Effect of Perfusate pH on Coronary Flow and Adenosine Release in Isolated Rabbit Heart

Sj, Mustafa; Mansour, Malek

doi:10.3181/00379727-176-41836

Cited by 18 publications

(14 citation statements)

References 10 publications

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“…A reduction in pH to 6-8 by C02 has previously been reported to cause an increase in adenosine release from Langendorf-perfused guinea-pig hearts (Mustafa & Mansour, 1984), whereas both cardiac function and adenosine release were depressed when a similar pH change was induced by HCl infusion (Bardenheuer, Whelton & Sparks, 1987). Similarly, the adenosine released from cultured vascular smooth muscle is reported to be increased by raising the C02 but reduced by lowering the pH (Belloni, Bruttig, Rubio & Berne, 1986).…”

Section: Discussionmentioning

confidence: 93%

The influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs.

Ballard

1991

The Journal of Physiology

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SUMMARY1. In anaesthetized and artificially ventilated dogs, a gracilis muscle was vascularly isolated and perfused at a constant flow rate of 11P9+2-2 ml min-' 100 g-(mean + S.E.M., n = 16; equivalent to 170 2 + 21'3 % of its resting free flow).2. Stimulation (3 Hz) of the obturator nerve produced twitch contractions of the gracilis muscle, reduced venous pH from 7'366 + 0027 to 7-250 + 0-031 (n = 5), increased oxygen consumption from 0-62 + 0-24 to 2-76 + 046 ml min-1 100 g-' (n = 5) and increased adenosine release from -0-40+0-14 (net uptake) to 1-36 +0 50 nmol min-1 100 g-1 (n = 8).3. Infusion of lactic acid (4-2 mM) into the artery reduced venous pH to 7-281 + 0026 (n = 5) and increased adenosine release to 0-96 + 0'40 nmol min-' 100 g-1 (n = 8), but did not significantly alter oxygen consumption (0-80+0-19 ml min-' 100 g-1; n = 5). Stimulation (3 Hz) in the presence of lactic acid infusion produced no further significant changes in venous pH or adenosine release, but increased oxygen consumption to 2-53 + 0-37 ml min-' 100 g-1 (n = 5). 4. Infusion of a range of lactic acid concentrations ( > 1-83 mM) produced dosedependent increases in adenosine release. The maximum lactic acid concentration tested (5 95 mM) reduced venous pH to 7-249 + 0-023 (n = 5) and increased adenosine release to 2-64+ 1-26 nmol min-1 100 g-1 (n = 6).5. A strong correlation existed between the adenosine release and the venous pH (r = -0-92); points obtained during muscle stimulation and/or lactic acid infusion fell on a single correlation line.6. The vasoactivity of adenosine administered by close-arterial injection was unaltered by infusion of either lactic acid (7-2 mM) or saline.7. These results suggest that the release of adenosine from skeletal muscle can be induced by a decrease in pH (probably at an intracellular site), and that this mechanism may contribute to the release of adenosine during muscle contractions.

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Section: Discussionmentioning

confidence: 93%

The influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs.

Ballard

1991

The Journal of Physiology

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“…3B), and also that C02 is known to cause adenosine release from isolated heart and cultured vascular smooth muscle (Mustafa & Mansour, 1984;Belloni, Bruttig, Rubio & Berne, 1986), it remains possible that the elevation in Pco2 also contributed to the adenosine release here. This question is the subject of further investigation in our laboratory.…”

Section: Adenobine and Lactate Concentration8mentioning

confidence: 99%

“…Finally, we wished to determine the relationship between muscle Pco2 and adenosine 108 ADENOSINE, LACTATE AND C02 FROM MUSCLE output, since CO2 influences muscle pH, and an elevated Pco2 has been shown to stimulate adenosine release from cardiac muscle (Mustafa & Mansour, 1984). A range of stimulation parameters were applied to an isolated gracilis muscle, in order to vary the amounts of adenosine, lactate and CO2 added to the venous blood, and correlation analysis of these variables was performed.…”

Section: Introductionmentioning

confidence: 99%

Influence of stimulation parameters on the release of adenosine, lactate and CO2 from contracting dog gracilis muscle.

Achike

Ballard

1993

The Journal of Physiology

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SUMMARY1. The addition of adenosine, CO2 and lactate to the venous blood draining an isolated constant-flow perfused gracilis muscle was studied in anaesthetized and artificially ventilated dogs during twitch and tetanic contractions.2. Venous adenosine concentration increased from 154+33 nm (mean+S.E.M.) to 279 + 121 or 280 + 125 nm after 10 min of 1P5 or 3 Hz twitch contractions and to 240+ 120 or 276+ 139 nm after 10 min of 1 or 5 s tetani occurring at 0 1 Hz. Twitch contractions at 0-1 or 0 5 Hz for 10 min did not significantly elevate venous adenosine.3. Venous lactate concentration was significantly increased after 10 min of 1-5 or 3 Hz twitches or 5 s tetani at 0-1 Hz. There was a good correlation (r = 0 70; P < 0-001) between venous adenosine and lactate concentrations.4. Venous partial pressure of C02 (PC02) was significantly elevated after 10 min of 1P5 or 3 Hz twitch contractions or 1 or 5 s tetani at 0-1 Hz. There was also a good correlation (r = 0-58; P < 0-001) between venous adenosine concentration and Pco2.5. Venous partial pressure of 02 (PO2) decreased during all contractions except those at 0-1 Hz, but the oxygen cost per unit of tension x time was similar during every pattern of stimulation, and the percentage of the total energy production achieved by anaerobic means during muscle contractions did not exceed that at rest, indicating that there had been no limitation to the oxygen supply. Venous Po2 was poorly correlated with venous adenosine concentration (r = 028), but quite well correlated with venous lactate concentration (r = 0-53; P < 0 001). If the indirect influence of Po2 on venous adenosine concentration via an increase in lactate concentration was eliminated by partial correlation, then the coefficient for the relationship between venous adenosine concentration and venous Po2 became 0-15.6. There was a significant correlation between the venous adenosine concentration and the venous pH (r = 0 53; P < 0-001). If the influence of oxygenation on venous adenosine and pH was eliminated by partial correlation, the coefficient for the relationship between venous adenosine and pH increased to 0-95.

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“…Coronary blood flow is known to be regu lated by a variety of factors, including coro nary perfusion pressure (aortic pressure), myocardial extravascular compression, and metabolic, neural, and hormonal mediators [1], Of the metabolic factors, many investi gators have demonstrated that slight changes in the pH of the circulating blood affect cor onary blood flow [2][3][4][5][6][7][8]. Since an increase in coronary blood flow was associated with adenosine production during acidosis, Mus tafa and Mansour [1,2] suggested that the effects of hydrogen ions on the coronary blood flow are due to metabolic factors, such as adenosine, mediated by the change in pH.…”

Section: Introductionmentioning

confidence: 99%

Effects of Hydrogen Ion on the Changes in Adenosine Production in the Isolated Rat Heart Perfused at a Constant Flow System

Ochi¹,

Tanaka²,

Yoshihara³

et al. 1991

Cardiology

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This study was designed to clarify the relationship between the change in H⁺ and the nucleoside concentration at a constant coronary flow rate using a Langendorff system. Wistar rat hearts were perfused with Krebs-Henseleit solution (control, pH 7.4) modified to be either acidotic or alkalotic. Coronary perfusion presssure (CPP), left ventricular pressure, and myocardial oxygen consumption were decreased in the acidotic perfusate. On the other hand, these parameters increased in the alkalotic perfusate. Adenosine production in the acidotic perfusate significantly decreased while it significantly increased in the alkalotic perfusate. Furthermore, there was a significant positive correlation between both the percent change in adenosine production and the percent change in CPP in acidosis and alkalosis. It is suggested from these results that the hydrogen ion affects the adenosine metabolism and that the change in coronary blood flow by H⁺ is at least partly regulated by adenosine.

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Effect of Perfusate pH on Coronary Flow and Adenosine Release in Isolated Rabbit Heart

Cited by 18 publications

References 10 publications

The influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs.

The influence of lactic acid on adenosine release from skeletal muscle in anaesthetized dogs.

Influence of stimulation parameters on the release of adenosine, lactate and CO2 from contracting dog gracilis muscle.

Effects of Hydrogen Ion on the Changes in Adenosine Production in the Isolated Rat Heart Perfused at a Constant Flow System

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