前列腺素E1控制性降压对肝,肾,脑血流量的影响

研究了前列腺素Ｅ１控制性降压对肝、肾、脑血流量的影响。杂种犬１６只，随机分为前列腺素Ｅ１组和对照组，输注前列腺素Ｅ１使平均动脉压下降３０％～４０％，维持３０分钟，分别于降压前、降压后１５分。３０分及停止降压后１５分钟测定肝、肾、颈内动脉血流量。结果表明控制胜降压期间右侧颈内动脉血流量、肝固有动脉血流量、肾动脉血流量均无显著变化，门静脉血流量显著降低，停止降压后１５分钟门静脉血流量恢复降压前水平。     

三磷酸腺苷控制性降压对器官血流量的影响

研究了三磷酸腺苷（ＡＴＰ）控制性降压对器官血流量的影响，杂种犬１６只，随机分为ＡＴＰ组和对照组，输注ＡＴＰ使平均动脉压下降３０％￣４０％，维持３０分钟，分别于降压前、降压后１５分钟、３０分钟及停止降压后１５分钟用电磁血流量计测定器官血流量。结果表明控制性降压期间右侧颈内动脉血流量、肝动脉、血流量、肾动脉血流量均无显著变化、门静脉血流量显著增加，停止降压后１５分钟静脉血流量恢复到降压前水平。     

中度低温治疗犬出血性休克的作用

低温治疗出血性休克的作用一直存有争议。本文旨在探讨低温加严重出血性休克时中度低温对心血管功能、局部血流量与氧耗量的影响,以评价其在治疗严重出血性休克中可能具有的保护和治疗作用。取18条16～28kg的犬。在以硫贲妥钠诱导和α-三氯醛糖维持的麻醉下,作股动脉与肱动脉插管直达降主动脉以便放血、     

神经安定镇痛普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠…

实验研究神经安定镇痛、普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响。结果表明，神经安定镇痛、普鲁卡因静脉复合麻醉抑制失血性休克状态下的心血管功能，降低心肌血流量，使得心肌氧供需失衡，心肌缺血缺氧。     

神经安定镇痛普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响

实验研究神经安定镇痛、普鲁卡因静脉复合麻醉对失血性休克犬体循环和冠脉循环血流动力学及心肌代谢的影响。结果表明，神经安定镇痛、普鲁卡因静脉复合麻醉抑制失血性休克状态下的心血管功能，降低心肌血流量，使得心肌氧供需失衡，心肌缺血缺氧。     

亚甲蓝对感染性休克犬肠道灌注和氧合的影响

目的　研究鸟苷酸环化酶抑制药亚甲蓝对感染性休克犬肠道灌注和氧合的影响。方法　静脉注入内毒素诱导的 7只感染性休克犬模型 ,输注 0 9%氯化钠复苏后 15分钟内注入亚甲蓝2mg/kg。血流量仪测定基础、休克 1小时后、复苏后和亚甲蓝注入后 30分钟肠系膜上动脉血流量。分析动脉和肠系膜上静脉血气 ,计算肠道氧合。结果　犬感染性休克后 ,肠系膜上动脉 (肠道 )血流减少 6 1 8% (P <0 0 1) ,氧输送 (DO2 )减少 6 2 1% (P <0 0 1) ,氧摄取 (O2 extr)增加 2 3 5 %。复苏至肺动脉嵌压为 (12 1± 1 4 )mmHg后 ,肠道血流增加 5 4 6 % (P <0 0 1) ,DO2 增加 12 8% (P <0 0 1) ,O2 extr增加 2 0 9%。亚甲蓝注入后 ,肠道血流增加 19 4 % (P <0 0 1) ,DO2 则无明显变化 (P >0 0 5 ) ,O2 extr增加 14 8%。结论　感染性休克后肠道血流灌注减少 ,氧耗增加 ;液体复苏仅部分恢复肠道灌注 ;亚甲蓝增加肠道灌注和氧摄取     

选择性脾胃区减断分流术后血流动力学变化的实验研究

目的 研究门静脉高压症犬行选择性脾胃区减断分流术(selective decongestive devascular-ization shunt of gastrosplenic region,SDDS-GSR)后血流动力学变化.方法 用正常犬制备门静脉高压脾亢模型并进行SDDS-GSR术.制模前、成模后,分流术后30 d和术后60 d观察门静脉压力,门静脉、肝动脉、脾静脉和脾动脉的内径、血流速度和血流量参数的变化,作自身对照研究.结果 SDDS-GSR术后30 d的脾胃区静脉压力显著下降(P<0.01),门静脉、脾动脉和脾静脉内径显著缩小(P<0.01),门静脉、脾动脉和脾静脉血流量参数减少(P<0.01),肝动脉内径和血流量参数显著增加(P<0.01),术后60 d上述指标改变仍保持稳定.结论 sDDS-GSR术通过减少脾动脉血流和改善脾静脉回流,有效地降低了脾胃区的静脉压力,并保持肠系膜区的相对高压,同时增加肝动脉向肝血流量,保证了门脉的向肝血流量,术后血流动力学变化较持久稳定,是一种合理而可取的治疗门静脉高压症的术式.     

肝动脉缓冲效应：机制及临床意义

肝动脉缓冲效应是肝脏自身调节血流量的重要生理功能，能够维持肝脏总血流量的相对稳定。“腺苷清除假说”是目前对肝动脉缓冲效应机制研究中较为公认的一种学说。肝动脉缓冲效应不仅在正常机体中具有重要的生理功能，而且在肝硬化、肝癌、肝移植、气腹术、休克等病理情况下具有重要的临床意义。     

多巴胺复合去甲肾上腺素对内毒素休克犬肾脏的影响

目的了解内毒素休克时低剂量去甲肾上腺素和多巴胺对肾血流量和肾功能的影响.方法21只犬(14-30kg)戊巴比妥钠麻醉,静脉注射内毒素2mg/kg,1h后将犬分成3组,Ⅰ组静滴去甲肾上腺素40ng.kg-1@min-1,Ⅱ组静滴多巴胺4μg.kg-1@min-1,Ⅲ组静滴去甲肾上腺素和多巴胺(剂量同上),给药1h停药并再观察2h.观察血流动力学(MAP、HR、CVP、PCWPCOSVISVR、)、肾血流量(电磁流量计)和肾功能(血清Na+、K+、肌酐、尿素氮、尿酸).结果休克后MAP显著下降(P＜0.01),CO明显减少(P＜0.01),肾血流量减少(P＜0.05),肾功能无显著改变.给予多巴胺、去甲肾上腺素和两药合用后MAP、SVI和CO增加,肾血流量无显著改变,肾功能基本无变化,仅给去甲肾上腺素2h及3h后尿素氮增加(P＜0.05),血肌酐显著增加(P＜0.01).结论低剂量去甲肾上腺素,特别是与多巴胺合用后能改善血流动力学,维持肾血流量,对肾功能无显著影响.     

麻黄碱纠正硬膜外阻滞低血压前后的血流动力学改变

对１７只犬用有创监测研究硬膜外阻滞后低血压和麻黄碱纠正其低血压的血流动力学改变。结果表明：硬膜外阻滞后肝血管阻力、肾血管阻力均降低．每搏肝动脉血流量、每搏门静脉血流量、每博肾动脉血流量有不同程度增加。麻黄碱纠正硬膜外阻滞低血压时，肝、肾血流量均能保持在较好的正常水个。     

Pneumatic antishock garment decreases hemorrhage and mortality from splenic injury

The effect of the pneumatic antishock garment (PASG) in controlling hemorrhage and death from splenic injury was studied in a canine model. Twelve (two groups of 6) anesthetized dogs had their spleens crushed. Carotid blood pressure, carotid blood flow, splenic artery flow and abdominal aortic flow, as well as the death rate and blood loss, were measured. Group 1 dogs did not have PASG inflation, but group 2 dogs had PASG inflation to an intraperitoneal pressure of 60 mm Hg. All group 1 dogs died within 27 to 58 minutes, but all group 2 dogs survived. Blood loss was 9.4 +/- 1.4 mL/min in group 1 and 1.6 +/- 0.9 mL/min in group 2. In group 1 carotid artery blood pressure, carotid artery flow, splenic artery flow and abdominal aortic flow fell from 120 +/- 10 mm Hg, 284 +/- 12 mL/min, 194 +/- 18 mL/min and 285 +/- 10 mL/min respectively to 0 with death of the animals. By 2 hours in group 2 dogs the carotid artery blood pressure had dropped from 116 +/- 12 to 99 +/- 12 mm Hg, and over the same period carotid artery flow, splenic artery flow and abdominal aortic flow fell from 296 +/- 8 mL/min, 190 +/- 26 mL/min and 279 +/- 16 mL/min respectively to 259 +/- 14 mL/min, 39.0 +/- 6 mL/min and 45 +/- 11 mL/min respectively. Thus, inflation of the PASG maintained carotid artery blood pressure wh ile decreasing splenic, abdominal and aortic flow as well as splenic hemorrhage, with a decrease in the death rate, over a 2-hour period.     

An experimental study on direct revascularization of bronchial circulation by microvascular anastomosis.

The effects of direct revascularization of the bronchial artery after bronchoplasty were estimated by laser Doppler velocimetry and india ink injection in dogs. Bronchoplastic surgery at the right main bronchus was performed in all dogs, and the bronchial artery was reconstructed using the internal thoracic artery in the reconstruction group. The mucosal blood flow was measured at the distal side of the anastomosis. India ink was injected into the aorta in the nonreconstruction group and into the internal thoracic artery in the reconstruction group. The peripheral blood flow had diminished immediately after surgeries to 59% of the baseline value and took 14 days to recover to the baseline value in the nonreconstruction group. However, in the reconstruction group, the blood flow recovered at once to 78% of the baseline value and had returned to that value in 5 days. Statistically significant differences were noted between the groups from just after operation to day 7. India ink data confirmed these findings. In the nonreconstruction group, no ink was observed in the peripheral bronchial vessels on day 3; it was noted in part of the vessels on day 7 and in most on day 14. On the other hand, a relatively large number of vessels were stained just after operation in the reconstruction group. Thus reconstruction of the bronchial artery by means of the anastomosis with the internal thoracic artery can be said to be a useful and effective method for preventing airway ischemia.     

Myocardial tissue oxygen during coronary artery constriction and hypotension in dogs

BACKGROUND: Sodium nitroprusside (SNP) may decrease myocardial tissue oxygenation in dogs with normal coronary arteries. We compared SNP- with desflurane-induced hypotension on myocardial tissue oxygen and pH in dogs with left anterior descending artery constriction. METHODS: Twenty-four dogs were anesthetized with 8% desflurane for baseline anesthesia. Catheters were inserted into the femoral artery and vein and the coronary sinus. A flow probe and flow restriction device was placed on the left anterior descending (LAD) artery. A probe that measured myocardial oxygen pressure was inserted into the middle myocardium in the LAD region. Baseline measures were made of LAD artery flow, arterial and coronary sinus blood gases, and myocardial tissue gases. A 30% decrease in blood pressure was induced with SNP with unrestricted LAD flow (n=6) or when LAD artery flow was restricted by 30% from baseline (n=6). In separate dogs, a 30% decrease in blood pressure was produced with 14 +/- 1% desflurane with unrestricted LAD flow (n=6) or with baseline LAD artery flow restricted by 30% (n=6). RESULTS: During SNP-induced hypotension with no LAD constriction, LAD artery flow and coronary sinus oxygen tension increased but myocardial tissue oxygen tension (PmO2) decreased by 40%. When baseline artery flow was decreased by 30% by LAD constriction, SNP-induced hypotension decreased tissue oxygen pressure by 80%, and ischemic acidosis was produced. During unrestricted LAD artery flow or with a 30% flow restriction, desflurane-induced hypotension produced no significant change from baseline myocardial tissue oxygen tension or pH. CONCLUSION: During coronary artery constriction, desflurane-induced hypotension maintained myocardial tissue oxygenation and pH better than did SNP-induced hypotension. The divergence between tissue and coronary sinus oxygen tension during SNP suggests that arteriovenous shunting may occur.     

Immediate Changes in the Pulmonary Blood Flow After Various Vascular Anastomoses in Lung Autotransplantation

The purpose of the present study was to investigate, by means of radioactive Xe 133, the different effects produced on the distribution of the pulmonary blood flow by various vascular anastomoses in lung autotransplantation.

Twenty mongrel dogs of varying weights were used. In Group I, which consisted of 7 dogs, the pulmonary artery was severed and resutured end-to-end. The distribution of the pulmonary blood flow was measured with Xe 133 pre- and postoperatively. Group II consisted of 5 dogs, whose pulmonary arteries also were severed, but a Dacron Velour patch was used in the resuturing to dilate the site of anastomosis as much as possible. The pre- and postoperative distributions were measured as for Group I. The 5 dogs of Group III were treated by severing and resuturing the pulmonary veins using the atrial cuff. The distribution of blood flow was measured as before. The remaining 3 dogs made up Group IV, the control group. Their treatment consisted of a thoracotomy incision and opening of the pleural cavity, and the closure of the incision without further interference. The pre- and postoperative distributions were measured as for the other groups. Pressure measurements revealed no pressure gradient at the anastomotic line of the pulmonary artery. Nor did the atrial suture, judging from pressure measurements, produce any constriction. The pre- and postoperative measurements with radioactive Xe 133 disclosed that thoracotomy alone did not affect the distribution of the pulmonary blood flow. Nor did the severing and resuturing of the pulmonary veins alone change the distribution. But in Group I, after the severance and end-to-end anastomosis of the pulmonary artery, a distinct, statistically highly significant fall was recorded in the distribution to the operated lung. The reduction in the blood volume was of the order of 38%. However, in the experimental animals whose pulmonary artery had been similarly severed, but where the site of anastomosis had been dilated by means of a Dacron Velour patch, the distribution did not change. The great importance of the pulmonary arterial anastomosis in the search for the causes of increased vascular resistance in autotransplantation is discussed. This detail, however, cannot be claimed to solve the whole problem.     

Effects of celiac plexus block on splanchnic circulation--II: Changes in the systemic hemodynamics and the blood flow of the liver and kidney in dogs

Effects of celiac plexus block (CPB) on systemic and splanchnic circulation, especially of liver and kidney, were investigated in twenty nine mongrel dogs. CPB was performed by an anterior approach through a catheter placed in a paraaortic compartment using 7 mg.kg-1 of 2% mepivacaine. Tissue blood flow measurement was performed by a hydrogen clearance method in eleven dogs, and vascular blood flow was measured in eighteen dogs by an electromagnetic flow meter. Swan-Ganz catheter was inserted to measure mean arterial pressure (ABP), heart rate (HR), central venous pressure (CVP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP) and cardiac output (CO). Then stroke volume (SV), systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR) were calculated. Following CPB, ABP, HR, CVP and C.O. were significantly decreased at 7 to 9%. PAP decreased at 5%. PCWP, SV, SVR and PVR were unchanged. The hepatic arterial blood flow increased significantly, and portal venous blood flow decreased after CPB transiently, and then recovered to control value or to a higher level at 60min after CPB. The tissue blood flow of the liver tended to increase, but the change was not significant. In the kidney, both arterial and tissue blood flows increased significantly after CPB. The results suggest that following CPB, hepatic and renal tissue blood flows increased because of the increments of their arterial blood flows, unless a profound systemic hemodynamic depression occurred.     

Nitrous oxide impairs functional recovery of stunned myocardium in barbiturate-anesthetized, acutely instrumented dogs.

The purpose of this investigation was to characterize the effects of nitrous oxide or nitrogen (70%) on systemic and regional hemodynamics and myocardial tissue perfusion after a brief coronary artery occlusion (15 min) and reperfusion (3 h). Two groups of experiments (14 experiments total) were completed with 24 open-chest, barbiturate-anesthetized dogs. Coronary collateral blood flow was diverted from the ischemic zone during coronary artery occlusion to eliminate a source of variability in degree of ischemia produced by differences in degrees of collateral blood flow among animals. Seven of 16 dogs treated with nitrous oxide and 7 of 8 dogs treated with nitrogen survived coronary occlusion and reperfusion (P less than 0.05). Coronary artery occlusion produced paradoxical systolic bulging in the ischemic zone in both groups of experiments. After reperfusion, segment shortening gradually returned toward control levels but remained depressed from the preocclusion state after 3 h in the nitrogen-treated control group. Similar results were observed after reperfusion in the nitrous oxide group; however, segment function in the ischemic region was significantly (P less than 0.05) depressed throughout the 3-h reperfusion period compared with the control group. Transmural coronary collateral blood flow during occlusion was not significantly different (P greater than 0.05) between groups, indicating that differences in recovery of contractile function observed between groups could not be attributed to differences in myocardial oxygen supply. In addition, the similarity in systemic hemodynamics between the nitrous oxide and control groups indirectly suggests that differences in recovery of function could not be attributed to differences in myocardial oxygen demand. The results indicate that 70% nitrous oxide produces greater mortality after coronary artery occlusion and reperfusion and reduces functional recovery of post-ischemic, reperfused myocardium compared with 70% nitrogen in open-chest, acutely instrumented dogs.     

Coronary Vasodilator Reserve in Young Dogs with Moderate Right Ventricular Hypertrophy

The effects of experimental right ventricular (RV) pressure overload and RV hypertrophy on coronary vasodilator reserve in young animals is not well established. Therefore, we measured coronary vasodilator reserve in the right ventricle of dogs from 7 to 12 months old with moderate RV hypertrophy due to pulmonary artery banding performed 3 to 7 days after birth. In the 5 dogs with pulmonary artery banding, substantial RV hypertension developed (RV pressure at rest, 73 ± 11 mm Hg) as did RV hypertrophy (ratio of RV free wall/left ventricular free wall weight, 1.86 ± 0.41 gm/kg). The reactive hyperemic response following brief coronary occlusions was used as an index of coronary vasodilator reserve. The ratios of peak reactive hyperemic response to resting flow, however, were not significantly different in the 5 banded dogs compared with 7 control animals (3.6 ± 1.0 versus 2.6 ± 0.6); this implies that the extent of vasodilator reserve was similar with or without moderate RV hypertrophy. In addition, myocardial blood flow, as determined using radioactive microspheres, was not significantly different at rest: 0.57 ± 0.09 ml/min per gram in the banded dogs versus 0.48 ± 0.12 ml/min per gram in the controls. Uniform transmural distribution of blood flow was maintained during infusion of isoproterenol, which was used to increase myocardial oxygen requirements in both groups. Minimum coronary vascular resistance was significantly lower in the banded than the control dogs (1.5 ± 0.6 versus 6.2 ± 2.3; p < 0.01). This difference suggests that the cross-sectional area of the right coronary vascular bed increased with the development of RV hypertrophy.     

An experimental study on viability of the devascularized trachea

This experiment was designed to evaluate the effect of varying extents of devascularization to the viability of the trachea, and the influence of preservation of the right bronchial artery on the ischemia of the widely devascularized trachea. In experiment 1, the canine trachea was devascularized in a stepwise manner, and the regional blood flow was measured in each situation. This experiment revealed that the regional blood flow decreased to one-third of the non-treated trachea when the bilateral bronchial arteries were transected, and to nil when the cervical and mediastinal trachea was devascularized. In experiment 2, in which dogs were divided into 2 groups depending on preservation of the right bronchial artery, the trachea was stepwisely devascularized and the regional blood flow measured. This experiment indicated that the regional blood flow in the trachea when the right bronchial artery was preserved did not so remarkably diminish, though the cervical and mediastinal trachea was devascularized. In experiment 3, dogs were divided into 3 groups according to the extent of devascularization of the trachea and to the presence or absence of the preserved right bronchial artery, and were followed for 2 months postoperatively. This experiment demonstrated that the preservation of the right bronchial artery prevented tracheal necrosis caused by devascularization of the cervical and mediastinal trachea. We concluded that the regional tracheal blood flow markedly decreased and that tracheal necrosis occurred following devascularization of the cervical and mediastinal trachea when the bilateral bronchial arteries were transected. The preservation of the right bronchial artery however, prevented a decrease in the regional blood flow and necrosis of the widely devascularized trachea.     

Experimental study of hepatic inflow occlusion in extrahepatic obstructive jaundice--effects on systemic and hepatic hemodynamics and oxygen metabolism]

The effect of clamping both the hepatic artery and portal vein for 20 min in extrahepatic obstructive jaundice on systemic and hepatic hemodynamics and oxygen metabolism were studied in dogs, and the following results was obtained. 1) Dogs with obstructive jaundice were in a hyperdynamic state before hepatic inflow occlusion, showing an increased demand for oxygen in the liver. 2) After declamping, cardiac index and systemic oxygen delivery were decreased in normal dogs, but a further decrease was found in dogs with jaundice. 3) After declamping, hepatic arterial blood flow was increased in normal dogs. Portal blood flow was decreased just after declamping, but was soon restored. In dogs with jaundice, hepatic arterial blood flow increased to a lesser extent, and recovery of portal blood flow was delayed. 4) Hepatic oxygen consumption and oxygen extraction ratio were already increased markedly just after declamping in normal dogs, whereas the degree of the increase in these parameters was much smaller in dogs with jaundice. Thus, hepatic inflow occlusion in extrahepatic obstructive jaundice induces evident disorder of hepatic oxygen metabolism, and is suggested to be dangerous.