Relationship of cardiac oxygen usage, adenosine content, and coronary resistance in dogs.

Saito, Daiji; Nixon, Debra G.; Vomacka, Robert B.; Olsson, Ray A.

doi:10.1161/01.res.47.6.875

Cited by 37 publications

(12 citation statements)

References 23 publications

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“…This is consistent with the observation by several groups of investigators, who found parallel relationships between V02, m' coronary blood flow and myocardial adenosine production (Miller, Belardinelli, Bacchus, Foley, Rubio & Berne, 1979;Saito, Nixon, Vomacka & Olsson, 1980; Bacchus, Ely, Knabb, Rubio & Berne, 1982;Knabb et al 1983). Since (Fig.…”

Section: Discussionsupporting

confidence: 92%

The role of adenosine in functional hyperaemia in the coronary circulation of anaesthetized dogs.

Karim

Goonewardene

1996

The Journal of Physiology

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1. The aim of this investigation was to determine the contribution of adenosine to coronary active hyperaemia in the dog denervated heart by using adenosine deaminase. 2. Beagles were anaesthetized with thiopentone sodium (500 mg, i.v.) and chloralose (100 mg kg-', i.v.) and artificially ventilated. The hearts were denervated by bilateral cervical vagotomy and cardiac sympathectomy. Blood samples were collected from the coronary sinus via a cannula passed through the right external jugular vein. The anterior descending or circumflex branch of the left coronary artery was cannulated and perfused with blood from the left subclavian artery under systemic blood pressure through an electromagnetic flow probe and a perfusion circuit. The heart was paced (3 V, 0 2 ms and a suitable frequency) via two electrodes attached to the right atrium from 109 + 7-3 to 170 + 9 8 beats min-' (means + S.E.M.) for 3-4 min, first during an infusion of the solvent, and then during an infusion of a solution of adenosine deaminase (5 U kg-' min-') into the circuit. 3. In seventeen tests in eight dogs, infusion of adenosine deaminase did not cause a significant change in the basal coronary blood flow nor in the immediate increase (within 10 s) in blood flow induced by pacing the heart from its basal rate to 170 beats min-'.However, adenosine deaminase did cause a significant attenuation by 58 + 5 2 % (P < 0 05) of the increase in coronary blood flow induced at 3-4 min of pacing from 31 + 4-6 to 43 + 5 8 ml min-' (100 g cardiac tissue)-'. Concomitantly, the pacing-induced increase in coronary vascular conductance (from 0-41 + 0-08 to 0 54 + 0-12 ml min-' (100 g)' mmHg-') was reduced by 75 + 6-6% (P < 0 02) and the increase in myocardial 02 consumption (from 13 + 3 5 to 21 + 4 2 ml min-' (100 g)-) was reduced by 50 + 12% (P < 0 05) but without significant changes in oxygen extraction or myocardial contractility. 4. The results show that although adenosine is unlikely to play a significant role in the regulation of the basal coronary blood flow, it can play a major role in the coronary active (functional) hyperaemia induced by atrial pacing to a high rate in the denervated heart of anaesthetized dogs.

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Section: Discussionsupporting

confidence: 92%

The role of adenosine in functional hyperaemia in the coronary circulation of anaesthetized dogs.

Karim

Goonewardene

1996

The Journal of Physiology

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“…Adenosine is an autacoid whose levels increase under stressful conditions such as ␤-adrenergic receptor stimulation, in which metabolic demand is increased (17,22,31). Adenosine binds to four adenosine receptors (A 1 AR, A 2a AR, A 2b AR, and A 3 AR), all of which are expressed in the heart.…”

mentioning

confidence: 99%

Sex differences and the effects of ovariectomy on the β-adrenergic contractile response

McIntosh

Chandrasekera

Lasley

2011

American Journal of Physiology-Heart and Circulatory Physiology

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The presence of sex differences in myocardial β-adrenergic responsiveness is controversial, and limited studies have addressed the mechanism underlying these differences. Studies were performed using isolated perfused hearts from male, intact female and ovariectomized female mice to investigate sex differences and the effects of ovarian hormone withdrawal on β-adrenergic receptor function. Female hearts exhibited blunted contractile responses to the β-adrenergic receptor agonist isoproterenol (ISO) compared with males but not ovariectomized females. There were no sex differences in β(1)-adrenergic receptor gene or protein expression. To investigate the role of adenylyl cyclase, phosphodiesterase, and the cAMP-signaling cascade in generating sex differences in the β-adrenergic contractile response, dose-response studies were performed in isolated perfused male and female hearts using forskolin, 3-isobutyl-1-methylxanthine (IBMX), and 8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphate (CPT-cAMP). Males showed a modestly enhanced contractile response to forskolin at 300 nM and 5 μM compared with females, but there were no sex differences in the response to IBMX or CPT-cAMP. The role of the A(1) adenosine receptor (A(1)AR) in antagonizing the β-adrenergic contractile response was investigated using both the A(1)AR agonist 2-chloro-N(6)-cyclopentyl-adenosine and A(1)AR knockout (KO) mice. Intact females showed an enhanced A(1)AR anti-adrenergic effect compared with males and ovariectomized females. The β-adrenergic contractile response was potentiated in both male and female A(1)ARKO hearts, with sex differences no longer present above 1 nM ISO. The β-adrenergic contractile response is greater in male hearts than females, and minor differences in the action of adenylyl cyclase or the A(1)AR may contribute to these sex differences.

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“…Although MVO 2 was raised equally by the two stimuli, adenosine release after 10 minutes was elevated in the presence of catecholamine, but not pacing. Also, Saito et al (1980) found that tissue adenosine content of dog hearts increased in response to several stimuli, but not cardiac pacing. On the other hand, Berne et al (1983) found that cardiac pacing of anesthetized and unanesthetized dogs increased adenosine release into venous blood and adenosine content of pericardial fluid.…”

Section: Increased Myocardial Oxygen Consumptionmentioning

confidence: 97%

“…Studies from several laboratories support this possibility. We have already described studies in which cardiac pacing (Weidmeier and Spell, 1977;Saito et al, 1980;Manfredi and Sparks, 1982) and increased afterload (Bardenheuer and Shrader, 1983) did not result in increased steady state adenosine formation, even though MVO 2 was markedly enhanced. Furthermore, when catecholamines or calcium are infused, the release of adenosine is phasic in the face of a steady increase in MVO 2 (DeWitt et al, 1983).…”

Section: Myocardial O 2 Consumptionmentioning

confidence: 99%

“…The increase in myocardial O 2 consumption (MVO2) in response to catecholamine administration is associated with increased tissue (Saito et al, 1980), venous (Manfredi and Sparks, 1982), and pericardial adenosine (Berne and Rubio, 1979). In general, there is a positive correlation between the increase in MVO 2 and the increase in adenosine (Berne et al, 1983).…”

Section: Increased Myocardial Oxygen Consumptionmentioning

confidence: 99%

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Regulation of adenosine formation by the heart.

Sparks¹,

Bardenheuer²

1986

Circulation Research

190

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We think that the available data on adenosine formation suggest the two signals are responsible for adenosine release from cardiac myocytes: (1) the ratio of oxygen supply to demand and (2) agonist-triggered release of extracellular adenine nucleotides. We do not believe that the available data support the oxygen consumption hypothesis. The few studies which allow us to judge the relative importance of these two signals suggest that both hypoxia and sympathetic nerve stimulation release adenosine primarily by decreasing O2 supply:demand. Agonist triggered nucleotide release may be quantitatively important in situations in which decreased O2 supply/demand cannot explain increased release, i.e., isoproterenol and acetylcholine administration.

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Relationship of cardiac oxygen usage, adenosine content, and coronary resistance in dogs.

Cited by 37 publications

References 23 publications

The role of adenosine in functional hyperaemia in the coronary circulation of anaesthetized dogs.

The role of adenosine in functional hyperaemia in the coronary circulation of anaesthetized dogs.

Sex differences and the effects of ovariectomy on the β-adrenergic contractile response

Regulation of adenosine formation by the heart.

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