MYOCARDIAL OXYGENATION DURING ACUTE NORMOVOLEMIC HEMODILUTION: IMPACT OF HYPOCAPNIC ALKALOSIS.

Edward A Czinn, M Ramez Salem, George J Crystal
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Abstract

Background: Increases in myocardial blood flow preserve myocardial oxygenation during moderate acute normovolemic hemodilution. Hypocapnic alkalosis (HA) is known to cause coronary vasoconstriction and increase hemoglobin-oxygen affinity. We evaluated whether these effects would compromise myocardial oxygenation during hemodilution.

Methods: Eighteen anesthetized dogs were studied. Myocardial blood flow (MBF) was measured with radioactive microspheres. Arterial and coronary sinus samples were analyzed for oxygen content and plasma lactate. Myocardial oxygen supply, oxygen uptake, and lactate uptake were calculated. HA (PaCO2, 23 ± 2 (SD); pHa, 7.56 ± 0.03) was induced by removal of dead space tubing at baseline (n = 8) and during hemodilution (n = 10), with hematocrit at 43 ± 4% and 19 ± 2%, respectively.

Results: Hemodilution during normocapnia caused decreases in arterial oxygen content (19.9 ± 2.4 to 9.3 ± 1.2 ml/100; P < 0.05) and the coronary arteriovenous 02 difference (13.0 ± 3.0 to 6.4 ± 0.9 ml/100ml; P < 0.05). MBF increased (52 ± 12 to 111 ± 36 ml/min/100g; P < 0.05) to maintain myocardial oxygen supply and oxygen uptake. Myocardial lactate uptake increased (31 ± 19 to 68 ± 35 µeq/min/100g; P < 0.05). At normal hematocrit, HA decreased MBF (57 ± 18 to 45 ± 10 ml/min/100; P < 0.05), implying vasoconstriction, accompanied by decreased myocardial oxygen supply. These myocardial effects of HA were not apparent during hemodilution. HA did not alter myocardial lactate uptake during hemodilution.

Conclusion: When HA was induced during hemodilution, its ability to cause coronary vasoconstriction was lost, and myocardial oxygenation remained well preserved.

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急性等容血液稀释时心肌氧合:低碳酸碱中毒的影响。
背景:在中度急性等容血液稀释期间,心肌血流量增加可保持心肌氧合。低碳酸碱中毒(HA)已知引起冠状动脉血管收缩和增加血红蛋白-氧亲和力。我们评估了这些影响是否会损害血液稀释过程中的心肌氧合。方法:对18只麻醉犬进行研究。用放射性微球测定心肌血流量(MBF)。分析动脉和冠状窦标本的氧含量和血浆乳酸。计算心肌供氧量、摄氧量和乳酸摄氧量。HA (PaCO2, 23±2 (SD);在基线(n = 8)和血液稀释(n = 10)时切除死腔管诱导pHa为7.56±0.03,红细胞比容分别为43±4%和19±2%。结果:正常碳酸血症时血液稀释导致动脉血氧含量降低(19.9±2.4 ~ 9.3±1.2 ml/100);P < 0.05),冠状动脉动静脉02差异(13.0±3.0 ~ 6.4±0.9 ml/100ml;P < 0.05)。MBF从52±12增至111±36 ml/min/100g;P < 0.05)维持心肌供氧和摄氧量。心肌乳酸摄取增加(31±19 ~ 68±35µeq/min/100g);P < 0.05)。在正常红细胞压积下,HA降低MBF(57±18 ~ 45±10 ml/min/100);P < 0.05),提示血管收缩,并伴有心肌供氧减少。血凝素对心肌的影响在血液稀释过程中不明显。血凝素没有改变血液稀释过程中心肌乳酸的摄取。结论:血凝素在血液稀释过程中诱导后,其引起冠状血管收缩的能力丧失,心肌氧合保持良好。
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来源期刊
Middle East Journal of Anesthesiology
Middle East Journal of Anesthesiology Medicine-Anesthesiology and Pain Medicine
CiteScore
0.20
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期刊介绍: The journal is published three times a year (February, June, and October) and has an Editorial Executive Committee from the department and consultant editors from various Arab countries. A volume consists of six issues. Presently, it is in its 42nd year of publication and is currently in its 19th volume. It has a worldwide circulation and effective March 2008, the MEJA has become an electronic journal. The main objective of the journal is to act as a forum for publication, education, and exchange of opinions, and to promote research and publications of the Middle Eastern heritage of medicine and anesthesia.
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