Tear propagation in isolated, pressurized porcine thoracic aortas.

OBJECTIVE: To determine the pressure required for the initial medial tear, and for propagtion of dissections, within the media of isolated pressurized porcine thoracic aorta, and to determine whether these vary with tear depth. DESIGN: India ink-stained saline was injected into the media of 48 fresh porcine descending thoracic aorta that were distended with 130 mmHg pressure. The fluid was infused into the media through a 25 gauge needle connected to a constant infusion pump, and the pressure at the entrance to the needle was monitored with a Cobe pressure transducer. The two lumens were not connected. Blebs were made at different depths and measured at the end of the experiment with a Starrett gauge. Seven casts were made in pressurized aortas and nine in nonpressurized ones to determine the shape of the blebs by injecting different volumes of mercox casting material into the media by hand. RESULTS: Mean tearing pressure, expressed as the transmural pressure between the bleb and the true lumen (which was at 130 mmHg) was 547 mmHg (range 208 to 995). Mean propagation pressure was 54 mmHg (range 25 to 93). The ratio of the two pressures was 10.1 (range 5.2 to 21.7). None of these pressures was correlated with tear depth. Casts showed that the leading edge was sharp in all directions. Small blebs were roughly spherical, and large ones were cylindrical with roughly hemispherical ends between the cylinder and the sharp leading edge. CONCLUSIONS: Dissections can propagate at pressures that could be reached under physiological and certainly pathological conditions. The initial tear requires pressures that are too high to create biologically except with trauma. The leading edge of the dissection appears to be very sharp and likely explains why the dissection propagates at relatively low pressures. Tear depth does not affect the results.     

制备犬胸主动脉脱细胞血管支架的新方法

目的 研究制备犬胸主动脉脱细胞血管支架的新方法,制备出理想的犬胸主动脉脱细胞基质,从而为构建组织工程血管提供支架材料.方法 在无菌条件下从成年比格犬体内取出胸主动脉血管段（28根）,随机分成4组：A组血管段设为正常对照组;B组血管段置于-70℃的冰箱和4℃冰箱内反复冻融2次;C组血管段在0.1％的SDS溶液中持续震荡1d;D组血管段经历反复冻融后置于1％ Triton X-100的PBS溶液和1μmol/L PMSF的混合液中常温下震荡2d,于0.01％的SDS溶液中持续震荡1d,最后加入核酸酶Dnase 0.2 mg/L和Rnase0.02 mg/L消化24h.四组血管段经历不同的过程后,全部从大体形态、光镜、电子显微镜观察、力学性能测试、免疫组化等角度进行检测并做统计学分析.结果 0.1％ SDS法虽能完全脱除细胞,但制备的脱细胞基质弹力纤维排列紊乱,部分发生断裂,且不能保持良好的形状和张力强度,管腔有不同程度的塌陷;反复冻融＋1％ Triton X-100＋PMSF＋0.01％ SDS法不仅能完全脱除细胞,保持基质纤维的正常排列结构,而且制备的脱细胞基质能保持良好的形状和力学性能,管腔无塌陷.结论 联合应用反复冻融、Triton X-100、PMSF和SDS的方法能够将犬胸主动脉的细胞成分除去,是一种制备脱细胞血管支架的有效方法.     

Segmental impairment of endothelium-mediated relaxation in thoracic aortas from atherosclerotic rabbits. Comparison to cholesterol infiltration and energy metabolism

Three sets of parameters, (i) relaxation to acetylcholine (Ach), ATP and NaNO2, (ii) cholesterol content in aortic tissue, and (iii) energy metabolism were compared in normal and atherosclerotic rabbits, fed 1% cholesterol for eight weeks. A special protocol was envisaged to permit a strict comparison between Ach, ATP and NaN O2 at different levels of thoracic aorta, in each rabbit. A gradual impairment of the endothelium-dependent relaxation to Ach and ATP was found at different levels of the thoracic aorta from hypercholesteromic rabbits. By contrast, NaNO2--endothelium-independent--maintained its relaxing power quite normally at all aortic levels. A close correlation was evident between the impairment of aorta relaxation to Ach and the cholesterol infiltration in the vessel wall, being the correlation coefficient -0.85 (P less than 0.001). A correlation was also evident for ATP, but to a lower degree, being the correlation coefficient -0.61 (P less than 0.01). Energy metabolism and related parameters (ATP, ADP, AMP, adenosine, inosine, GTP, GDP, guanosine, NAD, NADP, total adenylate nucleotides and adenylate energy charge) were not modified by the cholesterol diet. These data show that the gradual impairment of endothelium-dependent relaxation, decreasing down the thoracic aorta of hypercholesterolemic rabbits, and correlated with cholesterol content in the aortic wall, may be considered as an index of a very early atherogenic damage, prior to variation in the parameters of energy metabolism and purine turnover.     

The vascular resistance of arterial stenoses in series

The vascular resistance of stenoses in series has been studied in vitro by use of fiber optic laser Doppler anemometry to measure the cross-sectional areas of the stenoses. Pressure gradients across each of the stenoses were measured while both the severity and the separation of the stenoses were altered. The individual resistances were compared with the combined resistance. Resistance at a stenosis is a nonlinear function of the severity of the stenosis. The resistance is a complex function of the perfusion pressure and the cross-sectional area of the stenosis and cannot be accurately predicted from a single plane angiographic image. With multiple stenoses an approximate assessment of the combined effect can be obtained by summing the value of the resistance for each stenosis but not the degree of the stenoses. The nonlinear relationship of resistance to stenosis severity means that if one stenosis is more severe than the other, the combined effect can be regarded as the same as the effect of the more severe stenosis acting by itself. The distance between the stenoses does not change their combined effect.     

Value of clinical screening for detection of asymptomatic hemodialysis vascular access stenoses.

Measurement of recirculation and intradialytic venous line pressures may aid in the detection of hemodialysis vascular access stenoses. The authors screened 29 consecutive asymptomatic patients for recirculation values exceeding 15% or venous pressures greater than 150 mmHg. All 13 patients requiring and agreeing to angiography on the basis of the screening protocol proved to have high-grade stenoses of their vascular access outflow or inflow. Asymptomatic vascular access pathology is common. High-risk asymptomatic populations may be detected by simple screening procedures.     

Pulmonary vascular effects of endotoxin in leukopenic dogs.

We have demonstrated previously that in the dog, small doses of endotoxin abolish the pulmonary vasoconstrictor reponse to hypoxia, apparently by stimulating the production of a vasodilator prostaglandin. We previously ruled out platelets as mediators of this endotoxin effect. To evaluate leukocytes as possible mediators, we rendered dogs leukopenic by means of a leukocyte antiserum. However, this did not modify the inhibitory effect of endotoxin on hypoxic pulmonary vasoconstriction. Hence, neither leukocytes nor platelets appear to mediate the endotoxin effect. In the near absence of both platelets and leukocytes, the endotoxin effect can be prevented by inhibiting prostaglandin synthesis with meclofenamate. This suggests that endotoxin prevents hypoxic pulmonary vasoconstriction by acting on the systemic circulation or on the lung (possibly directly on the pulmonary blood vessels) to stimulate the production of a vasodilator prostaglandin.     

Relation of sinusoidal stenoses following hepatocyte swelling to hepatic vascular resistance in experimental liver cirrhosis

To investigate the significance of sinusoidal stenoses and a decrease in the sinusoidal bed due to hepatic cell swelling as a factor increasing hepatic vascular resistance in liver cirrhosis, hepatic vascular resistance in choline-deficient diet-induced cirrhotic rats was measured by an isolated liver perfusion method. In the cirrhotic rats, the swollen hepatic cells resulting from accumulation of fat droplets narrowed the sinusoids and decreased the sinusoidal bed. Consequently, the hepatic vascular resistance was increased by 2.7 times normal (8.60 +/- 2.32 mm H2O.ml-1.min; controls, 3.13 +/- 0.67 mm H2O.ml-1.min), and portal hypertension was also recognized (188.1 +/- 26.3 mm H2O; controls, 114.2 +/- 12.8 mm H2O). In the cirrhotic rats fed with ordinary rat pellets for 2 months, however, the sinusoidal stenoses and the decreased sinusoidal bed recovered to nearly normal as a result of disappearance of the fat droplets in the hepatic cells. The increased hepatic vascular resistance was decreased to 1.5 times normal (4.68 +/- 0.82 mm H2O.ml-1.min), and the elevated portal vein pressure was reduced (141.5 +/- 17.4 mm H2O). These findings clearly demonstrate that an important factor leading to an increase in hepatic vascular resistance is sinusoidal stenoses and a decrease in the sinusoidal bed resulting from swollen hepatic cells.     

Renin-angiotensin system in dogs following chronic bile-duct ligation. Relation to vascular reactivity

The pressor response to angiotensin II, blood volume, angiotensin II in arterial blood, renin substrate, renin concentration, renin activity and aldosterone in venous blood, liver function tests, kidney function tests, glucose, sodium, potassium, plasma osmolality and complete blood count were examined before and 1, 2, 3 and 5 weeks after ligation of bile ducts in nine conscious trained dogs. The pressor response to angiotensin II was markedly suppressed after bile-duct ligation, especially at 1-3 weeks postoperation. A maximal decrease in plasma renin substrate, and maximal increases in plasma renin concentration, plasma renin activity and aldosterone were noted at 1 week postoperatively. Plasma angiotensin II levels were elevated at 1 and 5 weeks postoperatively but were near normal 2 weeks postoperatively despite suppression of the angiotensin II pressor response. Endogenous levels did not correlate with suppression of the pressor response to exogenous angiotensin II.     

Anomalous origins of the posterior intercostal arteries from 915 thoracic aortas: Their role in fractures of the ribs

Nine hundred fifteen aortas were collected from various hospitals during the years 1934 to 1937. All had been fixed in a 10 per cent solution of formalin, and all but three were believed to have been opened anteriorly. The subclavian artery was considered the upper limit of the thoracic aorta, and the diaphragm, the lower.Nine pairs of intercostal arteries should arise in the posterior midline of the aorta above the diaphragm. With allowances for variations, this was found to be true in 25.2 per cent of the cases.In 74.8 per cent they deviated to the right, to the left, or to the anterior wall, or were scattered in their placement of origin, constituting a devious delivery of blood.In the 915 aortas, 673, or 73.6 per cent, had thickening or destruction of the aortic intima, further interfering with the nutritional function of the branches.In 84 patients there had been syphilis, and a tertiary lesion was recognized in fourteen, or 16.7 per cent, of the 84 aortas.Alcoholism was known to have been included in the history of 92 of the patients, and in these the aortas were smooth in twenty, or 21.7 per cent.     

Rupture of the distal thoracic esophagus by closed trauma]

Closed traumatic rupture of the esophagus is uncommon, usually located in the upper third of the esophagus. We report a case occurring in the lower third. This diagnosis must be envisaged when faced with delayed clinical and radiological signs. The prognosis is severe and the therapeutic decisions are controversial.