Coronary circulation in acute hypoxia

Kaijser, L.; Grubbström, J; Berglund, Bo

doi:10.1111/j.1475-097x.1990.tb00094.x

Cited by 20 publications

(19 citation statements)

References 7 publications

(4 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In controls, exercise-induced hyperemia at altitude was significantly increased by 38% (PϽ0.01) compared with normoxia, although target RPP was reached at a significantly lower workload level (Ϫ28%, PϽ0.0001), probably due to hypoxia-induced sympathetic activation, which might also increase myocardial contractility. This is in agreement with previous invasive measurements by Kaijser and coworkers,18 who found that during physical exercise, the hypoxia-induced reduction in O 2 content was compensated for mainly by an increase in MBF of 33%. So far, no data are available for patients with CAD.…”

Section: Discussionsupporting

confidence: 93%

“…28 However, only very few reports in the literature deal with the use of physical exercise in PET, 29 -31 and only recently has its reproducibility been documented. 18 In the present study, exercise-induced, hyperemic flow was higher in patients than in controls, possibly indicating an uncoupling of MBF and cardiac work due to inefficient contractility of the ischemic heart. In fact, as patients had a significantly decreased maximal adenosine-induced MBF, they utilized Ϸ90% of their available maximal MBF during physical exercise.…”

Section: Discussionsupporting

confidence: 41%

See 1 more Smart Citation

Influence of Altitude Exposure on Coronary Flow Reserve

et al. 2003

View full text Add to dashboard Cite

Background-Although no data exist on the effect of altitude exposure on coronary flow reserve (CFR), patients with coronary artery disease (CAD) are advised not to exceed moderate altitudes of Ϸ2500 m above sea level. We studied the influence of altitude on myocardial blood flow (MBF) in controls and CAD patients. Methods and Results-In 10 healthy controls and 8 patients with CAD, MBF was measured by positron emission tomography and 15 O-labeled water at rest, during adenosine stress, and after supine bicycle exercise. This protocol was repeated during inhalation of a hypoxic gas mixture corresponding to an altitude of 4500 m (controls) and 2500 m (CAD). Workload was targeted to comparable heart rate-blood pressure products at normoxia and hypoxia. Resting MBF increased significantly in controls at 4500 m (ϩ24%, PϽ0.01) and in CAD patients at 2500 m (ϩ24%, PϽ0.05). Altitude had no influence on adenosine-induced hyperemia and CFR. Exercise-induced hyperemia increased significantly in controls (ϩ38%, PϽ0.01) at 4500 m (despite a reduction in workload, Ϫ28%, PϽ0.0001) but not in CAD patients at 2500 m (moderate decrease in workload, Ϫ11%, PϽ0.05). Exercise-induced reserve was preserved in controls (ϩ10%, PϭNS) but decreased in CAD patients (Ϫ18%, PϽ0.005). Conclusions-At 2500 m altitude, there is a significant decrease in exercise-induced reserve in CAD patients, indicating that compensatory mechanisms might be exhausted even at moderate altitudes, whereas healthy controls have preserved reserve up to 4500 m. Thus, patients with CAD and impaired CFR should be cautious when performing physical exercise even at moderate altitude.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 41%

Influence of Altitude Exposure on Coronary Flow Reserve

et al. 2003

View full text Add to dashboard Cite

show abstract

“…However, this mechanism is protective for the heart, a vital organ that is also demanding for a high O 2 supply at exercise. The coronary fl ow reserve has been shown to be limited to 33 % above what is prevailing during maximal exercise at sea level [ 20 ]. Therefore, the compensation of decreased arterial O 2 content by increasing coronary blood fl ow is not possible above a certain altitude and the only option to preserve cardiac integrity is to decrease myocardial O 2 demand and therefore maximal heart rate.…”

Section: Adrenergic System and Preservation Of The Myocardium In Hypoxiamentioning

confidence: 99%

Physiological and Clinical Implications of Adrenergic Pathways at High Altitude

Richalet

2016

Advances in Experimental Medicine and Biology

View full text Add to dashboard Cite

The adrenergic system is part of a full array of mechanisms allowing the human body to adapt to the hypoxic environment. Triggered by the stimulation of peripheral chemoreceptors, the adrenergic centers in the medulla are activated in acute hypoxia and augment the adrenergic drive to the organs, especially to the heart, leading to tachycardia. With prolonged exposure to altitude hypoxia, the adrenergic drive persists, as witnessed by elevated blood concentrations of catecholamines and nerve activity in adrenergic fibers. In response to this persistent stimulation, the pathways leading to the activation of adenylate cyclase are modified. A downregulation of β-adrenergic and adenosinergic receptors is observed, while muscarinic receptors are upregulated. The expression and activity of Gi and Gs proteins are modified, leading to a decreased response of adenylate cyclase activity to adrenergic stimulation. The clinical consequences of these cellular and molecular changes are of importance, especially for exercise performance and protection of heart function. The decrease in maximal exercise heart rate in prolonged hypoxia is fully accounted for the observed changes in adrenergic and muscarinic pathways. The decreased heart rate response to isoproterenol infusion is another marker of the desensitization of adrenergic pathways. These changes can be considered as mechanisms protecting the heart from a too high oxygen consumption in conditions where the oxygen availability is severely reduced. Similarly, intermittent exposure to hypoxia has been shown to protect the heart from an ischemic insult with similar mechanisms involving G proteins and downregulation of β receptors. Other pathways with G proteins are concerned in adaptation to hypoxia, such as lactate release by the muscles and renal handling of calcium. Altogether, the activation of the adrenergic system is useful for the acute physiological response to hypoxia. With prolonged exposure to hypoxia, the autonomous nervous system adapts to protect vital organs, especially the heart, against a too high energetic state, via a purely local autoregulation mechanism necessary for the preservation of overall homeostasis.

show abstract

“…Kaijser et al, 18 our results show that there are no significant changes in MBF in healthy human beings at a moderate altitude of 2000 m. This may explain the fact that even patients with CAD and impaired left ventricular function tolerate these conditions well, 25 because no sizeable flow reserve seems to be required to meet the myocardial oxygen demand during the slight decrease in PO 2 at 2000 m. However, at high altitudes such as 4500 m, an increase in MBF of 62% is observed despite the concomitant decrease in PEtCO 2 . A hypoxia-induced increase in heart rate due to sympathetic activation and vagal withdrawal could increase myocardial oxygen consumption because of an increase in cardiac work 26 and thus could also account for increased MBF.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, MBF is regulated to maintain constant myocardial tissue oxygen tension. 17 However, Kaijser et al 18 found an enhanced oxygen extraction at rest during acute exposure to an altitude of 2300 m and no change in MBF, which increased during physical exercise. Thus it remains unclear whether a reduced coronary vasodilator capacity (such as that in patients with CAD) represents a risk factor during acute exposure to hypoxia.…”

mentioning

confidence: 99%