第四章 血液循环
2011-06-08 18:14:57   来源：   作者：  评论：0 点击：

第五节 器 官 循 环
(Organ circulation)
体内每一器官的血流量取决于主动脉压和中心静脉压之间的压力差，又取决于该器官阻力血管的舒缩状态。由于各器官的结构和功能的不同，器官血管的分布也各有特点，本节主要讨论心、肺、脑的循环特点。 一、冠脉循环
(Coronary circulation)
（一）冠脉循环的解剖特点
心肌的血液供应来自左、右冠状动脉。左冠状动脉主要供应左心室的前部，右冠状动脉主要供应左心室的后部和右心室。左冠状动脉的血液流经毛细血管和静脉后，主要经由冠状窦回流入右心房，而右冠状动脉的血液则主要经较细的心前静脉直接回流入右心房。另外还有一小部分冠脉血液可通过心最小静脉直接流入左、右心房和心室腔内。
冠脉循环的解剖特点：1、左、右冠状动脉主干行走于心脏表面，其分支常以垂直于心脏表面的方向穿入心肌，并在心内膜下层分支成网，这种分支方式使冠脉血管容易在心肌收缩时受压迫。2、心肌的毛细血管网分布极为丰富，毛细血管数与心肌纤维数的比例为1∶1。在心肌横断截面上，每平方毫米面积内约有2 500～3 000根毛细血管；因此，心肌与冠脉血液间物质交换迅速。3、冠脉动脉之间的侧支吻合较细小，血流量很少；因此当冠状动脉突然阻塞时不易很快建立侧支循环，常可导致心肌梗塞。但如果冠脉阻塞是缓慢形成的，侧支可逐渐扩张建立新的侧支循环，起代偿作用。
（二）冠脉循环的生理特点
1．途径短，血流快 冠脉循环的血液从主动脉根部，经全部冠状血管流回右心房，只需几秒钟就可完成。
2．血压较高 冠状动脉直接开口于主动脉根部，且血流途径短，并直接流入较小血管中，血压仍能维持在较高的水平。
3．血流量大 在安静状态下，人冠脉血流量为每百克心肌每分钟60～80ml。中等体重的人，总的冠脉血流量为225ml/min，占心输出量的4%～5%，而心脏的重量只占体重的0.5%。体力劳动时冠脉血流量可达静息时的4倍。心肌耗氧量大，需要大量血液供应，心肌主要通过有氧氧化而获得大量能量，以适应心脏长期持续活动。
4．平静时动-静脉血含氧量差很大 心肌富含肌红蛋白，摄氧能力很强。动脉血流经心脏后，其中65%～70%的氧被心肌摄取，从而满足心肌的耗氧量增加。心肌靠提高从单位血液中摄取氧的潜力较小，只能靠冠脉血管的扩张增加血流量来满足心肌对氧的需求。
5．血流量随心动周期波动 冠脉血流量取决于主动脉压和中心静脉压之间压力差，以及冠脉血管的口径和舒缩状态。由于冠脉血管的大部分分支深埋于心肌内，心肌的节律性收缩将压迫血管，影响冠脉血流。图4-29示狗的左、右冠状动脉血流在一个心动周期中的变化。当左心室等容收缩期开始，主动脉压低而心室壁张力升高，左冠状动脉受压而致血流量突然减少，甚至发生逆流。在左心室射血期，主动脉压升高，左冠状动脉受压程度相对减少，冠状动脉血压也随着升高，冠脉血流量增加，进入减慢射血期，主动脉压下降，冠脉血流量再次下降。在等容舒张期开始时，心肌对冠脉的挤压作用减弱或消失，冠脉血流阻力减小，而主动脉舒张压仍处于较高状态，冠脉血流量突然增加，到舒张的早期冠脉血流量最多，然后又逐渐减少。一般说来，左心室在收缩期血流量大约只有舒张期的20%～30%。当心肌收缩加强时，心缩期血流量所占的比例更小。由此可见，动脉舒张压的高低和心舒期的长短是影响冠脉血流量的重要因素，体循环外周阻力增大时，动脉舒张压升高，冠脉血流量增多。心率加快时，由于心动周期缩短主要是心舒期缩短，故冠脉血流量也减少。右心室肌肉比较薄弱，收缩时对血流的影响不如左心室明显，在安静情况下，右心室收缩期的血流量和舒张期的血流量相差不多，或甚至多于后者。
（三）冠脉血流量的调节
对冠脉血流量进行调节的各种因素中，最重要的是心肌本身的代谢水平。交感和副交感神经也支配冠脉血管平滑肌，但它们的调节作用是次要的。
1．心肌代谢水平对冠脉血流量的调节 心肌收缩的能量来源几乎唯一地依靠有氧代谢。实验证明，冠脉血流量和心肌代谢水平成正比，当心肌耗氧量增加或心肌组织中的氧分压降低时，都可引起冠脉舒张，增加血流量。
心肌组织中氧分压降低使冠脉血管舒张是由于某些代谢产物引起的，在各种代谢产物中，腺苷起主要作用。当心肌代谢增强而使局部组织中氧分压降低时，心肌细胞中ATP分解为ADP和AMP。存在于冠脉血管周围间质细胞中5'-核苷酸酶，可使ATP分解产生核苷，核苷对小动脉有强烈的舒张作用。心肌的其他代谢产物如H＋、CO2、乳酸、缓激肽、前列腺素E等也有舒张冠脉的作用。
2．神经调节 冠状动脉受迷走神经和交感神经的支配。刺激交感神经，可使冠脉先收缩后舒张。初期出现的冠脉收缩乃由于交感神经可激活冠脉平滑肌的a肾上腺素能受体，使血管收缩；而后期出现冠脉舒张，则因交感神经兴奋，激活心肌的b肾上腺素能受体，使心率加快、心肌收缩加强、耗氧量增加、代谢加速、代谢产物增多所造成的继发反应。如给予b肾上腺素能受体阻滞剂后，刺激交感神经只表现为a肾上腺素能受体兴奋，产生冠脉收缩反应。平时此缩血管作用往往被强大的继发性舒血管作用所掩盖，因此交感神经兴奋常引起冠脉舒张。
迷走神经对冠脉的直接作用是使冠脉舒张，但在完整机体内刺激迷走神经，对冠脉流量影响较小，这可能是由于迷走神经对冠脉的直接舒血管作用被心脏活动减弱，心肌代谢降低所引起的继发性缩血管作用所掩盖。
3．激素的调节 肾上腺素和去甲肾上腺素可通过增强心肌代谢活动和耗氧量使冠脉血流量增加；也可直接作用于冠脉血管的a或b肾上腺素能受体，引起冠脉血管收缩或舒张。甲状腺素增多时，心肌代谢增强，耗氧量增加，冠脉舒张，冠脉血流量增加。大剂量血管升压素和血管紧张素Ⅱ能使冠状动脉收缩，冠脉血流量减少。
二、肺 循 环
(Pulmonary circulation)
肺循环的功能是使右心室射出的血液通过肺泡壁进行气体交换，然后进入左心房；体循环中的支气管循环的功能是供给气管、支气管以及肺的营养需要。两种循环在末梢部分有少量吻合，少量支气管静脉血可通过吻合支直接进入肺静脉内，使主动脉的动脉血中掺入少量未经肺泡进行气体交换的静脉血，估计这部分血量约占心输出量的1%～2%。
（一）肺循环的生理特点
1．循环途径短、外周阻力小 肺动脉主干长4cm，随即分为左、右两支，再分为若干小支进入肺泡壁形成毛细血管网，最后汇入肺静脉流回左心房。整个肺循环途径比体循环短得多。肺动脉分支短、管径大、管壁薄，可扩张性大，血管的总横截面积大，加上肺循环的全部血管都位于比大气压低的胸腔内，因此肺循环的阻力小。因肺循环对血流阻力小，肺动脉压低于主动脉压，而致右心室每分心输出量与左心室每分心输出量相等。
2．血压较低 因右心室的收缩能力弱，肺循环的血压较低，仅为体循环的1/6～1/5。在正常人，右心室收缩压平均约为2.9kPa(22mmHg)，舒张压为0～0.13kPa(0～1mmHg)；肺动脉收缩压和右心室收缩压相同，平均为2.9kPa(22mmHg)，舒张压为1.1kPa(8mmHg)，平均压约1.7kPa(13mmHg)。用间接方法可测得肺循环毛细血管平均压为0.9kPa(7mmHg)。肺循环的终点，即肺静脉和左心房内压力为0.13～0.53kPa(1～4mmHg)，平均约0.27kPa(2mmHg)，可见肺循环的血压低。由于肺毛细血管的压力(0.9kPa)低于血浆胶体渗透压(3.3kPa或25mmHg)，因此肺泡间隙中基本上没有组织液。另外，由于肺部组织液的压力为负压，使肺泡膜与毛细血管壁互相紧密相贴，有利于肺泡与血液之间的气体交换。在左心衰竭时，肺静脉压及肺毛细血管血压升高，可导致液体积聚在肺泡或肺的组织间隙中而形成肺水肿(pulmonary edema)。
3．肺血管顺应性大，肺的血容量变化大 与体循环相比较，肺血管的顺应性大。肺部平静时的血容量约为450ml，占全身总血量的9%。用力呼气时，肺的血容量可减少至200ml左右；而在深吸气时可增加到约1 000ml左右。因其容量大，变化范围也大，故肺循环有"贮血库"的作用。当机体失血时，肺循环可将一部分血液转移至体循环，起代偿作用。肺循环的血容量还受呼吸周期的影响，并对左心室输出量和动脉血压发生影响。在吸气时，由腔静脉回流入右心房的血量增多，右心室射出血量增多。由于肺扩张时可将肺循环的血管牵拉扩张，使其容量增大，能容纳较多的血液，而由肺静脉回流入左心房的血液则减少。但经几次心搏后，扩张的肺循环血管已被充盈，故肺静脉回流入左心房的血液则逐渐增多。在呼气时，发生相反的过程。因此，在吸气开始时，动脉血压下降，到吸气相的后半期降至最低点，以后逐渐回升，在呼气相的后半期达到最高点。在呼吸周期中出现的这种血压波动，称为动脉血压的呼吸波。
（二）肺循环血流量的调节
1．神经调节 肺血管受交感和迷走神经支配。刺激交感神经可产生缩血管作用，肺血管阻力增大；刺激迷走神经则可引起轻度舒血管作用，肺血管阻力稍有降低。
2．肺泡气的氧分压 急性或慢性的低氧都能使肺部血管收缩，血流阻力增大。引起肺血管收缩的原因是肺泡气的氧分压低而不是血管内血液的氧张力低。血液氧分压降低可使体循环血管舒张，而肺血管则相反。当肺泡氧分压降低时，肺泡周围的微动脉收缩，局部血流阻力增大，血流量减少，这有利于较多的血液流经通气充足的肺泡，进行有效的气体交换。肺泡气中氧分压降低引起肺血管收缩的原因，目前还不清楚。有人推测低氧可能使肺组织产生一种缩血管物质，也有人认为必须有血管内皮存在才能发生这种缩血管反应。长期居住高海拔地区的人由于氧分压过低，引起肺微动脉广泛收缩，导致肺血流量阻力增大。产生肺动脉高压，这种因长期右心室负荷增加是造成右心室肥厚的主要原因。
3．血管活性物质对肺血管的影响 肾上腺素、去甲肾上腺素、血管紧张素Ⅱ、血栓素A2、前列腺素F2等能使肺循环的微动脉收缩。组胺、5-羟色胺能使肺循环的微静脉收缩。
三、脑 循 环
(Cerebral circulation)
脑的血液供应来自颈内动脉与椎动脉。大脑半球的前2/3脑区由颈内动脉供血，大脑半球的后1/3脑区及小脑和脑干由椎动脉供血。脑静脉注入静脉窦、主要通过颈内静脉注入腔静脉。脑循环主要是为脑组织供氧、供能、排出代谢产物以维持脑的内环境恒定。
（一）脑循环的特点
1．脑血流量大、耗氧量多 在安静情况下，每百克脑的血液量为50～60ml/min。整个脑的血流量约为750ml/min。可见，脑的重量虽仅占体重的2%，但血流量却占心输出量的15%左右。在安静情况下，每百克脑每分钟耗氧3～3.5ml；或者说，整个脑的耗氧量约占全身耗氧量的20%。
2．脑血流量变化小 脑位于骨性颅腔内，容积较为固定。颅内为脑、脑血管和脑脊液所充满，三者的容积的总和也是固定的。由于脑组织是不可压缩的，故脑血管舒缩受到相当的限制，血流量的变化较小。
3．局部化学环境对脑血管舒缩活动影响大 尤其以血液中CO2和O2分压对脑血流量影响更明显。
4．神经因素对脑血管活动的调节作用小
5．脑循环中存在血-脑屏障 脑循环的毛细血管壁内皮细胞相互接触紧密，并有一定的重叠，管壁上没有小孔。另外，毛细血管和神经元之间并不直接接触，而为神经胶质细胞所隔开。这一结构特征对于物质在血液和脑组织之间的扩散起着屏障的作用，称为血-脑屏障(blood-brain barrier)。
（二）脑血流量的调节
1．脑血管的自身调节 由于脑血管的舒缩受到限制，故脑的血流量主要取决于脑的动脉和静脉的压力差和脑血管的血流阻力。在正常情况下，颈内静脉压接近右心房压，变化不大，故影响脑血流量的主要因素是颈动脉压。颈动脉压升高时，脑血流量可相应增加；颈动脉降低时，则反之。正常情况下脑循环的灌注压为10.6～13.3kPa(80～100mmHg)。平均动脉压降低或颅内压升高都可使脑的灌注压降低。但当平均压在8.0～18.6kPa(60～140mmHg)的范围内变动时，脑血管可通过自身调节的机制使脑血流量保持恒定。平均动脉压降低到8.0kPa(60mmHg)以下时，脑血流量减少，引起脑的功能障碍。反之，当平均动脉压超过脑血管自身调节的上限时，脑血流量显著增加。
2．CO2和O2分压对脑血流量的影响 血液CO2分压升高时，脑血管舒张，血流量增加。其机制是血液中CO2进入组织与水分子结合生成H2CO3，后者在解离出H＋，H＋引起脑血管舒张，脑血流阻力减小，脑血流量增多，可将过多的H＋和CO2清除，使脑组织的酸碱度保持相对恒定，维持脑的正常功能；氧分压降低时，可使脑血管舒张。
3．脑的代谢对脑血流的影响 脑的各部分的血流量与该部分脑组织的代谢活动程度有关。当脑的某一部分活动加强时，该部分的血流量就增多。如握拳时，对侧大脑皮层运动区的血流量增加。代谢活动加强引起局部脑血流增加的机制，可能是通过代谢产物如H＋、K＋、腺苷以及氧分压降低，引起脑血管舒张。
4．神经调节 脑血管主要接受交感缩血管纤维和副交感舒血管纤维的支配，另外，脑血管还有血管活性肠肽等神经肽纤维末梢分布，但神经因素在脑血管活动调节中所起作用很小。切断支配脑血管的神经后，脑血流量无明显变化。在多种心血管反射中，脑血流量一般变化都很小。
（三）血-脑脊液屏障和血-脑屏障
脑脊液(cerebrospinal barrier)形成的原理与组织液不完全相同，它主要由脑室的脉络丛分泌而产生。此外，室管膜细胞也能分泌脑脊液。还有一部分脑脊液则来自血浆经毛细血管壁的滤过。脑脊液的成分与血浆不同，和身体其他部分的组织液也不相同。脑脊液中蛋白质的含量极微，葡萄糖含量也较血浆少，Na＋、Mg2＋的浓度较血浆中高，K＋、HCO3－和Ca2＋则较血浆中低。可见，血液和脑脊液之间的物质交换不是被动转运过程，而是主动转运过程。另外一些大分子物质也难从血液进入脑脊液。在血液和脑脊液之间似乎存在一种特殊屏障，称为血-脑脊液屏障(blood-cerebrospinal fluid barrier)。这种屏障对不同物质的通透性是不同的。如O2、CO2等脂溶性物质易通过屏障；但许多离子则很困难。血-脑脊液屏障的基础是，在无孔的毛细血管壁和脉络丛细胞中，有运输各种物质的特殊载体系统。
血液和脑组织之间也有类似屏障，可限制物质在血液和脑组织之间的自由交换，称为血-脑屏障。脂溶性物质如O2、CO2、以及某些麻醉药和乙醇等，易于通过血-脑屏障。而不同的水溶性物质的通透性有很大差别，并不一定和分子的大小有关。例如葡萄糖和氨基酸的通透性较高，而甘露醇、蔗糖和许多离子通透性很低，甚至不能通透。可见脑内毛细血管处的物质交换和身体其他部分的毛细血管处不同，它也是一种主动转运过程。在电镜下可见脑内大多数毛细血管表面都被星状胶质细胞伸出的突起（称血管周足）所包围，而毛细血管内的血液和神经元之间的物质交换可能要通过胶质细胞。因此，毛细血管的内皮、基膜和星状胶质细胞的血管周足等结构可能就是血-脑屏障的形态学基础。另外，毛细血管壁对各种物质特殊的通透性也和这种屏障作用有重要关系。
血-脑脊液屏障和血-脑屏障的存在，对于保持脑组织周围稳定的化学环境和防止血液中有害物质侵入脑内具有重要的生理意义。如循环血液中的去甲肾上腺素、乙酰胆碱、多巴胺、氨基酸等物质不易进入脑内，而保证脑内神经元正常功能活动不致因受血流中上述物质浓度变化而影响。
在脑室系统，脑脊液和脑组织之间为室管膜所分隔；在脑的表面，脑脊液和脑组织之间为软脑膜所分隔。室管膜和软脑膜的通透性都很高，脑脊液中的物质很容易通过室管膜或软脑膜进入脑组织。因此临床上将不易通过血-脑屏障的药物直接注入脑脊液，使其能很快进入脑组织，以达到治疗目的。
Summary
Cardiac innervation
Impulses in the noradrenergic sympathetic nerves to the heart increase the cardiac rate (positive chronotropic effect) and the force of cardiac contraction (positive inotropic effect). Impulses in the cholinergic vagal cardiac fibers decrease heart rate. There are a good deal of tonic discharge in the cardiac sympathetic and vagal nerves at rest. When the vagi are cut in experimental animals or after the administration of parasympatholytic drugs such as atropine, the cardiac rate in humans increases from its normal resting value of 70 to 150~180 beats per minute. In humans in whom both noradrenergic and cholinergic systems are blocked,the heart rate is approximately 100 beats/min.
Innervation of the Blood vessels
Noradrenergic fibers end on vessels in all parts of the body, but the fibers from the sympathetic ganglia to the cerebral vessels are of little functional importance. The noradrenergic fibers are vasoconstrictor in function.In addition to their vasoconstrictor innervation, the resistance vessels of the skeletal muscles are innervated by vasodialator fibers that, although they travel with the sympathetic nerves, are cholinergic (the sympathetic vasodilator system) nerve fiber.
There is no tonic discharge in the vasodilator fibers, but the vasoconstrictor fibers to most vascular beds have some tonic activity. When the sympathetic nerves are cut (sympathectomy), the blood vessels dilate.In most tissues,vasodialatation is produced by decreasing the rate of tonic discharge in the vasoconstrictor nerve,although in skeletal muscles it can also be produced by activiting the sympathetic vasodiator system. While stimulation of the vasodilator fiber of the parasympathetic nerves causes the vasodilation.
Nerves containing peptides are also found on many blood vessels. The peptides released from these peptidergic nerves include VIP, which produced vasodilation.
Afferent impulses in sensory nerves from the skin are relayed antidromically down branches of the sensory nerves, which inervate blood vessels and these impulses produce vasodilation. This local neural mechanism is called the axon reflex.
Cardiovascular regulatory mechanism
Nervous control:
Cardiovascular center: Cardiovascular center means a certain region that possesses the function to regulate the cardiovascular activity.
1. Medullary cardiovascular center:
Recent evidence strongly supports the view that the ventrolateral medullary (VLM) area functions to maintain vasomotor tone and mediate the cardiovascular reflexes.
The VLM includes the rostral ventrolateral medulla(rVLM) area that this area corresponds with the so-called vasoconstrictor center or C1 area where brain stem adrenaline containing neurones are located. The electrical or chemical stimulation of rVLM area elicits to an increase in arterial blood pressure (BP) and heart rate (HR). The VLM area still includes the caudal ventrolateral medulla(cVLM) that this area corresponds with the so-called vasodilator area or A1 area where brain stem noradrenaline containing neurones are located. The decrease in BP an HR of the cVLM stimulation may be mediated by activation of the GABA receptors in the rVLM.
In addition, the nucleus ambiguous and the dorsal motor nucleus of vagus in the medulla are areas sometimes called as the cardioinhibitory center.
2. Higher cardiovascular center
Above the medulla, a large number of areas throughout the reticular formation of the pons, mesencephalon and diencephalon can either excite or inhibit the medullary cardiovascular center. Among these areas, the hypothalamus plays an important role in the control of the cardiovascular activity. Besides, many parts of the cerebral cortex can also influence the cardiovascular activity. They are involved in regulating cardiovascular adjustments to exercise and emotion.
Cardiovascular reflexes
1. Sino-aortic baroreceptor reflex: A rise in arterial pressure stimulates the baroreceptors and causes them to transmit signals to the central nervous system. They are involved in following pathway: (1) N.IX.X-(EAA) NTS-(EAA) cVLM-(GABA) rVLM-(EAA) IML-(ACh) cardiac sympathetic nerve; (2) NTS -(EAA) N.Ambiguus -(ACh) cardiac vagus nerve. These cause a reduction of the arterial pressure toward the normal level and a decrease of HR.This homeostatic mechanism acts to maintain the constancy of arterial blood pressure.
2. Arterial chemorecepor reflex: The afferent nerve fibers from the carotid and aortic bodies pass with the baroreceptor afferents through the carotid sinus nerves and vagus nerves respectively. The chemoreceptor discharge increases rapidly when arterial PO2 falls or there is an increase in arterial PCO2 and hydrogen ion concentration. The main function of the chemorecepors is to regulate ventilation.
3.Cardiopulmonary receptor reflex: Experiments have shown that stretching atria or pulmonary arteries causes a reflex inhibition of the sympathetic nerve activity, a reduction of the release vasopressin and increase of atrial natriuretic peptide from the atrial myocardium. All the above mentioned reflex effects of the cardiopulmonary receptors tend to return the blood volume back to normal.
In addition to the above mentioned cardiovascular reflexes, stimulation of somatic or visceral nerves may also cause some other reflexes affecting the cardiovascular activity.
Humoral control
1. Noradrenaline and adrenaline: Noradrenaline (NA) causes vasoconstriction almost in every vascular bed by binding with a-adrenoceptors in the vascular smooth muscle. On the other hand, adrenaline(Adr) binds with both a-and b-adrenoceptors, leading to vasoconstriction and vasodilation respectively.
2. Angiotensin:AngiotensinⅡis one of the most potent vasoconstrictor agents and pressor effects.
3. Vasopressin (VP): Vasopressin is a nonapeptide hormone synthesized in the neurones of the paraventricular (PVN) and supraoptic nuclei (SON) in the hypothalamus. The principal physiological effect of VP is retention of water by increasing the permeability of the collecting ducts of the kidney and very potent vasoconstrictor and pressor effects. The baroreceptor reflex may be facilitated by the VP. In addition, the effect of VP on CNS, it also acts on the rVLM area in the brain to increase sympathetic vasomotor tone and arterial blood pressure.
Recent studies indicate that the effects of endothelium-relaxing factor (EDRF), bradykinin, prostaglandins (PG), b-endorphin histamie are vasodilataion.
Local control of basal vascular tone
This myogenic activity results in a basal vascular tone which keeps these vessels in a state of partial constriction. When the arterial blood pressure in a tissure vascular bed is suddenly raised, the transmural pressure increases, especially in the section of precapillary resistance vessels, thus giving rise to a mechanical stretch of smooth muscle and distension of the vessels. This causes a constriction of the smooth muscle.
Coronary Blood Flow
In human being the resting coronary blood flow averages 225ml/min which is 4 to 5 percent of the total cardiac output.The blood flow in the left ventricle falls to a low value during systole, because of strong compression of intramusclar vessels by the myocardial contraction. During diastole, however, the cardiac muscle relaxes and no longer obstructs the blood flow through the left ventricular blood vessels. Blood flow increases rapidly during diastole. The force of contraction of right ventricle is much less than that of the left ventricle. The phasic changes in blood flow are relatively small compared with those in the left ventricle.
Oxgen demand or consumption is a major factor in regulation of coronary blood flow, while the neural control is of secondary importance. Among metabolites known, adenosin is thought to be the most important which plays a role in the regulation of coronary blood flow.
Pulmonary circulation
The function of the pulmonary circulation is to oxygenate the mixed venons blood which comes from the right ventricle and remove its excess of CO2 by exchange between the capillaries and the air in the alveoli.
The blood volume of the lungs is apporoximately 450ml. Since blood volume in the pulmonary circulation is large and its volume variation is also large, the pulmonary vascular bed serves as a blood reservoir in the body. On the other hand,the pulmonary interstitial hydrostatic pressure is very low and even subatmospheric. This low pressure helps to pull fluid from the alveoli into the interstitial space and into the capillaries, keeping the alveoli dry. When alveolar oxygen concentration becomes low, the adjacent blood vessels slowly constrict in a few minutes, leading to an increase in the vascular resistance. This response may cause most of the blood to flow through other areas of the lungs that are better ventilated.
Stimulation of the sympathetic fibers, NA, Adr and AngⅡ cause vasoconstriction of the pulmonary circulation.
Cerebral Blood flow
Cerebral blood flow is autoregulated extremely well between the pressure range of 60 and 160mmHg in the arterial pressure. The mechanism of this autoregulation is probably due to a combination of myogenic and metabolic factors. An increase in CO2 or H＋ concentration in the arterial blood perfusing the brain greatly increases cerebral blood flow. Stimulation of the sympathetic nerves causes mild vasoconstriction, while stimulation of the parasympathetic nerves causes mild vasodilatation.
Blood-Brain and Blood-cerebrospinal fluid (CSF) Barrier
The morphological basis of the blood brain barrier is the endothelial cells, the basement membrane of the capillaries and the foot processes of glial cells (the perivascular end foot). This property of the blood-brain barrier helps to conserve the constancy of the local enviroment of the neurones, preventing fluctuation in plasma composition from being transmitted to the CSF.
The blood-CSF barriers also exists. Evidently, many large molecular substances hardly pass from the blood into the CSF.
(复旦大学上海医学院 郭学勤)