Changes in pulmonary hemodynamics in acute pulmonary edema

Summary Experiments were made on dogs to study the hemodynamic changes following intravenous injections of chloramine and adrenaline. Chloramine injections were followed by the development of a severe pulmonary edema in an of the dogs. In most of them, however, the capillary pressure in the pulmonary circulation increased, but insignificantly. The great increase in the pulmonary capillary pressure following adrenaline injection did not culminate in the development of edema or caused very slight edema. The conclusion is drawn that increase of filtration pressure is not an indispensable decisive factor for the development of pulmonary edema, even if it is concurrent with considerable disturbances in the pulmonary circulation.(Presented by Academician V. V. Parin) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 60, No. 8, pp. 25–29, August, 1965     

Solute permeability of the alveolar epithelium in acute hemodynamic pulmonary edema in dogs.

Ten anesthetized dogs, 48 h postintravenous 131I-albumin injection, had a segment of lung airspace isolated by a balloon-tipped catheter lodged in a bronchus. An isotonic saline solution containing trace amounts of Blue Dextran, 125I-albumin, and 57Co-cyanocobalamin was instilled into the lung segment. During control periods, lung saline was absorbed at a rate of 0.133% per minute as measured by indicator dilution of Blue Dextran. Only 57Co-cyanocobalamin crossed the epithelium. Acute hemodynamic pulmonary edema was produced by aortic constriction plus saline overload. In pulmonary edema the fluid volume in the airspace increased at the rate of 0.96% per minute, and there was a significant influx of 131I-albumin into the lung saline from the blood in all animals. However, neither 125I-albumin nor Blue Dextran diffused from the airspace into blood during edema; both were merely diluted by fluid influx. The rate of diffusion of 57Co-cyanocobalamin increased fivefold during edema. A small number of discrete breaks in the lung epithelium allowing bulk flow of interstitial fluid is proposed to account for the one-way movement of albumin in hemodynamic alveolar edema.     

The pathogenesis of acute pulmonary edema associated with hypertension

BACKGROUND: Patients with acute pulmonary edema often have marked hypertension but, after reduction of the blood pressure, have a normal left ventricular ejection fraction (> or =0.50). However, the pulmonary edema may not have resulted from isolated diastolic dysfunction but, instead, may be due to transient systolic dysfunction, acute mitral regurgitation, or both. METHODS: We studied 38 patients (14 men and 24 women; mean [+/-SD] age, 67+/-13 years) with acute pulmonary edema and systolic blood pressure greater than 160 mm Hg. We evaluated the ejection fraction and regional function by two-dimensional Doppler echocardiography, both during the acute episode and one to three days after treatment. RESULTS: The mean systolic blood pressure was 200+/-26 mm Hg during the initial echocardiographic examination and was reduced to 139+/-17 mm Hg (P< 0.01) at the time of the follow-up examination. Despite the marked difference in blood pressure, the ejection fraction was similar during the acute episode (0.50+/-0.15) and after treatment (0.50+/-0.13). The left ventricular regional wall-motion index (the mean value for 16 segments) was also the same during the acute episode (1.6+/-0.6) and after treatment (1.6+/-0.6). No patient had severe mitral regurgitation during the acute episode. Eighteen patients had a normal ejection fraction (at least 0.50) after treatment. In 16 of these 18 patients, the ejection fraction was at least 0.50 during the acute episode. CONCLUSIONS: In patients with hypertensive pulmonary edema, a normal ejection fraction after treatment suggests that the edema was due to the exacerbation of diastolic dysfunction by hypertension--not to transient systolic dysfunction or mitral regurgitation.     

Hemodynamic responses during acute normovolemic hemodilution in anesthetized dogs.

Acute normovolemic hemodilution was induced by progressive replacement of blood by dextran (molecular weight 150,000) in anesthetized artificially ventilated dogs. Experiments were performed on dogs with intact autonomic innervation, dogs with beta-adrenergic blockade, dogs with cholinergic blockade, dogs with bilateral vagotomy, and dogs with combined bilateral vagotomy plus beta-adrenergic blockade. Hemodilution induced an increase in cardiac-output in all the groups. However, in dogs with low control heart rate (dogs with intact autonomic innervation, and dogs with beta-adrenergic blockade), cardiac-output increase was almost wholly due to an increase in heart rate. Whereas, in dogs with high control heart rate (dogs with cholinergic blockade, dogs with bilateral vagotomy, and dogs with combined bilateral vagotomy plus beta-adrenergic blockade), the increase in cardiac-output was almost wholly due to an increase in the stroke-volume. The increase in heart rate in dogs with intact autonomic innervation was not significantly different from the heart rate increase in dogs with beta-adrenergic blockade. In dogs with low control heart rate (beta-receptor blockade), hemodilution induced tachycardia, which was not significantly different from the response induced in intact dogs. This shows that the cardioacceleration was primarily mediated through the efferent vagus nerves, and the efferent sympathetic nerves did not make significant contribution in the reflex.     

体外循环中急性肺水肿分析

目的:强调重视和加强体外循环中对肺功能的保护.方法:分析16例在体外循环中发生肺水肿患者术前的肺动脉高压、血红蛋白、肾功能和心功能情况.经PEEP+利尿药+激素和超滤器为主,辅以强心、扩血管药的协同治疗.结果:所有患者经治疗后气道阻力下降,均减小至术前水平.无酸中毒,尿量＞100ml/min.平均2.5天拔管停呼吸机,11例患者术后第-天均顺利脱离呼吸机.15例患者出院,1例死于MOF.结论:中度肺动脉高压、贫血和心肾功能功能不全可能是体外循环中急性肺水肿的诱发因素.体外循环时应采取措施预防和减轻肺功能损伤.     

Prevention of acute pulmonary edema in irradiated rats

Experiments on rats showed that preparations with a marked prophylactic action against the development of pulmonary edema in unirradiated animals are in some cases ineffective (or may even aggravate the development of edema) in irradiated (650 R) rats. Conversely, substances ineffective or detrimental in unirradiated animals may have a marked prophylactic action in irradiated rats.Department of Pathological Physiology, Yaroslavl' Medical Institute. (Presented by Acdemician of the Academy of Medical Sciences of the USSR P. D Gorizontov.) Translated from Byulleten' Éksperimental'noi Biologii, i Meditsiny, Vol. 84, No. 9, pp. 284–286, September, 1977.     

Hemodynamic reactions in the acute phase of massive pulmonary embolism

Massive pulmonary embolism is accompanied by the differences between a decrease in systemic and peripheral blood flow and imbalanced blood ejection from the ventricles. The results of the study suggest an association of these hemodynamic responses with redistribution of blood outflows from systemic veins whereby the relative proportion of blood outflowing to the right atrium decreases and that of blood outflowing to the left atrium increases via systemic-pulmonary collaterals. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 123, No. 5, pp. 579–583, May, 1997     

白细胞毒素引起大鼠急性肺水肿的实验研究

本文观察白细胞毒素(Lx)对无菌Wistar大鼠肺的毒性作用。实验依使用Lx剂量的不同分两组进行:Ⅰ组用Lx100,150,200,500μmol/kg静脉注射(每一剂量6只,下同),10min活杀;Ⅱ组用Lx50,100,150μmol/kg静脉注射分别于1h、6h、或12h后活杀,取肺组织行光镜及电镜检查。结果发现注射Lx后10min即引起急性肺水肿,肺泡上皮细胞及肺毛细血管内皮细胞损害;Ⅱ组除上述改变外,还有明显的炎症细胞浸润。提示Lx是引起肺水肿和肺部炎症病变的因素之一。     

Protein composition of lung fluids in acute alloxan edema in dogs.

In 11 anesthetized dogs with acute alloxan-induced pulmonary edema, we measured the protein composition of 1-mul samples of plasma, free interstitial fluid, alveolar fluid, and airway fluid. We obtained plasma and airway fluid at regular intervals as edema developed. We sampled alveolar fluid by pleural micropuncture in the unfrozen, excised lung and free interstitial fluid from perivascular cuffs in the frozen, excised lung. The average (+/- 1 SD) total protein concentration of plasma was 4.9 +/- 0.6, airway fluid 4.4 +/- 0.7, free interstitial fluid 4.9 +/- 0.7, and alveolar fluid 5.2 +/- 0.8 g/100 ml. The average fractions of albumin were 0.42 +/- 0.05, 0.50 +/- 0.05, 0.49 +/- 0.06, and 0.49 +/- 0.07, respectively. By paired analysis, the protein concentration of interstitial fluid was not significantly different from alveolar fluid. The protein concentration of airway fluid was significantly less than that in interstitial and alveolar fluid. The albumin fraction of the three lung fluids was identical but significantly different from plasma. We conclude that in alloxan-induced pulmonary edema the lung fluids contain high concentrations of protein and the alveolar epithelial membrane becomes freely permeable to protein molecules.