scholarly journals Effects of Beta Blockers on Cardiac Function and Myocardial Oxygen Consumption in the Isolated Supported Heart Preparation of the Dog

1975 ◽  
Vol 16 (5) ◽  
pp. 592-602 ◽  
Author(s):  
Seiji KUMAKURA ◽  
Takeshi OSHIMA
1983 ◽  
Vol 244 (6) ◽  
pp. H799-H806 ◽  
Author(s):  
K. A. Fox ◽  
H. Nomura ◽  
B. E. Sobel ◽  
S. R. Bergmann

Assessments of myocardial metabolism based on external detection of accumulation of radiolabeled substrates may be influenced, as a result of alterations in flow, by altered substrate delivery as well as altered work (with concomitant changes in metabolic requirements). To determine whether reduced delivery limits substrate utilization under defined conditions of reduced perfusion, an isolated rabbit heart preparation was employed in which flow was reduced but myocardial oxygen consumption (MVo2) and work were kept constant by adjustment of left ventricular end-diastolic pressure and heart rate. Flow was reduced from 1.5 to 0.5 ml . g-1 . min-1, while work was maintained constant in hearts functioning at either low or high levels of MVo2. Consumption of palmitate remained constant (48.8 +/- 11.6 and 68.8 +/- 23.3 nmol . g-1 . min-1), because the proportion of palmitate extracted increased (8.8 +/- 4 to 29.1 +/- 7.2% and 10.3 +/- 3.4 to 21.0 +/- 6.1%). The results indicate that, despite reduction of flow, hearts at constant work loads can extract increasing proportions of delivered substrates such that net utilization remains constant until flow is reduced below the level required to maintain cellular function. They suggest that, under conditions of low flow, impaired extraction of substrates reflects either primarily or secondarily depressed myocardial metabolism rather than simply decreased delivery of substrate.


2017 ◽  
Vol 8 (1) ◽  
pp. 204589321774312 ◽  
Author(s):  
Mona S. Hansen ◽  
Asger Andersen ◽  
Lars P. Tolbod ◽  
Nils H. Hansson ◽  
Roni Nielsen ◽  
...  

Levosimendan is an inotropic and vasodilator drug, which is known to improve cardiac function in animal models of right ventricular (RV) failure. The effects of levosimendan on oxygen consumption and myocardial efficiency in the failing RV is unknown. We investigated the effects of levosimendan on RV function, myocardial oxygen consumption, myocardial external efficiency (MEE), and myocardial metabolism in rats with RV hypertrophy and failure. RV hypertrophy and failure were induced by pulmonary trunk banding in rats. Rats were randomized to seven weeks of treatment with vehicle (n = 16) or levosimendan (3 mg/kg/day) (n = 13). Control animals without pulmonary banding received vehicle treatment (n = 11). RV MEE and RV metabolism were evaluated by echocardiography, 11C-acetate positron emission tomography (PET), 18F-FDG PET, and invasive pressure measurements. We found that levosimendan improved RV MEE (26 ± 3 vs. 14 ± 1%, P < 0.01) by increasing RV external work (0.62 ± 0.06 vs. 0.30 ± 0.03 mmHgċmL, P < 0.001) without affecting RV myocardial oxygen consumption ( P = 0.64). The improvement in RV MEE was not associated with a change in RV myocardial glucose uptake (1.3 ± 0.1 vs. 1.0 ± 0.1 µmol/g/min, P = 0.44). In conclusion, in the hypertrophic and failing RV of the rat, levosimendan improves RV function without increasing myocardial oxygen consumption leading to improved MEE. The improvement in RV MEE was not associated with a change in myocardial glucose uptake. This study emphasizes the potential therapeutic value of chronic levosimendan treatment RV failure. It extends previous observations on the effect profile of levosimendan and motivates clinical testing of levosimendan in RV failure.


1960 ◽  
Vol 198 (5) ◽  
pp. 965-970 ◽  
Author(s):  
Koroku Hashimoto ◽  
Tatauro Shigei ◽  
Shoichi Imai ◽  
Yoshiharu Saito ◽  
Nagataka Yago ◽  
...  

An improved method of determining the coronary flow and myocardial oxygen consumption of the Langendorf dog heart preparation with ventricular fibrillation is described. Stable levels of these two functions are obtained for a 6-hour period. The effects of acetylcholine, epinephrine, levarterenol, isoproterenol, methoxamine and Pitressin are studied. Further, the effects of the sympathomimetic amines are studied before and afteŕ treatment with Dibenzyline and the dichloroanalogue of isoproterenol. A significant correlation between coronary flow and myocardial oxygen consumption is found in all cases. It is concluded that epinephrine and levarterenol cause coronary vasodilation by increasing the myocardial oxygen consumption though initially producing a vasoconstriction. Isoproterenol affects myocardial oxygen consumption and has no direct vascular effect. These studies are interpreted as revealing the existence of sympathetic vasoconstrictor and parasympathetic vasodilator receptors and the absence of pure sympathetic vasodilator receptors in the coronary vessel wall.


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