The systemic and coronary hemodynamic effects of adenosine triphosphate and adenosine

Rowe, George G.; Afonso, Skoda; Gurtner, H. P.; Chelius, Carl J.; Lowe, William C.; Castillo, Cesar A.; Crumpton, Charles W.

doi:10.1016/0002-8703(62)90334-4

Cited by 50 publications

(16 citation statements)

References 6 publications

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“…In our experiments, cardiac output remained unchanged during ATP hypotension, but Rowe et al (1962) reported an increase in cardiac output from adenine nucleotides in dogs.…”

Section: Cardiac Outputcontrasting

confidence: 53%

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Hashimoto

Rigor

Moreno

1982

Tohoku J. Exp. Med.

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Effects of Hypotension Induced by Adenosine Triphosphate and Sodium Nitroprusside on Dogs with Denervated Hearts. Tohoku J, exp. Med., 1982, 138 (1), 27-37 Adenosine triphosphate (ATP) and sodium nitroprusside (SNP) are administered to patients to induce and control hypotension during anesthesia. SNP is authorized for clinical use in USA and UK, and ATP is clinically used in other countries such as Japan. We investigated how these two drugs act on the cardiovascular systems of 20 dogs whose hearts had been denervated by a procedure we had devised. ATP (10 dogs) or SNP (10 dogs) was administered to reduce mean arterial pressure by 30% to 70% of control. Before, during and after induced hypotension, we measured major cardiovascular parameters. Hypotension induced by ATP was accompanied by significant decreases in mean pulmonary arterial pressure (p<0.001), central venous pressure (p<0.001), left ventricular end-diastolic pressure (p<0.001), total peripheral resistance (p<0.001), rate pressure product (p <0.001), total body oxygen consumption (p <0.05), and heart rate (p<0.001); all these variables returned normal within 30 min after ATP was stopped. Cardiac output did not change. During hypotension produced by SNP similar decreases were observed in mean pulmonary arterial pressure (p<0.01), central venous pressure (p <0.001), left ventricular end-diastolic pressure (p <0.01), total peripheral resistance (p <0.001), rate pressure product (p <0.001), and oxygen content difference between arterial and mixed venous blood (p <0.05), while heart rate (p <0.001) and cardiac output (p<0.05) were increased. Recoveries of heart rate and left ventricular end-diastolic pressure were not shown within 60 min after SNP had been stopped. Both ATP and SNP should act on the pacemaker tissue of the heart. adenosine triphosphate; sodium nitroprusside; denervated heart; induced hypotension; cardiovascular effects Adenosine triphosphate (ATP) is known to produce profound changes in the cardiovascular system and has been administered intravenously for controlled

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“…In our experiments, cardiac output remained unchanged during ATP hypotension, but Rowe et al (1962) reported an increase in cardiac output from adenine nucleotides in dogs.…”

Section: Cardiac Outputcontrasting

confidence: 53%

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Hashimoto

Rigor

Moreno

1982

Tohoku J. Exp. Med.

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“…This dosage of adenosine previously has been shown to result in maximum dilation of the coronary vasculature since (1) no further increase in coronary flow was observed during infusion of larger dosages of adenosine and (2) no further increase in flow occurred following brief periods of coronary occlusion. 8 ' 9 Adenosine was dissolved in warm normal saline so that the desired dosage would be delivered by an infusion rate of 0.7 ml/min. The infusion of adenosine was begun 10 minutes before the first pacing intervention was begun and continued at a constant rate until the conclusion of the study.…”

Section: Methodsmentioning

confidence: 99%

Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in the awake dog.

Bache

Cobb

1977

Circulation Research

181

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We studied the influence of active coronary vasomotion on transmural myocardial perfusion during tachycardia. Regional myocardial blood flow was estimated in chronically prepared awake dogs by injecting radioactive microspheres (7-10 /xm in diameter) into the left atrium. Studies were performed during ventricular pacing at 100, 150, 200, and 250 beats/min under control conditions with intact coronary vasomotor tone, and during maximal coronary vasodilation induced by intravenous infusion of adenosine. During control conditions, mean myocardial blood flow was 1.27 ± 0.12 ml/min per g of myocardium at a heart rate of 100 beats/min, and increased regularly with increasing heart rates. Transmural myocardial perfusion remained essentially uniform as heart rates were increased from 100 to 250 beats/min. During administration of adenosine, mean myocardial blood flow increased to 5.49 ± 0.39 ml/min per g at a heart rate of 100 beats/min, and transmural myocardial perfusion was uniform. As heart rates were increased, flow to the subendocardium decreased as a linear function of heart rate while subepicardial flow was maintained so that the ratio of subendocardial-subepicardial flow fell from 1.00 at a heart rate of 100 beats/min to 0.40 at a heart rate of 250 beats/min. The reduction of subendocardial perfusion with increasing heart rate was most marked in the deepest myocardial layers. This rate-dependent decrease in subendocardial blood flow resulted in a decrease in mean myocardial blood flow with increasing heart rates (mean change at 250 beats/min = -18%; P < 0.05). These data indicate that active coronary vasomotion is necessary for maintenance of uniform transmural myocardial perfusion during tachycardia.

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“…Purines were shown to alter systemic blood pressure (Flesher et al. 1960, Gordon & Hesse 1961, Rowe et al. 1962, Haddy & Scott 1968) and change the tone of isolated arteries from the mesentery, kidney and skeletal muscle (Hashimoto & Kumukura 1965, Scott et al.…”

Section: Early Studies Of the Extracellular Effects Of Purinesmentioning

confidence: 99%

The birth and postnatal development of purinergic signalling

et al. 2010

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The purinergic signalling system is one of the most ancient and arguably the most widespread intercellular signalling system in living tissues. In this review we present a detailed account of the early developments and current status of purinergic signalling. We summarize the current knowledge on purinoceptors, their distribution and role in signal transduction in various tissues in physiological and pathophysiological conditions.

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The systemic and coronary hemodynamic effects of adenosine triphosphate and adenosine

Cited by 50 publications

References 6 publications

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Cardiovascular effects of hypotension induced by adenosine triphosphate and sodium nitroprusside on dogs with denervated hearts.

Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in the awake dog.

The birth and postnatal development of purinergic signalling

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