胸内压

在胸膜的壁层和脏层之间有一个密闭的、潜在的腔隙叫胸膜腔,胸膜腔中的压力叫做胸内压。胸膜的壁层由于受到坚实胸廓的支持,大气压不能通过胸廓作用于胸膜腔,胸膜的脏层覆盖在肺的表面,肺内压通过胸膜的脏层作用于胸膜腔,胸内压应等于肺内压。但是,由于胸廓和肺的自然容积相差较大,肺泡壁中的弹性纤维产生弹性回缩力(约占肺总回缩力的1/3),再加上肺泡表面的液层产生的表面张力(约占肺总回缩力的2/3),它们的作用方向和肺内压相反,所以,胸内压=肺内压(大气压)-肺回缩力。若用特制的检压计来测量胸内压,可测得在整个平静呼吸过程中,胸内压均低于大气压(正常人约低3-10mmHg),一般称为胸内负压,其实称为胸内负压是不正确的,只是人们长期的应用已经习惯     

呼吸周期中的胸内压和肺内压的变化

本文重点说明在一个呼吸周期中,胸内压和肺内压的改变。呼吸运动的强弱是影响肺内压高低的最重要的因素,而胸廓运动的强度和气道的通畅状态,影响胸内压的大小。     

胸内正压对正常人左室功能影响及其力学原理

目的：探讨胸内正压对正常人左室射血及充盈的影响及其力学原理。方法：超声心动图观测30例正常人初始时与标准乏氏动作张力期10s时左室舒张末容积（LVEDV）、左室收缩末容积（LVESV）、每搏量（SV）、射血分值（EF）、流入道血流速度（E峰、A峰）、E／A值、二尖瓣环舒张早期运动速度（e）及舒张早期充盈压（E/e）的变化。结果：与初始时比较,标准乏氏动作张力期LVEDV、LVESV及SV减低而心率（陬）增快（P均〈0．001）,EF值增加,但无统计学意义（P〉0．05）;E峰与E／A值减低（P均〈O．05）;e没有变化（P〉0．05）．E／e值减低（P〈O．05）。结论：胸内正压对左室游离壁的力学作用促进了左室收缩运动而阻碍了左室舒张运动,会引起EF值增加,E峰及E／A值减低;2,胸内正压降低了肺静脉系统与心脏的跨壁压力,增加了血流阻力也是导致肺静脉系统与左室血液回流减少．E峰减低．E／e值减低的一个原因。     

非容积依赖性呼吸力学参数估计的敏感度分析

研究呼吸运动过程中呼吸驱动压P(t)、呼吸气体流率V(t)及肺容积V(t)三者间的数量关系,建立相应数学模型,进而估计气道阻力(R_W)、肺顺应性(C_L)等呼吸力学参数,不仅有重要理论意义,并且在临床医学、环境医学等领域也有重要应用价值。一、呼吸力学模型呼吸过程中,胸膜腔压力相对于口腔压力的变化与呼吸气体流率。肺容积之间的关系     

胸内正压对正常人左室功能影响及其力学原理

目的:探讨胸内正压对正常人左室射血及充盈的影响及其力学原理。方法:超声心动图观测30例正常人初始时与标准乏氏动作张力期10s时左室舒张末容积(LVEDV)、左室收缩末容积(LVESV)、每搏量(SV)、射血分值(EF)、流入道血流速度(E峰、A峰)、E/A值、二尖瓣环舒张早期运动速度(e)及舒张早期充盈压(E/e)的变化。结果:与初始时比较,标准乏氏动作张力期LVEDV、LVESV及SV减低而心率(HR)增快(P均<0.001),EF值增加,但无统计学意义(P>0.05);E峰与E/A值减低(P均<0.05);e没有变化(P>0.05),E/e值减低(P<0.05)。结论:胸内正压对左室游离壁的力学作用促进了左室收缩运动而阻碍了左室舒张运动,会引起EF值增加,E峰及E/A值减低;2,胸内正压降低了肺静脉系统与心脏的跨壁压力,增加了血流阻力也是导致肺静脉系统与左室血液回流减少,E峰减低,E/e值减低的一个原因。     

110例开胸病人引流管的护理

胸膜腔负压是维持气体交换的重要条件.开胸手术后,由于气体进入胸膜腔,肺因其本身的弹性回缩而塌陷.又由于手术创伤造成胸膜腔内渗血渗液,术后在胸腔内放置引流管,以排出积气、积液.     

Valsalva氏实验引起的实验性芤脉

中医学认为“芤主失血”。临床各种原因引起的大失血,导致血容量急剧减少时,均可以出现芤脉。有关芤脉的实验研究很少,其脉图特征及形成原理均未见详细报道。可能是因为芤脉多出现在急性大出血等危急情况下,必须采取急救措施,不便做某些实验观察的缘故。在Valsalva氏实验中,令受试者紧闭声门,用力呼气,使胸内压和腹内压迅速升高,静脉回流受阻,血液聚集于外周四肢。在适宜的情况下,     

呼吸力学参数的强迫振荡识别方法及其应用

呼吸力学参数包括呼吸气体的压力、流率、胸肺系统的顺应性、气道阻力、惯性阻力以及呼吸功等。测量这些参数可进一步从生物力学角度分析呼吸过程,在理论上与实际上均有一定意义。例如,测量胸内压、各级气道阻力、肺顺应性等,有助于深入了解肺内气体的传输和分布问题;定量研究气道阻力或肺顺应性的改变,对于阐明慢性阻塞性肺疾病(COPD)     

浅谈胸腔闭式引流术的护理体会

胸腔闭式引流术是利用重力学的原理引出胸膜腔内的积液、积气,恢复、重建胸膜腔内负压,平衡压力,促进肺部复张,恢复肺脏有效的呼吸功能,改善缺氧状态。胸腔闭式引流术广泛应用于临床,是胸外科重要的治疗手段之一,是治疗胸外伤血气胸、脓胸、自发性气胸的有效治疗方法[1]。     

一氧化氮对大鼠胸膜淋巴孔调控及淋巴吸收的影响

实验研究了一氧化氮（nitric oxide,NO）对大鼠胸膜淋巴孔的调控和胸膜腔淋巴吸收的影响。NO供体和NOS（nitric oxide synthase）抑制剂分别经腹腔给药,示踪剂（台盼蓝）胸膜腔内注射后,处死大鼠,测定血清NO和台盼蓝浓度;在扫描电镜下观察各组胸膜淋巴孔,用计算机图像处理,统计学分析。结果显示,NO供体组血清NO浓度为49.34±18.47μmol/L,淋巴孔的面积和密度分别为6.80±1.13 μm2和170.24±66.60/0.1mm2;NOS抑制剂组血清NO浓度为17.72±6.58μmol/L,淋巴孔的面积和密度分别为5.72±1.54μm2和61.71±12.73/0.1mm2。血清NO浓度与淋巴孔开放的面积和密度成正相关（P<0.05）。在胸膜腔给示踪剂后,NO供体组血清台盼蓝的浓度为74.68±33.67mg/L,与对照组比较有显著差异（P<0.05）。提示,NO可以调控胸膜淋巴孔,促进胸膜腔淋巴吸收。     

冠状动脉狭窄对血流量的影响

在22条开胸犬上观察了冠脉狭窄对血流量(CBF)的影响。用一可调节的微米缩窄器定量调节左旋支缩窄程度,测量了主动脉平均压(Pa)、冠脉远端小动脉平均压(Pc)和狭窄端压力降(ΔP)。冠脉狭窄程度与血流量变化曲线显示:在冠脉狭窄程度小于85％时,CBF相对稳定;随着狭窄程度的进一步增加,CBF急剧下降;而在狭窄程度大于95％后,CBF又缓慢下降。冠状动脉狭窄程度与CBF下降的曲线可用下列方程式表达: CBF=1.48×10~(10)e~(-27.6A)(A=冠脉狭窄程度) 冠脉狭窄程度大于50％时,狭窄程度与Pc呈负相关:Pc=159.1—1.36A(r=-0.73,P<0.01)。Pc与CBF呈正相关;Pc=16.9 1.3CBF(r=0.74,P<0.01)     

在正常和冠状动脉狭窄犬中扩张胃对冠脉血流动力学的影响

饱餐和扩张胃对心血管的影响早已引起人们的注意,但结论是不一致的。以往的实验都是在正常冠脉的动物上进行。本文在造成冠脉狭窄的情况下进行观察。在22条开胸狗的左旋支上,用微米狭窄器造成临界狭窄和重度狭窄。把一个气球送入胃中并充气600ml连续观察30min。正常冠脉组在扩张胃的最初15min内(前期)冠脉流量增多,主动脉压升高,血管总阻力下降,冠脉扩张;在扩张胃后15分钟(后期)无显著变化。冠脉临界狭窄组,前期冠脉流量增多,血管总阻力下降,冠脉扩张;后期流量减少,壁内血管阻力增加,冠脉收缩。冠脉重度狭窄组,前期冠脉流量无明显增加;后期流量显著减少,血管总阻力及心外膜、壁内血管阻力均增加,提示左旋支血管各段都发生收缩。 我们认为,餐后心绞痛的发作可能主要是在原有冠脉狭窄基础上冠脉流量进一步减少的结果。     

Effects of systole-specific pericardial pressure increases on coronary flow

It has been postulated that intrathoracic pressure increases may impair cardiac function by decreasing coronary flow. To determine whether altered coronary flow causes or results from change in cardiac function, we used 14 anesthetized dogs in propranolol-induced heart failure following atrioventricular node ablation. After thoracoabdominal binding, the animals were paced and ventilated at the same frequency, and inspiration was synchronized with cardiac systole, resulting in systole-specific pericardial pressure increases (SSPPI). At SSPPI magnitudes of 15 and 30 mmHg, left atrial transmural pressure decreased and cardiac output increased, whereas decreases in left ventricular end-systolic transmural pressure and myocardial O2 consumption were directly related. Concurrent decreases in coronary sinus flow (CSF) and coronary arteriovenous O2 gradient with SSPPI 15 mmHg indicate autoregulation. However, the arteriovenous O2 gradient remained unaltered with SSPPI 30 mmHg, despite further decrease in CSF. Because the absolute diastolic aortic pressure decreased, a limit may exist for increasing SSPPI above which CSF may be directly affected.     

Upstream pressure for systemic to pulmonary flow from bronchial circulation in dogs

Systemic to pulmonary flow from bronchial circulation, important in perfusing potentially ischemic regions distal to pulmonary vascular obstructions, depends on driving pressure between an upstream site in intrathoracic systemic arterial network and pulmonary vascular bed. The reported increase of pulmonary infarctions in heart failure may be due to a reduction of this driving pressure. We measured upstream element for driving pressure for systemic to pulmonary flow from bronchial circulation by raising pulmonary venous pressure (Ppv) until the systemic to pulmonary flow from bronchial circulation ceased. We assumed that this was the same as upstream pressure when there was flow. Systemic to pulmonary flow from bronchial circulation was measured in left lower lobes (LLL) of 21 anesthetized open-chest dogs from volume of blood that overflowed from pump-perfused (90-110 ml/min) pulmonary vascular circuit of LLL and was corrected by any changes of LLL fluid volume (wt). Systemic to pulmonary flow from bronchial circulation upstream pressure was linearly related to systemic arterial pressure (slope = 0.24, R = 0.845). Increasing Ppv caused a progressive reduction of systemic to pulmonary flow from bronchial circulation, which stopped when Ppv was 44 +/- 6 cmH2O and pulmonary arterial pressure was 46 +/- 7 cmH2O. A further increase in Ppv reversed systemic to pulmonary flow from bronchial circulation with blood flowing back into the dog. When net systemic to pulmonary flow from bronchial circulation by the overflow and weight change technique was zero a small bidirectional flow (3.7 +/- 2.9 ml.min-1 X 100 g dry lobe wt-1) was detected by dispersion of tagged red blood cells that had been injected.(ABSTRACT TRUNCATED AT 250 WORDS)     

Simulated breath-hold diving to 20 meters: cardiac performance in humans

Cardiac performance was assessed in six subjects breath-hold diving to 20 m in a hyperbaric chamber, while nonsubmersed or submersed in a thermoneutral environment. Cardiac index and systolic time intervals were obtained with impedance cardiography and intrathoracic pressure with an esophageal balloon. Breath holding at large lung volume (80% vital capacity) decreased cardiac index, probably by increasing intrathoracic pressure and thereby impeding venous return. During diving, cardiac index increased (compared with breath holding at the surface) by 35.1% in the nonsubmersed and by 29.5% in the submersed condition. This increase was attributed to a fall in intrathoracic pressure. Combination of the opposite effects of breath holding and diving to 20 m left cardiac performance unchanged during the dives (relative to the surface control). A larger intrathoracic blood redistribution probably explains a smaller reduction in intrathoracic pressure observed during submersed compared with nonsubmersed diving. Submersed breath-hold diving may entail a smaller risk of thoracic squeeze (lesser intrathoracic pressure drop) but a greater risk of overloading the central circulation (larger intrathoracic blood pooling) than simulated nonsubmersed diving.     

迷走神经与乙酰胆碱对缩窄的犬冠状动脉节段阻力的影响

在麻醉开胸犬,用电起搏维持心率恒定,研究了电刺激颈迷走神经(VNS)及冠状动脉内注入乙酰胆碱(ACh)对缩窄的冠状动脉的节段阻力及血流量的影响。在左旋支主干造成不同程度的冠状动脉缩窄。分别测定左旋支血流量(CBF_(cx))、主动脉压和主旋支远端冠状动脉压,记录心电图。实验发现,在冠状动脉临界狭窄和重度狭窄时,VNS 或冠脉给ACh 引起心外膜大冠状动脉阻力及冠状动脉主旋支总阻力增大,CBF_(cx)减少;随着缩窄程度加重,这些改变也愈明显,然而,心肌内小冠状动脉阻力却无显著改变。     

Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs.

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.     

冠状动脉血流信号的计算机测量与分析

本文介绍在药效学研究的实验中，应用计算机技术测量，处理血流信号的新方法，通过分离实验运动左冠状动脉的旋支，接入电磁流量计探头，直接引出血流波形，经计算机采集，得到与左室压，动态压，心电图等同步的血流信号，再由计算机对血流信号的基本参数进行计算分析，为深入进行有关药效学研究提供了新手段。     

Coronary vascular volume remodelling in rainbow trout Oncorhynchus mykiss

The 34% increase in relative ventricular mass (M_rv) resulting from chronic anaemia (induced by an intraperitoneal injection of phenylhydrazine hydrochloride) was accompanied by a 117% increase in coronary vascular volume of diploid rainbow trout Oncorhynchus mykiss. Coronary vascular volume of normocythemic triploid fish was similar to that of normocythemic diploid fish despite a larger M_rv. These observations, in combination with previous studies, suggest that the vascularity of compact myocardium in O. mykiss can vary independently of M_rv.