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大鼠、兔和猫失血性低血压期间出现明显的脾充血。

Marked splenic hyperaemia during post-haemorrhagic hypotension in the rat, rabbit and cat.

作者信息

Iversen P O, Benestad H B, Nicolaysen G

机构信息

Department of Physiology, Institute of Basic Medical Sciences, University of Oslo, Norway.

出版信息

J Physiol. 1992 Mar;448:437-52. doi: 10.1113/jphysiol.1992.sp019050.

Abstract
  1. The regulation of the splenic perfusion during normal and pathological conditions is incompletely understood. We studied the time course of splenic blood flow during the initial (0-24 h) development of haemorrhagic anaemia in awake and anaesthetized rats, as well as in awake rabbits and cats. Another group of rats had either normovolaemic anaemia or beginning polycythaemia. 2. The microsphere method was used to measure splenic blood flow. The awake rats were rendered anaemic either by a heavy (1.5% of body weight) or a moderate (0.7% of body weight) bleeding (hypovolaemia), by haemolysis (normovolaemia) or by bleeding (1.5% of body weight) followed by transfusion of autologous plasma (normovolaemia). Polycythaemia was induced with injections of erythropoietin. The anaesthetized rats as well as the awake rabbits and cats were also bled heavily (1.5% of body weight). 3. In awake rats, splenic blood flow increased to 215% of control within the first 5 min after bleeding. The perfusion declined nearly to baseline over the next 24 h. A similar, but less prominent splenic hyperaemia was detected in the awake rabbits and cats. However, this hyperaemic response was not detected in the normovolaemic, the polycythaemic or the anaesthetized and bled rats. 4. Administration of the adrenergic beta-blocking agent propranolol prior to bleeding significantly attenuated the splenic hyperaemia in the awake rats, while the alpha-blocking agent phentolamine or the cholinergic blocking agent atropine had no effect. 5. Concomitant with the initial increase in splenic perfusion, cardiac output increased to 123% of control in the awake, heavily bled rats. In the bled, anaesthetized rats cardiac output decreased to 91% of control 5 min after bleeding. A decrease in cardiac output to 64 and 70% of control was observed in the awake rabbits and cats, respectively. 6. Immediately following the bleeding, we noticed a substantial release of platelets from the rat spleen. 7. It appears that a heavy acute blood loss in awake rats, rabbits and cats elicits a marked reduction in splenic vascular tone, perhaps mediated by beta-adrenergic receptor activity. Anaesthesia abolished this response in rats. Possibly, the induced hypovolaemia triggered an accelerated release of platelets from the rat spleen, dependent on an augmented splenic blood flow.
摘要
  1. 正常和病理状态下脾脏灌注的调节尚未完全明确。我们研究了清醒和麻醉大鼠、清醒兔和猫在出血性贫血初始阶段(0 - 24小时)脾脏血流的时间进程。另一组大鼠患有正常血容量性贫血或初期红细胞增多症。2. 采用微球法测量脾脏血流。清醒大鼠通过大量(体重的1.5%)或中度(体重的0.7%)出血(低血容量)、溶血(正常血容量)或出血(体重的1.5%)后输注自体血浆(正常血容量)造成贫血。通过注射促红细胞生成素诱导红细胞增多症。麻醉大鼠以及清醒兔和猫也进行大量出血(体重的1.5%)。3. 在清醒大鼠中,出血后最初5分钟内脾脏血流增加至对照值的215%。在接下来的24小时内灌注几乎降至基线。在清醒兔和猫中检测到类似但不太明显的脾脏充血。然而,在正常血容量、红细胞增多症或麻醉和出血的大鼠中未检测到这种充血反应。4. 出血前给予肾上腺素能β受体阻滞剂普萘洛尔可显著减轻清醒大鼠的脾脏充血,而α受体阻滞剂酚妥拉明或胆碱能阻滞剂阿托品则无作用。5. 与脾脏灌注的初始增加同时,清醒、大量出血的大鼠心输出量增加至对照值的123%。出血的麻醉大鼠在出血后5分钟心输出量降至对照值的91%。在清醒兔和猫中,心输出量分别降至对照值的64%和70%。6. 出血后立即观察到大鼠脾脏有大量血小板释放。7. 似乎清醒大鼠、兔和猫的急性大量失血会引起脾脏血管张力显著降低,可能由β肾上腺素能受体活性介导。麻醉消除了大鼠的这种反应。可能诱导的低血容量触发了大鼠脾脏血小板的加速释放,这依赖于脾脏血流的增加。

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