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无基质血红蛋白溶液的冠状动脉收缩效应。

Coronary constrictor effect of stroma-free hemoglobin solutions.

作者信息

Vogel W M, Dennis R C, Cassidy G, Apstein C S, Valeri C R

出版信息

Am J Physiol. 1986 Aug;251(2 Pt 2):H413-20. doi: 10.1152/ajpheart.1986.251.2.H413.

Abstract

A coronary vasoconstrictor effect of human stroma-free hemoglobin (SFH) was identified in isolated rabbit hearts perfused with Krebs-Henseleit buffer or whole rabbit blood at a constant coronary flow rate. In buffer-perfused hearts, SFH in concentrations of 5 to 200 mg/dl produced dose-related increases of coronary perfusion pressure. At a concentration of 150 mg/dl, SFH, equilibrated with CO to form carboxyhemoglobin, caused an increase in perfusion pressure (55 +/- 7 mmHg), similar to that observed with oxyhemoglobin (57 +/- 6 mmHg); addition of potassium ferricyanide to form methemoglobin reduced the increase of perfusion pressure to 34 +/- 5 mmHg (P less than 0.05). The vasoconstrictor activity could not be eliminated by dialyzing against the perfusion buffer. Human SFH prepared by different methods had similar vasoconstrictor activity. Rabbit SFH and human SFH were equi-effective in the rabbit heart. Less constrictor activity of SFH was evident in rat and guinea pig heart. Polymerized, pyridoxalated SFH had greatly reduced constrictor effect compared with unmodified or pyridoxalated tetramer SFH. In blood-perfused hearts, increasing plasma hemoglobin to 1.6 +/- 0.1 g/dl, without changing total hemoglobin or arterial O2 content, increased coronary perfusion pressure by 36 +/- 13 mmHg (P less than 0.05). We conclude that stroma-free hemoglobin solutions exert a coronary vasoconstrictor effect that is unrelated to O2 delivery.

摘要

在以恒定冠脉血流量用克雷布斯 - 亨塞尔特缓冲液或全兔血灌注的离体兔心脏中,发现人无基质血红蛋白(SFH)具有冠脉血管收缩作用。在缓冲液灌注的心脏中,浓度为5至200mg/dl的SFH可使冠脉灌注压呈剂量相关增加。在浓度为150mg/dl时,与CO平衡形成羧基血红蛋白的SFH使灌注压升高(55±7mmHg),与氧合血红蛋白引起的升高(57±6mmHg)相似;加入铁氰化钾形成高铁血红蛋白可使灌注压升高降至34±5mmHg(P<0.05)。通过与灌注缓冲液透析不能消除血管收缩活性。用不同方法制备的人SFH具有相似的血管收缩活性。兔SFH和人SFH在兔心脏中效果相当。在大鼠和豚鼠心脏中,SFH的收缩活性较弱。与未修饰或吡哆醛化的四聚体SFH相比,聚合的、吡哆醛化的SFH的收缩作用大大降低。在血液灌注的心脏中,在不改变总血红蛋白或动脉血氧含量的情况下,将血浆血红蛋白增加至1.6±0.1g/dl,可使冠脉灌注压升高36±13mmHg(P<0.05)。我们得出结论,无基质血红蛋白溶液发挥的冠脉血管收缩作用与氧输送无关。

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