Effect of beta-adrenergic blockade on nucleoside release from the hypoperfused isolated heart

Wangler, Roger D.; Dewitt, Donald F.; Sparks, Harvey V.

doi:10.1152/ajpheart.1984.247.2.h330

Cited by 10 publications

(4 citation statements)

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“…This idea is consistent with studies which show that catecholamines cause the release of cAMP from isolated rodents hearts (O'Brien and Strange, 1975;Imai et al, 1978). The 0-adrenergic receptor blocker, dlpropranolol reduces the early release of adenosine during ischemia, which is consistent with the above model (Wangler et al, 1984).…”

supporting

confidence: 90%

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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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supporting

confidence: 90%

“…During steady state conditions, release falls to approximately half the peak value and is sustained at that level for up to 3 hours (Wangler et al, 1984). The reduction in adenosine release is not accompanied by changes in coronary flow or myocardial O 2 consumption.…”

Section: Decreased Oxygen Supplymentioning

confidence: 87%

Regulation of adenosine formation by the heart.

Sparks¹,

Bardenheuer²

1986

Circulation Research

190

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“…The isolated, non-working, non-blood-perfused heart preparation used in this study has been well characterized by our laboratory (DeVVitt et al, 1983; Wangler et al, 1984). It has several distinct advantages.…”

Section: Discussionmentioning

confidence: 99%

Effect of development on coronary vasodilator reserve in the isolated guinea pig heart.

Toma¹,

Wangler²,

Dewitt³

et al. 1985

Circulation Research

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SUMMARY. Morphological studies have demonstrated an age-related decrease in capillary density and capillary surface area in the developing heart. However, the consequences of these changes on myocardial perfusion are not known. We tested the hypothesis that the decreased capillary density is associated with a reduction in coronary blood flow reserve. To test this hypothesis, we studied coronary responses to adenosine and sodium nitroprusside administration, reactive hyperemia, and autoregulatory capacity. We used a Langendorff-perfused heart preparation from guinea pigs of five different age groups (1 week and 1, 2, 12, and 18 months). Data are expressed as mean ± SEM. Maximal coronary flows (ml/min per g) in response to adenosine (10~* to 10~3 M) infusion are: 27 ± 1.3, 18.5 ± 1.4, 12.2 ± 0.4, 10.3 ± 0.3, and 10.6 ± 0.8 at 1 week, 1, 2, 12, and 18 months, respectively, with the flows at 1 week and 1 month significantly higher than those at 2, 12, and 18 months. There is a similar trend for a decreased maximum coronary perfusion in response to sodium nitroprusside (10"* to 10~5 M) and following a 45-second occlusion of the coronary inlet flow. Despite the decreased maximal pharmacological and reactive hyperemic flow reserve, autoregulation of flow is not altered with growth. The pressure-flow relationship exhibits autoregulation between 25 and 55 mm Hg perfusion pressure for all but the 1-week age group, which autoregulates within a narrower range of pressures (20-45 mm Hg). Total maximal coronary flow (ml/min) increases during development; this indicates that the growth of vessels continues with development. However, since coronary perfusion, corrected per unit cardiac mass, decreases significantly, we conclude that the vascular growth lags behind that of the parenchyma. (Circ Res 57: 538-544, 1985)

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“…In isolated hearts the nonselective beta-blocker propranolol exerts an energy-sparing effect during ischemia [9,10] and has strong chain-breaking antioxidant properties [11]. Beta-blockers, administered intravenously or intracoronarily, diminish ischemia during acute coronary occlusion in humans [12,13].…”

mentioning

confidence: 99%

Absence of beneficial effect of intravenous metoprolol given during angioplasty in patients with single-vessel coronary artery disease

Jong

Bonnier

Huizer

et al. 1993

Cardiovasc Drug Ther

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Summary. In a double-blind, randomized, placebo-controlled trial, the possible antiischemic effect of metoprolol during percutaneous transluminal coronary angioplasty was tested. Electrocardiograms, hemodynamics, and metabolism were studied in 27 patients with a stenosis in the left anterior descending coronary artery. Measurements took place before angioplasty, after each of four 1-minute occlusions and 15 minutes after the last balloon deflation. Patients were randomly given placebo or metoprolol (15 mg as a bolus intravenously, followed by an infusion of 0.04 mg/kg/hr). At the end of the procedure, the rate-pressure product had decreased by 15% (NS) and 23% (p = 0.001) in the placebo and metoprolol groups, respectively, mainly due to similar decreases in heart rate. Metoprolol tended to lower chest pain and reduce precordial ST-segment elevation due to angioplasty, but the effects were not statistically significant. Lactate, hypoxanthine, and urate release immediately after deflation was similar in both groups. Metoprolol reduced arterial plasma hypoxanthine throughout the procedure by about 30% (p -< 0.02 vs. placebo). Thus, intravenous infusion of metoprolol did not significantly attenuate chest pain and ST-segment elevation, and failed to decrease cardiac lactate and oxypurine release. It did, however, reduce arterial hypoxanthine concentrations during angioplasty, possibly indicating that the beta-blocker inhibits extracardiac ATP catabolism.

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Effect of beta-adrenergic blockade on nucleoside release from the hypoperfused isolated heart

Cited by 10 publications

References 0 publications

Regulation of adenosine formation by the heart.

Regulation of adenosine formation by the heart.

Effect of development on coronary vasodilator reserve in the isolated guinea pig heart.

Absence of beneficial effect of intravenous metoprolol given during angioplasty in patients with single-vessel coronary artery disease

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