The Metabolic Effects of Epinephrine and Related Amines

Ellis, Sydney

doi:10.1097/00132586-195710000-00091

Cited by 42 publications

(55 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These changes in FFA level appeared to bear a reciprocal relation to changes in blood glucose levels. Norepinephrine has insignificant glycogenolytic properties compared with epinephrine (22), and no rise in blood glucose is seen with the former. Norepinephrine was therefore chosen for the following experiments in which sustained FFA levels were desired.…”

Section: Resultsmentioning

confidence: 91%

The Role of Plasma Free Fatty Acids in Development of Fatty Liver

Feigelson¹,

Pfaff²,

Karmen³

et al. 1961

J. Clin. Invest.

201

View full text Add to dashboard Cite

Section: Resultsmentioning

confidence: 91%

The Role of Plasma Free Fatty Acids in Development of Fatty Liver

Feigelson¹,

Pfaff²,

Karmen³

et al. 1961

J. Clin. Invest.

201

View full text Add to dashboard Cite

“…Results collected by Ellis (1956) show that figures given by various workers for the relative stimulation of oxygen consumption by these amines in different species vary from noradrenaline being 0.9 of that of adrenaline to being equal. Lee (1953) recorded the oxygen consumption of cat papillary muscle and found the two drugs indistinguishable in their effects.…”

Section: The Effects Of Noradrenaline and Adrenalinementioning

confidence: 91%

Some Factors Influencing the Recovery of Isolated Myocardium From Acute Anoxia

Penn

1965

British Journal of Pharmacology and Chemotherapy

View full text Add to dashboard Cite

The heart is fundamentally aerobic in contrast to skeletal muscle. This is obvious from the rich supply of oxidative enzymes, the numerous mitochondria and the high ratio of one capillary to each muscle fibre (Olson & Schwartz, 1951). It has been previously held that the myocardium is unable to support an oxygen debt. Recent work (Coffman & Gregg, 1961) has modified this view but still indicates that, although the myocardium can derive a considerable portion of its energy requirements anaerobically during transient periods of oxygen deprivation, the capabilities of the normal heart are very limited in this respect. It is a fundamental concept that, for normal function, the heart must be adequately oxygenated.In some circumstances the heart may, for a time, be partially or completely deprived of its usual oxygen supply. These circumstances include coronary insufficiency and some modem heart surgery. The determination of the safe length of myocardial anoxia and the factors influencing the length of this period are important problems. Some workers have also emphasized the possibility of treating or preventing the oxygen deficit by means of compounds which affect the myocardial metabolism directly.The work described in this paper was performed in an attempt to delineate some of the factors involved in the recovery of isolated myocardium from acute anoxia and to see how this recovery could be modified by the application of such drugs as adrenaline, noradrenaline, reserpine, iproniazid, dipyridamole and sodium nitrite. METHODSThe preparations used were the isolated heart and the isolated atria of the rabbit. Isolated hearts were perfused by the Langendorff technique with Locke solution at 50 cm of water pressure. The constitution (g/100 ml.) of the Locke solution was: NaCl 0.9, KCl 0.042, CaCl2 0.024, NaHCO3 0.05 and glucose 0.1. It was gassed with 97% oxygen and 3% carbon dioxide. The rabbits were mainly albino and averaged between 1 and 1.2 kg body weight.The apparatus was based on that of Baker (1951). The coronary input was measured as drops making contact across silver wires connected to a Thorp impulse counter. The amplitude of the beat was recorded by a spring-loaded Brodie Universal lever writing on a smoked drum. The lever was attached by thread to a small hook in the right ventricular apex. Drugs were given by continuous perfusion of a fixed concentration.

show abstract

“…Nicotine causes activation of the sympathetic nervous system and the release of catechols (23,24), which increase EE in humans (25,26). CS or catechol administration increases serum FFA concentrations (27)(28)(29).…”

Section: Introductionmentioning

confidence: 99%

Effects of cigarette smoking and its cessation on lipid metabolism and energy expenditure in heavy smokers.

Hellerstein

Nl²,

Neese³

et al. 1994

J. Clin. Invest.

148

107

View full text Add to dashboard Cite

The relationship between thermogenic and potentially atherogenic effects of cigarette smoking (CS) and its cessation was investigated. Heavy smokers (n = 7, serum cotinine > 200 ng/ ml, > 20 cigarettes/d) were maintained on isoenergetic, constant diets for 2 wk, 1 wk with and I wk without CS. Stable isotope infusions with indirect calorimetry were performed on day 7 of each phase, after an overnight fast. CS after overnight abstention increased resting energy expenditure by 5% (not significant vs. non-CS phase; P = 0.18). CS increased the flux of FFA by 77%, flux of glycerol by 82%, and serum FFA concentrations by 73% (P < 0.02 for each), but did not significantly affect fat oxidation. Hepatic reesterification of FFA increased more than threefold (P < 0.03) and adipocyte recycling increased nonsignificantly (P = 0.10). CS-induced lipid substrate cycles represented only 15% (estimated 11 kcal/d) of observed changes in energy expenditure. De novo hepatic lipogenesis was low (< 1-2 g/d) and unaffected by either acute CS or its chronic cessation. Hepatic glucose production was not affected by CS, despite increased serum glycerol and FFA fluxes. Cessation of CS caused no rebound effects on basal metabolic fluxes. In conclusion, a metabolic mechanism for the atherogenic effects of CS on serum lipids (increased hepatic reesterification of FFA) has been documented. Increased entry of FFA accounts for CS-induced increases in serum FFA concentrations. The thermogenic effect of CS is small or absent in heavy smokers while the potentially atherogenic effect is maintained, and cessation of CS does not induce a rebound lipogenic milieu that specifically favors accrual of body fat in the absence of increased food intake. (J. Clin. Invest. 1994. 93:265-272).

show abstract

The Metabolic Effects of Epinephrine and Related Amines

Cited by 42 publications

References 0 publications

The Role of Plasma Free Fatty Acids in Development of Fatty Liver

The Role of Plasma Free Fatty Acids in Development of Fatty Liver

Some Factors Influencing the Recovery of Isolated Myocardium From Acute Anoxia

Effects of cigarette smoking and its cessation on lipid metabolism and energy expenditure in heavy smokers.

Contact Info

Product

Resources

About