Local vasoactivity of oxygen and carbon dioxide in the right coronary circulation of the dog and pig.

Ely, Stephen W.; Sawyer, Donald C.; Scott, Jerry B.

doi:10.1113/jphysiol.1982.sp014422

Cited by 26 publications

(10 citation statements)

References 32 publications

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“…ventilated with open chest. Hyperoxia may induce vasoconstriction of coronary arteries (4,32), whereas hypoxia may induce vasodilation (17). We did not see vasoconstricting effects, because, as stated in Table 1, global oxygen extraction was on average 70% in our experiments, which is normal for the anesthetized pig, but somewhat lower than found in awake pigs breathing air (16,31).…”

Section: Discussionmentioning

confidence: 67%

Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery

Alders¹,

Groeneveld²,

Kanter³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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and correlated well (r ϭ 0.85, P ϭ 0.02, n ϭ 7) with oxygen consumption calculated from blood flow, hemoglobin, and blood gas measurements (mean 22.8 Ϯ 4.7 mol⅐min Ϫ1 ⅐g dry wt Ϫ1). Local blood flow and oxygen consumption were significantly correlated (r ϭ 0.63 for pooled normalized data, P Ͻ 0.0001, n ϭ 60). We calculate that, in the heart at normal workload, the variance of left ventricular oxygen delivery at submilliliter resolution is explained for 43% by heterogeneity in oxygen demand. regional blood flow; metabolism; myocardium; magnetic resonance spectroscopy MYOCARDIAL BLOOD FLOW is highly heterogeneous, as demonstrated in many different species, with various methods (radioactive, colored and fluorescent microspheres, molecular tracers, MRI, and PET), and under different experimental circumstances, such as open-versus closed-chest and anesthetized versus awake animals (5,9,19,22,26,27). Myocardial perfusion shows similar heterogeneity in the human heart (47). This heterogeneity is largely of spatial nature, although there is also some temporal variation (27). Local blood flow can differ by a factor five among small areas of the left ventricle, even in the normal heart. Interestingly, regional blood flow is rather stable over a substantial time period, at least for several hours, but some data even indicate a relatively stable local blood flow over days (44). From an anatomic and mechanical point of view, this heterogeneity is difficult to understand because the heart appears rather homogeneous and biomechanical models predict homogeneous contraction. The question thus remains: which factors contribute to heterogeneous blood flow? Heterogeneity in oxygen consumption (V O 2 ) between different areas of the left ventricle may explain at least part of the heterogeneity of myocardial blood flow. Indeed, it has been shown in previous studies (9,19) that indirect indicators of local aerobic metabolism show heterogeneity. For instance, a correlation between local blood flow and fatty acid uptake has been shown (24). Others (38, 39) have reported a rather good correlation between local myocardial blood flow and local myocardial V O 2 (MV O 2 ) measured by [18 O]water in the isolated buffer-perfused rabbit heart. Low-flow areas had lower V O 2 and highflow areas had higher V O 2 . Further studies showed that areas of the left ventricle that receive a relatively low amount of blood flow are not in a hypoxic state, suggesting local adaptation of blood flow to oxygen demand (8,11,14). However, direct measurement of aerobic metabolic flux in small myocardial regions became possible only recently. Regional V O 2 and regional blood flow can be estimated with PET, although this technique still does not permit analysis at sufficiently high spatial resolution to study cardiac heterogeneity in small tissue areas (1,34,37).To investigate the distribution of MV O 2 at high spatial resolution, a new combination of isotope labeling protocol and mathematical analysis of 13 C incorporation into the tricarboxylic acid (TCA) cycle ...

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Section: Discussionmentioning

confidence: 67%

Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery

Alders¹,

Groeneveld²,

Kanter³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

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“…Several studies have shown increased Effects of acid-base imbalance on vascular reactivity www.bjournal.com.br coronary blood flow during hypercapnia (18,19). Whether P CO 2 or pH exerts a direct effect on the smooth muscle of coronary vessels or whether the vascular response is mediated through other mechanisms is currently not known.…”

Section: Respiratory Acidosismentioning

confidence: 99%

Effects of acid-base imbalance on vascular reactivity

Celotto

Capellini

Baldo

et al. 2008

Braz J Med Biol Res

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Acid-base homeostasis maintains systemic arterial pH within a narrow range. Whereas the normal range of pH for clinical laboratories is 7.35-7.45, in vivo pH is maintained within a much narrower range. In clinical and experimental settings, blood pH can vary in response to respiratory or renal impairment. This altered pH promotes changes in vascular smooth muscle tone with impact on circulation and blood pressure control. Changes in pH can be divided into those occurring in the extracellular space (pH o ) and those occurring within the intracellular space (pH i ), although, extracellular and intracellular compartments influence each other. Consistent with the multiple events involved in the changes in tone produced by altered pH o , including type of vascular bed, several factors and mechanisms, in addition to hydrogen ion concentration, have been suggested to be involved. The scientific literature has many reports concerning acid-base balance and endothelium function, but these concepts are not clear about acid-base disorders and their relations with the three known mechanisms of endothelium-dependent vascular reactivity: nitric oxide (NO/cGMP-dependent), prostacyclin (PGI 2 /cAMP-dependent) and hyperpolarization. During the last decades, many studies have been published and have given rise to confronting data on acid-base disorder and endothelial function. Therefore, the main proposal of this review is to provide a critical analysis of the state of art and incentivate researchers to develop more studies about these issues.

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“…The increased MBF, CS So2, and CS Po2 caused by hypercapnia have been characterized as a myocardial "over perftision" (Case et al 1975;Ely et al 1982;Wexels et al 1985). However, if hyprcapnia causes an increased myocardial arte-'Current address: Department of Surgery, County Hospital of Alesennd, N-6017 Asestranda, Norway.…”

Section: Introductionmentioning

confidence: 97%

Myocardial oxygen supply during hypocapnia and hypercapnia in the dog

Wexels¹

1986

Can. J. Physiol. Pharmacol.

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It has been postulated that a coronary vasoconstriction during hypocapnia might be opposed by a compensating coronary vasodilatation due to impaired myocardial oxygen supply. The present study was performed first to examine whether a maximal decline in coronary sinus (CS) oxygen content was reached during hypocapnia. During hypercapnia a myocardial "over perfusion" has been demonstrated. The second purpose of the present study was to examine whether a myocardial "over perfusion" is essential to maintain a sufficient myocardial tissue oxygen supply during hypercapnia. Closed-chest dogs were anesthetized with pentobarbital and hypocapnia was induced by hyperventilation. Nitrogen gas and carbon dioxide could both be added to the inspiratory gas to create arterial hypoxemia (arterial SO2 65%) and hypercapnia, respectively. Arterial hypoxemia during hypocapnia increased myocardial blood flow (MBF) by 50%, while CS SO2 decreased significantly. The decrease in CS SO2 demonstrates a reserve capacity of myocardial oxygen extraction during hypocapnia, thereby ruling out any major coronary vasoconstriction during hypocapnia. Hypercapnia during normoxemia increased MBF, myocardial oxygen delivery, and CS SO2 substantially, but this was not observed when hypercapnia was created during arterial hypoxemia. From the present results we conclude that hypocapnia does not cause any major coronary vasoconstriction, while hypercapnia results in a myocardial "over perfusion," which is a luxury perfusion not essential to maintain sufficient myocardial oxygen supply during hypercapnia.

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Local vasoactivity of oxygen and carbon dioxide in the right coronary circulation of the dog and pig.

Cited by 26 publications

References 32 publications

Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery

Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery

Effects of acid-base imbalance on vascular reactivity

Myocardial oxygen supply during hypocapnia and hypercapnia in the dog

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Local vasoactivity of oxygen and carbon dioxide in the right coronary circulation of the dog and pig.

Cited by 26 publications

References 32 publications

Myocardial O2consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O2delivery

Myocardial O2consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O2delivery

Effects of acid-base imbalance on vascular reactivity

Myocardial oxygen supply during hypocapnia and hypercapnia in the dog

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Product

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Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery

Myocardial O₂consumption in porcine left ventricle is heterogeneously distributed in parallel to heterogeneous O₂delivery