtmax, and cardiac output were markedly reduced to only 32 ± 13, 26 ± 11, and 28 ± 12% of the changes observed in control. In HTN, α1-adrenergic blockade restored the coronary vasodilation and increased in ventricular function to the levels observed when normotensive. We conclude that exaggerated MMA-induced increases in SNA functionally vasoconstrict the coronary vasculature impairing increases in CBF, which limits oxygen delivery and ventricular performance in HTN. [ABSTRACT FROM AUTHOR]

Published
2017
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results