Experimental studies on respiratory insufficiency after endoscopic injection sclerotherapy using ethanolamine-oleate

To study the influence of Ethanolamine-Oleate (EO) used for endoscopic injection sclerotherapy for esophageal varices on the pulmonary hemodynamics, extra vascular lung water (EVLW), and pulmonary and systemic pressures measurements, and blood gas analysis were performed after injection of EO directly into the right atrium in 18 mongrel dogs. Studies were made in three groups, group A (6 dogs) in which the bolus of 1 ml/kg of EO was injected with 1 second; group B (6 dogs) in which 0.25 ml/kg of EO was injected for four times successively within a minute; and controls (6 dogs) the bolus of 1 ml/kg of saline was injected within 1 second. EVLW was measured by thermal-green dye double indicator dilution method. Pulmonary pressures were measured using Swan-Ganz catheter. Results were as follows. In group A, 4 of the 6 dogs died with a symptom of pulmonary edema within several minutes. In the other two, systemic and pulmonary artery pressure did not change, but EVLW and pulmonary artery resistance significantly increased compared to the controls. Intrapulmonary shunt ratio and PO2 were reduced significantly compared to the controls. In group B no systemic hemodynamic changes were observed. But again EVLW significantly increased. These results suggest that the injection sclerotherapy using EO affects pulmonary hemodynamics. And this effect of EO doesn't depend on the total amount of injected EO, but on the concentration of EO reaching the lung. Careful respiratory monitoring seems necessary in patients undergoing injection sclerotherapy.     

不同时间浅低温对蛛网膜下腔出血犬脑血管痉挛的影响

目的 探讨不同时间浅低温对蛛网膜下腔出血犬脑血管痉挛的影响.方法 成年健康犬30只,雌雄不拘,体重14～20 kg,采用枕骨大孔二次注血法制备犬蛛网膜下腔出血模型.随机分为5组(n=6),人工脑脊液组(ACSF组):枕骨大孔处注入ACSF 0.5 ml/ks;蛛网膜下腔出血组(SAH组):制备蛛网膜下腔出血模型,维持直肠温度38～39℃;不同时间浅低温组(H_(1～3)组):在第2次注血后分别立即实施8、16和32 h浅低温(33.5℃),随后复温至38～39℃.于第1次注血或注入ACSF前和第2次注血或注入ACSF 5、12和19 d时行整体功能分级(OPC),并采用ELISA法和硝酸还原酶法分别测定血浆和脑脊液内皮素-1(ET-1)和一氧化氮(NO)代谢产物NO_2~-/NO_3~-的浓度,采用CT血管造影动态测量脑基底动脉直径.结果 与ACSF组比较,SAH组和H_1,2组OPC分级升高,血浆和脑脊液ET-1浓度升高,NO_2~-/NO_3~-浓度降低,基底动脉直径减小(P＜0.05),H_3组上述指标差异无统计学意义(P＞0.05);与SAH组比较,H_2,3组OPC分级降低,血浆和脑脊液ET-1浓度降低,NO_2~-/NO_3~-浓度升高,基底动脉直径增大(P＜0.05),H_1组各时点上述指标差异无统计学意义(P＞0.05);与H_2组比较,H_3组血浆和脑脊液ET-1浓度降低,NO_2~-/NO_3~-浓度升高,基底动脉直径增大(P＜0.05).结论 浅低温16～32 h可缓解蛛网膜下腔出血犬脑血管痉挛,且随浅低温时间延长该作用增强,其机制可能与降低全身和脑组织ET-1水平,升高NO水平,调节脑血管收缩-舒张平衡有关.     

Hemodynamic and morphological changes in the dog kidney after injection of 5% ethanolamine oleate into the superior vena cava

The effect of the sclerosant 5% ethanolamine oleate (EO) on renal circulation was evaluated in 20 mongrel dogs into which we injected 5% EO (0.5 ml/kg) into the superior vena cava. There was a marked hemolysis and a significant decrease in creatinine clearance from 104.4 +/- 17.1 (mean +/- SD) to 40.7 +/- 5.0 ml/min (p less than 0.01) at 120 min. The renal arterial blood flow (RAF) decreased biphasically; from 75.3 +/- 13.1 to 9.8 +/- 9.3 ml/min during an average of 2.3 min, immediately after the injection (p less than 0.01) and gradually decreased after reaching the pretreatment level to 43.2 +/- 8.6 ml/min at 120 min (p less than 0.01). Cardiac output significantly decreased from 1.86 +/- 0.08 to 1.54 +/- 0.08 l/min (p less than 0.01). Tubular necrosis was histologically evidenced in the tissues examined at 6 h after the injection of EO. Biphasic decrease in renal arterial blood flow can be explained by the possible occurrence of spasm of the peripheral renal arteries in the acute phase and tubular necrosis in the late phase. This study suggests to us that the tubular necrosis induced by decreases in RAF as well as hemolytic nephropathy play a significant role in cases of renal dysfunction following the endoscopic injection of 5% EO to sclerose esophageal varices.     

Red blood cells are essential for late vasospasm following experimentally induced subarachnoid hemorrhage in dogs.

The in vivo spasmogenic activity of various blood components was examined in dogs. Each blood fraction was injected into the cisterna magna at 0.5 or 1.0 ml/kg body weight, after the removal of 0.5 ml/kg body weight of cerebrospinal fluid, and vertebral angiography was then performed. Whole blood induced both early and late arterial spasm. Platelet-rich and platelet-poor plasma produced only early spasm, and no arterial narrowing was observed on days 1, 3, and 7 after injection. On the contrary, intracisternal injection of washed red blood cells (0.5 ml/kg body weight) produced no arterial narrowing for 6 hours after injection and induced moderate arterial narrowing on days 1, 3, and 7 after injection. Hemolysate (a 10-gm/dl concentration of hemoglobin) produced prolonged monophasic arterial narrowing after injection. These results imply that red blood cells are required for late, prolonged arterial narrowing after experimental subarachnoid hemorrhage.     

Net fluid leakage (LN) in experimental pulmonary oedema in the dog

Net fluid leakage (LN) from the intravascular to the extravascular pulmonary space was estimated in anaesthetised dogs after injection of oleic acid (OA) (n = 8), or after hydrostatic pressure elevation by inflation of a left atrial balloon (n = 5). LN was calculated as the sum of: (i) rate of change in extravascular lung water (delta EVLW), (ii) thoracic lymph flow, and (iii) pleural fluid formation per time unit. Pleural fluid formation was measured in five dogs with hydrostatic or OA induced pulmonary oedema and was 1.8 +/- 0.9 ml/kg/h. In OA-induced pulmonary oedema, LN increased to a peak of 9.2 ml/kg/h within 2 h after OA injection. Thereafter LN fell and was 2-4 ml/kg/h during the succeeding 2-4 h. During hydrostatic pulmonary oedema LN was increased to as much as 13 ml/kg/h, but it became negative, -5 to -8 ml/kg/h (reabsorption of extravascular fluid) as soon as pulmonary vascular pressures returned to normal following deflation of the left atrial balloon. We conclude that in both forms of oedema there is an initial rapid leakage. In OA-induced oedema this leakage continues, although at a slower rate, whereas in hydrostatic oedema there is a considerable net fluid absorption from the pulmonary extravascular to the intravascular space as soon as vascular pressures are brought to normal levels.     

Neurologic and histologic outcome after intraneural injections of lidocaine in canine sciatic nerves

BACKGROUND: Inadvertent intraneural injection of local anesthetics may result in neurologic injury. We hypothesized that an intraneural injection may be associated with higher injection pressures and an increase in the risk of neurologic injury. METHODS: The study was conducted in accordance with the principles of laboratory animal care, and was approved by the Laboratory Animal Care and Use Committee. Fifteen dogs of mixed breed (16-21 kg) were studied. After general endotracheal anesthesia, the sciatic nerves (n= 30) were exposed bilaterally. Under direct vision, a 25-gauge, long-beveled needle (30 degrees) was placed either epineurally (n= 10) or intraneurally (n= 20), and 4 ml of preservative-free lidocaine 20 mg/ml was injected using an automated infusion pump (4 ml/min). Injection pressure data were acquired using an in-line manometer coupled to a computer via an analog-to-digital conversion board. After injection, the animals were awakened and subjected to serial neurologic examinations. One week later, the dogs were killed, the sciatic nerves excised and histologic examination was performed by pathologists blind to the purpose of the study. RESULTS: All perineural injections resulted in low pressures (< or = 5 psi). In contrast, eight of 20 intraneural injections resulted in high pressures (20-38 psi) at the beginning of the injection. Twelve intraneural injections, however, resulted in pressures of less than 12 psi. Neurologic function returned to baseline within 3 h after perineural injections and within 24 h after intraneural injections, when the measured injection pressures were less than 12 psi. Neurologic deficits persisted throughout the study period after all eight intraneural injections that resulted in high injection pressures. Histologic examination of the affected nerves revealed fascicular axonolysis and cellular infiltration. CONCLUSIONS: The data in our canine model of intraneural injection suggest that intraneural injections do not always lead to nerve injury. High injection pressures during intraneural injection may be indicative of intrafascicular injection and may predict the development of neurologic injury.     

胶体扩容对异氟醚-硬膜外阻滞复合麻醉时肝血流的影响

目的：探讨硬膜外阻滞复合异氟醚吸入全麻对血流动力学和肝血流的影响及其静脉输入3.5%尿素交连明胶（UG）的作用。方法：18只犬分两组，行胸段硬膜外阻滞后吸入0.5和1.0MAC异氟醚。实验组硬膜外阻滞前开始静脉输入UG12ml/kg。监测体循环、肺循环、肝动脉、门静脉血流动力学。肝血流用电磁血流仪测定。结果：对照组硬膜外阻滞后BP、HR、肝动脉阻力和门静脉血流均下降，加吸0.5MAC异氟醚使外周血管阻力（SVR）、肺动脉压和门静脉压降低；1.0MAC后心排血量下降、肝动脉血流也比0.5MAC时减少。心博量（SV）于吸入异氟醚后有所升高。实验组硬膜外阻滞后HR减慢、SV、增加而SVR下降，肝脏循环稳定。吸入异氟醚后全身和肝脏血流动力学变化显著轻于对照组。结论：硬膜外阻滞后，随异氟醚浓度升高，体循环、肺循环、肝动脉、门静脉血流动力学发生显著变化；胶体液扩容对比有明显的防治作用。     

Furosemide, when used in combination with positive end-expiratory pressure, facilitates the resorption of extravascular lung water in experimental hydrostatic pulmonary oedema

The study aimed to establish whether furosemide given intravenously improved resorption of hydrostatic pulmonary oedema in 14 dogs mechanically ventilated with positive end-expiratory pressure (PEEP). Hydrostatic pulmonary oedema was created by simultaneous inflation of a left atrial balloon and rapid intravenous infusion of isotonic saline. The hydrostatic process was terminated by deflating the balloon and reducing the infusion rate. A PEEP of 10 cmH2O (1.0 kPa) was applied in all animals; in seven, furosemide was administered (diuretic group), 1 mg/kg intravenously as a bolus followed by an infusion of 0.5 mg/kg per hour, while the remaining seven dogs served as a control group. All dogs were studied for a period of 4 h. The extravascular lung water measured with the double indicator dilution technique was 28.3 +/- 3.8 (diuretic group) and 28.2 +/- 6.8 ml/kg (control group) during maximum oedema. It was reduced to 16.4 +/- 2.2 (diuretic group) vs 19.8 +/- 3.7 ml/kg (control group) after 4 h of resorption, P less than 0.05. Postmortem gravimetric values of extravascular lung water were 9.1 +/- 3.4 (diuretic group) vs 12.6 +/- 5.0 g/kg (control group). In the diuretic group the urinary output increased threefold, and haemoglobin and serum protein concentrations were higher than in the control group. There was a significantly greater decrease in cardiac output and central blood volume in the diuretic group. In conclusion, furosemide given intravenously improved lung fluid resorption in hydrostatic pulmonary oedema, probably by increasing the plasma colloid osmotic pressure.     

The effects of halothane and pentobarbital on the threshold of transpulmonary passage of venous air emboli in dogs

The influence of halothane, pentobarbital, and their interaction on the passage of air across the pulmonary circulation was studied in 12 dogs using transesophageal M-mode echocardiography for air detection in the left atrium and/or aorta. Air was detected in the left atrium and/or aorta after pulmonary artery air injection of 0.04 ml/kg during 1% halothane anesthesia (n = 5). Addition of pentobarbital changed the threshold to 1.0 ml/kg. During pentobarbital anesthesia with and without halothane (n = 7), the thresholds were 1.1 and 1.2 ml/kg, respectively. The authors conclude that the threshold for transpulmonary passage of venous air is higher during anesthesia with pentobarbital with or without halothane than during anesthesia with halothane alone.     

Suppressive effect of doxorubicin on liver recurrence after resection of colonic VX2 cancer lesions: Difference in efficacy according to the injection protocol

An animal model with liver cancer recurrence was induced by resecting colonic VX2 cancer lesions in 57 rabbits, and the effects of doxorubicin (ADR) on the recurrence were examined. Animals were divided into a control group and three chemotherapeutic groups: a portal injection group, to which ADR was injected into the portal vein after resection of the primary lesions; a peripheral injection group, to which ADR was injected into a peripheral vein after resection; and a preoperative injection group, to which an ADR dose of 0.5 mg/kg was peripherally injected 0, 1, and 2 days prior to resection followed by a portal injection of ADR 0.5 mg/kg after resection. The rate of liver recurrence was 100% in the control group, whereas it was 0% and 60% in the portal ADR 1.0 and 0.5 mg/kg injection groups, and 60% and 100% in the peripheral ADR 1.0 and 0.5 mg/kg injection groups. In the preoperative group, the rate was 0%, 100%, and 67% in the animals injected 2, 1, and 0 days prior to resection, respectively. These results suggest that portal injection or appropriate combinations of preoperative peripheral and portal injections of ADR are more effective than peripheral or portal injection alone in the suppression of liver recurrence.     

Cardiovascular effects of pregnanolone emulsion: an experimental study in artificially ventilated dogs

The acute cardiovascular effects of pregnanolone emulsion, a new steroid preparation for intravenous anaesthesia, were investigated in artificially ventilated dogs. The anaesthetic was administered as repeated intravenous bolus injections, doubling the dosage with each injection. The plasma concentration of pregnanolone, and the haemodynamic, respiratory and metabolic variables were determined after each injection. Cardiac output and heart rate increased from the first bolus dose of the anaesthetic (0.5 mg/kg), which produced anaesthesia lasting 10 to 15 min. Both continued to increase after administration of 1.0, 2.0 and 4 mg/kg, whereas reductions of systemic arterial pressure and estimated myocardial contractility were observed only at the two highest dosages. A decrease in vascular resistance was calculated in the systemic circulation, whereas vascular resistance increased in the pulmonary circulation. A state of circulatory shock followed administration 8, 16 and 32 mg/kg of the anaesthetic.     

Relaxant effect of calcitonin gene-related peptide on cerebral arterial spasm induced by experimental subarachnoid hemorrhage in dogs

This study examines the relaxant effect of calcitonin gene-related peptide (CGRP), a 37-amino acid peptide with a potent vasodilator action, on cerebral arterial spasm after subarachnoid hemorrhage (SAH). The spasm was induced by injecting autologous arterial blood percutaneously into the cisterna magna in adult mongrel dogs. The single-injection model of SAH was produced by injection of 1.0 ml/kg body weight of blood (on Day 0), and the double-injection model involved two successive injections of 0.5 ml/kg body weight of blood made 48 hours apart (on Day 0 and Day 2). On vertebral angiograms, arterial narrowing of the major cerebral arteries was most prominent on Day 3 after SAH in the single-injection model and on Day 7 in the double-injection model. When 10(-10) mol/kg of CGRP was administered intracisternally in the single-injection model on Day 3, the diameter of the spastic cerebral arteries, as determined by angiography, recovered to normal. After intracisternal administration of 10(-11) to 2 X 10(-10) mol/kg of CGRP on Day 7 in double-injection models, spastic cerebral arteries dilated in a dose-dependent manner. The dilatory effect of CGRP continued for a few hours after administration. The results suggest that CGRP injected intracisternally may reverse cerebral arterial spasm after SAH.     

脱氢野百合碱诱导犬肺动脉高压模型的建立

目的用药物法建立犬肺动脉高压模型。方法野百合碱经脱氢处理成脱氢野百合碱 (dehydromonocrotaline,DMCT),经心导管注射入犬右心房,于注射药物后4周、8周测定肺动脉压力等血液动力学参数,并行肺组织病理检查,评估周围肺肌性动脉肌化情况、肌性肺动脉中膜肥厚程度。结果 DMCT(3 mg／kg)组8只犬存活2只,DMCT(2 mg／kg)组8只犬与对照组犬均存活。DMCT组4周后平均肺动脉压(mMPAP)(20．7±3．1)mm Hg(1 mm Hg=0．133 kPa),8周后mPAP(30．2±2．6)mm Hg,肺动脉收缩压(sPAP)和肺动脉楔压(PCWP)亦升高,与给药前相比,差异有统计学意义(P<0．01)。DMCT组8周后 mPAP、sPAP与PCWP亦明显高于溶剂对照组,差异有统计学意义,P<0．01。8周后DMCT组直径为15- 50μm的肺肌性动脉肌化数(54．3±6．6)％,直径为100-200μm的肺肌性动脉的中膜厚度百分比(27．3± 5．7)％,均高于溶剂对照组,差异有统计学意义(P<0．01),右心肥大指数增加(P<0．05)。光学显微镜下观察到DMCT组肺泡区肺肌性动脉中膜肥厚,新生内膜形成,管腔变小。结论 DMCT可成功诱导犬肺动脉高压模型,模拟人类终末期肺高压的病理特点。     

Detection of venous air embolism by continuous mixed venous oximetry in dogs

Continuous mixed venous oxygen saturation (SvO 2) was evaluated as a monitor of venous air embolism in a canine model. Nineteen dogs were anesthetized, paralyzed, and mechanically ventilated. Invasive monitoring included SvO 2, systemic and pulmonary artery blood pressures, and thermodilution cardiac outputs. Air boluses of 0.25 and 0.5 ml/kg were injected in six dogs and 1 ml/kg in all. All 1 ml/kg emboli were detected by greater than or equal to 5% decreases in the SvO 2. The SvO 2 decreased from 82 +/- 8% to 72 +/- 11% (mean +/- SD), an average decrease of 9 +/- 5% (p = 0.004). Time to the SvO 2 nadir was 2.6 +/- 2.5 min. Of the 0.5 and 0.25 ml/kg emboli, 50% and 17% were detected, respectively. Cardiac output decreased from 2.9 +/- 0.8 to 2.1 +/- 0.8 L/min after the 1 ml/kg emboli (p = 0.02). The 1 ml/kg emboli increased pulmonary artery pressures and decreased systemic blood pressure in 100% and 75% of animals, respectively. Peak changes in pulmonary artery pressure occurred at 1.2 +/- 0.8 min. In the present study, time to maximum change was greater for SvO 2 than for pulmonary artery pressure changes. Use of fiberoptic pulmonary artery catheters for continuous measurement of SvO 2 can add a new diagnostic modality to venous air embolism detection in patients who require a pulmonary artery catheter for other medical indications.     

Heparinase I (Neutralase) Reversal of Systemic Anticoagulation

Background: Protamine causes multiple adverse reactions. Heparinase I, a specific enzyme that inactivates heparin, is a possible alternative to protamine. In this study, the authors examined the efficacy of heparinase I to reverse heparin-induced anticoagulation in vitro and compared heparinase I to protamine as an antagonist of heparin-induced anticoagulation in dogs.

Methods: In the in vitro study, blood was obtained from the extracorporeal circuits of 12 patients, and activated clotting times were determined after adding different concentrations of heparinase I. In the in vivo study, 24 anesthetized dogs received 300 units/kg heparin injected intravenously for 5 s, then 10 min later, 3.9 mg/kg protamine, 5-41 micro gram/kg heparinase I, or the vehicle (n = 4/group) were administered intravenously, and activated clotting times and hemodynamics were measured.

Results: In the in vitro study, heparin concentrations of 3.3 +/-1.0 (mean+/-SD) units/ml (approximately 0.033 mg/ml; n = 12) were reversed in the blood of patients by heparinase I at concentrations > 0.490 micro gram/ml. In the canine study, heparinase at all doses studied and protamine effectively reversed the anticoagulating effects of heparin within 10 min of administration. Protamine produced adverse hemodynamic effects, whereas heparinase or its vehicle produced no significant change in arterial pressure.     

Effect of halothane, fentanyl, and ketamine on the threshold for transpulmonary passage of venous air emboli in dogs.

We assumed that the capacity of the lungs to filter gas bubbles would vary as a function of anesthetic management. The effects of halothane (1% inspired concentration [group 1, n = 8]), fentanyl (100 micrograms/kg IV, followed by 1 micrograms.kg-1.min-1 [group 2, n = 7]), and ketamine (10 mg/kg IV, followed by 0.2 mg.kg-1.min-1 [group 3, n = 6]) on the passage of bolus injections of air across the pulmonary circulation were studied in dogs by using transesophageal echocardiography to detect air in the left atrium or the aorta, or both. The thresholds for bolus air detection during halothane, fentanyl, and ketamine administration were 0.05 mL/kg (range 0.01-0.1), 0.5 mL/kg (range 0.2-1.0), and 0.35 mL/kg (range 0.1-0.5), respectively. We conclude that the threshold during fentanyl- or ketamine-induced anesthesia was significantly higher than during halothane-induced anesthesia. Therefore, halothane interferes with the capacity of the lungs to filter air from the pulmonary circulation.     

Detection of air embolism by transesophageal echocardiography

In this study transesophageal echocardiography was utilized for detecting air embolism in dogs in the supine position and in patients undergoing neurosurgery in the sitting position. In dogs, the threshold dose of venous air for detection was determined using either a bolus injection or continuous infusion of air via the jugular vein for up to three minutes. The ability to detect air in the aorta also was determined by a bolus injection into the left ventricular via an arterial catheter. For venous injection of air, the threshold dose by bolus was 0.02 ml/kg. When given by infusion, air could be detected in all cases by both contrast echocardiogram and Doppler sound changes at the rate of 0.05 ml . kg-1 . min-1. When air was injected into the left ventricle, the threshold dose was 0.001 ml/kg using contrast echocardiogram. In the clinical evaluation, air was clearly demonstrated in five of six patients by transesophageal echocardiogram along with appropriate changes in Doppler sounds, pulmonary artery pressure, and end-tidal carbon dioxide concentration. Our results suggest that transesophageal echocardiography may be a more sensitive and accurate method for detecting venous air embolism than other commonly used monitors for patients undergoing neurosurgical procedures in the sitting position. This device may also be able to detect air in the aorta in patients experiencing paradoxical air embolism during surgery due to intracardiac or pulmonary shunts.     

Intra-aortic injection of propofol prevents spinal cord injury during aortic surgery.

OBJECTIVE: We investigated whether propofol, a widely used anesthetic, injected into clamped aortic segments quickly attenuated transcranial spinal motor-evoked potential (MEP) amplitudes and protected against spinal cord injury during thoracoabdominal aortic surgery. METHODS: Eighteen beagle dogs were divided into three groups (n=6, each group): group 1 (20 ml of saline, intra-aortic injection), group 2 (1.5 mg/kg of propofol, intravenous injection), and group 3 (1.5 mg/kg of propofol, intra-aortic injection). Aortic cross-clamping was performed for 30 min. In each group, MEP amplitudes were recorded before, during, and after aortic cross-clamping. Tarlov score and histopathological examination were used to evaluate the protective effects of intra-aortic propofol injections. RESULTS: MEP amplitudes in group 3 attenuated to a value that was 60% of the control in just a minute after aortic cross-clamping, but maintained 40% of the control value during aortic cross-clamping. However, MEP amplitudes in groups 1 and 2 gradually attenuated and almost disappeared. Groups 1 and 2 amplitudes were lower than those in group 3, 30 min after aortic cross-clamping (p<0.001). Twenty-four hours after ischemia, the Tarlov score in group 3 was 3.5+/-0.5 and was higher than scores from groups 1 and 2, which were 0.5+/-0.5 and 1.3+/-1.2 (mean+/-SD, p<0.001, and p<0.001), respectively. Histopathologically, normal spinal cord motor neurons in group 3 were preserved to a significantly greater extent than in groups 1 and 2 (p=0.0031, and p=0.0282, respectively). There was a strong correlation between Tarlov scores at 24h and the number of normal motor neurons in the anterior horns of spinal cords (r=0.897; p<0.001). CONCLUSIONS: Intra-aortic propofol injections produce the quick suppression of MEP amplitudes and protect spinal cords from ischemia during aortic cross-clamping.     

细针直接穿刺枕大池二次注入自体血致犬脑血管痉挛模型的建立

目的 评价采用细针直接穿刺枕大池二次注入自体血致犬脑血管痉挛模型建立的可行性.方法 成年健康杂种犬6只,雌雄不拘,体重14～ 18 kg.腹腔注射3%戊巴比妥钠30～40 mg/kg麻醉下,保留自主呼吸.用细针穿刺枕大池后,缓慢放出脑脊液0.3 ml/kg,然后注入自体股动脉血0.5 ml/kg,速率0.5 ml/s;48 h后再次注入等容量自体股动脉血.于第1次注血前(T1)、第2次注血后7 d(T2)、14 d(T3)和21 d(T4)时,行神经功能评分,并进行CT血管造影,测量基底动脉直径.结果 术中和术后无一只犬死亡.与T1时比较,T2.3时神经功能评分升高,基底动脉直径缩短(P＜0.05),T4时神经功能评分和基底动脉直径差异无统计学意义(P＞0.05).结论 采用细针直接穿刺枕大池二次注入自体血可成功建立犬蛛网膜下腔出血后脑血管痉挛模型,术后生存率高,对动物损伤小.     

细针直接穿刺枕大池二次注入自体血致犬脑血管痉挛模型的建立

目的 评价采用细针直接穿刺枕大池二次注入自体血致犬脑血管痉挛模型建立的可行性.方法 成年健康杂种犬6只,雌雄不拘,体重14～ 18 kg.腹腔注射3%戊巴比妥钠30～40 mg/kg麻醉下,保留自主呼吸.用细针穿刺枕大池后,缓慢放出脑脊液0.3 ml/kg,然后注入自体股动脉血0.5 ml/kg,速率0.5 ml/s;48 h后再次注入等容量自体股动脉血.于第1次注血前(T1)、第2次注血后7 d(T2)、14 d(T3)和21 d(T4)时,行神经功能评分,并进行CT血管造影,测量基底动脉直径.结果 术中和术后无一只犬死亡.与T1时比较,T2.3时神经功能评分升高,基底动脉直径缩短(P＜0.05),T4时神经功能评分和基底动脉直径差异无统计学意义(P＞0.05).结论 采用细针直接穿刺枕大池二次注入自体血可成功建立犬蛛网膜下腔出血后脑血管痉挛模型,术后生存率高,对动物损伤小.