Sympathetic Control of the Coronary Circulation in the Unanesthetized Dog

2015 ◽  
pp. 89-97 ◽  
Author(s):  
B. Pitt
Keyword(s):  
Coronary Circulation ◽  
Sympathetic Control

scholarly journals Sympathetic Control of Coronary Circulation During Cold Pressor Test

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Maitê Gondim ◽  
Helena Rocha ◽  
Thiago Cavalcanti ◽  
Luis Olveira ◽  
Pedro Mira ◽  
...  
Keyword(s):  
Coronary Circulation ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Sympathetic Control ◽  
Pressor Test

Sympathetic Control of the Coronary Circulation

1990 ◽  
pp. 197-209
Author(s):  
Ishio Ninomiya ◽  
Tsuyoshi Akiyama ◽  
Toshihiro Honda ◽  
Naoki Nishiura
Keyword(s):  
Coronary Circulation ◽  
Sympathetic Control

scholarly journals The coronary circulation

1928 ◽  
Vol 65 (4) ◽  
pp. 357-373 ◽  
Author(s):  
G. V. Anrep ◽  
H. Häusler
Keyword(s):  
Coronary Circulation

Myocardial CO2 buffering: role of transmembrane transport of H+ or HCO3-ions

1976 ◽  
Vol 230 (4) ◽  
pp. 1037-1041 ◽  
Author(s):  
DR Strome ◽  
RL Clancy ◽  
NC Gonzalez
Keyword(s):  
Small Volume ◽  
Coronary Circulation ◽  
Myocardial Cell ◽  
Ringer Solution ◽  
Red Cells ◽  
Transmembrane Transport ◽  
High Degree

Isolated rabbit hearts were perfused with rabbit red cells suspended in Ringer solution. A small volume of perfusate was recirculated for 10 min at Pco2 of 33.4 +/- 0.9 or 150.8 +/- 7.5 mmHg. Hypercapnia resulted in an increase in perfusate HCO3- concentration that was smaller than that observed when isolated perfusate was equilibrated in vitro with the same CO2 tensions (delta HCO-3e = 1.6 mM, P less than 0.01). This difference is consistent with a net movement of HCO3- into or H+ out of the mycardial cell, and cannot be accounted for by dilution of HCO3- in the myocardial interstitium. Recirculation of perfusate through the coronary circulation at normal Pco2 for two consecutive 10-min periods was not followed by changes in perfusate HCO3- concentration. A high degree of correlation (r = 0.81) was observed between intracellular HCO-3e concentration and the corresponding delta HCO-3e in individual experiments. The results suggest that transmembrane exchange of H+ or HCO3- is a buffer mechanism for CO2 in the myocardial cell.

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