Adenosine exacerbates ischemic myocardial injury during regional coronary hypoxemia in the dog.

Murakami, Hironori; Kim, Song-Jung; Lee, Shang Chiun; Strete, Denis; Downey, H. Fred

doi:10.1536/ihj.31.365

Cited by 3 publications

(2 citation statements)

References 17 publications

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“…Experiments tested the hypothesis that the contribution of nitric oxide, K V , and/or K ATP channels increase in response to acute isovolemic hemodilution in open-chest, anesthetized domestic swine. Our findings are consistent with prior studies which have demonstrated that progressive augmentation of coronary blood flow in response to anemia is sufficient to maintain overall myocardial oxygen delivery, although subendocardial ischemia is apparent as hematocrit falls to ≤ 10% [1, 3, 37, 45, 64]. Overall, coronary blood flow corresponds with MVO 2 , is dependent on arterial driving pressures ≥ 60 mmHg, and occurs with little/no change in myocardial oxygen extraction (coronary venous PO 2 ) [10, 19, 34, 35, 47, 64, 67, 68].…”

Section: Discussionsupporting

confidence: 92%

“…This progressive augmentation of coronary flow maintains overall myocardial oxygen delivery and occurs with a ~2-fold increase in MVO 2 and little/no change in myocardial oxygen extraction [10, 19, 34, 35, 47, 64, 67, 68]. However, evidence of enhanced myocardial lactate release and impairments to both sub-endocardial blood flow and cardiac contractile function have been reported with more severe reductions in hematocrit (≤ 10%) [1, 3, 37, 45, 64]. Earlier studies have suggested a role for reduced blood viscosity in the coronary response to anemia [5, 31, 33, 46, 62].…”

Section: Introductionmentioning

confidence: 99%

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Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

et al. 2017

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This study was designed to identify mechanisms responsible for coronary vasodilation in response to progressive decreases in hematocrit. Isovolemic hemodilution was produced in open-chest, anesthetized swine via concurrent removal of 500 ml of arterial blood and the addition of 500 ml of 37°C saline or synthetic plasma expander (Hespan, 6% hetastarch in 0.9% sodium chloride). Progressive hemodilution with Hespan resulted in an increase in coronary flow from 0.39 ± 0.05 to 1.63 ± 0.16 ml/min/g (P < 0.001) as hematocrit was reduced from 32 ± 1% to 10 ± 1% (P < 0.001). Overall, coronary flow corresponded with the level of myocardial oxygen consumption, was dependent on arterial pressures ≥ ~60 mmHg, and occurred with little/no change in coronary venous PO2. Anemic coronary vasodilation was unaffected by the inhibition of nitric oxide synthase (L-NAME: 25 mg/kg iv; P = 0.92) or voltage-dependent K+ (KV) channels (4-aminopyridine: 0.3 mg/kg iv; P = 0.52). However, administration of the KATP channel antagonist (glibenclamide: 3.6 mg/kg iv) resulted in an ~40% decrease in coronary blood flow (P < 0.001) as hematocrit was reduced to ~10%. These reductions in coronary blood flow corresponded with significant reductions in myocardial oxygen delivery at baseline and throughout isovolemic anemia (P < 0.001). These data indicate that vasodilator factors produced in response to isovolemic hemodilution converge on vascular smooth muscle glibenclamide-sensitive (KATP) channels to maintain myocardial oxygen delivery and that this response is not dependent on endothelial-derived nitric oxide production or pathways that mediate dilation via KV channels.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

et al. 2017

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Adenosine and myocardial protection

Gatell

Barrier

Shevde

1993

Journal of Cardiothoracic and Vascular Anesthesia

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Adenosine

Faulds¹,

Chrisp²,

Buckley³

1991

Drugs

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Adenosine (adenine riboside), administered either as the free base or as the 5'-triphosphate (ATP) by rapid intravenous bolus, depresses atrioventricular (AV) nodal conduction, resulting in transient AV block. Adenosine is the active agent and ATP is rapidly converted to adenosine after exogenous administration. By blocking the anterograde AV nodal limb of a re-entrant circuit, adenosine 6 to 12 mg (or ATP 10 to 20 mg) converts almost all episodes of paroxysmal supraventricular tachycardia (PSVT) involving the AV node within 30 seconds of administration. This is at least equivalent in efficacy to verapamil in adults, and superior to lanatoside C in children, with a considerably more rapid onset of action. Furthermore, if a dose of adenosine is ineffective, the exceptionally short plasma half-life of the adenyl nucleosides (less than 10 sec) allows rapid upward dosage titration until PSVT is terminated. Because the induced conduction block primarily affects the AV node, adenosine is a useful diagnostic tool in patients with broad or narrow QRS complex tachycardia; it terminates arrhythmias dependent on the AV node, unmasks other supraventricular mechanisms during transient AV block, but almost always has no effect on ventricular tachycardia. Noncardiac adverse effects, i.e. flushing, dyspnoea and chest pain, may occur during acute arrhythmia termination or diagnosis with adenosine, and arrhythmias may develop; however, these effects are usually transient (lasting less than 1 minute). Adenosine has also been used to induce coronary vasodilation in patients undergoing thallium-201 single photon emission computed tomography (201Tl SPECT), 2-dimensional echocardiography or positron emission tomography to evaluate suspected coronary artery disease. Intravenous infusion of adenosine 140 micrograms/kg/min for 6 minutes was generally associated with only mild adverse effects. These usually resolved within 1 to 2 minutes of discontinuing adenosine, although occasionally patients required aminophylline and/or nitroglycerin (glyceryl trinitrate). Diagnoses based on the results of scintigraphy were of a sensitivity, specificity and predictive accuracy comparable to those achieved with exercise- or dipyridamole-201Tl SPECT. Adenosine is therefore particularly suitable for the diagnosis of tachycardias and the acute management of PSVT involving the AV node in all age groups, without the risks of cardiac arrest and hypotension associated with verapamil. Furthermore, intravenous adenosine infusion may be used to induce coronary vasodilation in patients unable to perform exercise stress tests for 201Tl scintigraphy, and is well tolerated.

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Adenosine exacerbates ischemic myocardial injury during regional coronary hypoxemia in the dog.

Cited by 3 publications

References 17 publications

Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

Regulation of myocardial oxygen delivery in response to graded reductions in hematocrit: role of K+ channels

Adenosine and myocardial protection

Adenosine

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