MEMSurgery: an integrated test-bed for vascular surgery

Many surgical procedures require skillful manipulations of blood vessels, especially in conventional invasive or minimally invasive surgical procedures. Current surgical methods do not allow the surgeon to receive any real time feedback of the tissue properties when operating on the vessel. As a result, the unintentional application of excessive force may damage the blood vessel. To minimize such trauma, and to study the interaction of surgical instruments with the vessel structure, we have developed an integrated surgical testbed called MEMSurgery (Microelectromechanical Sensory augmented Surgery). The test-bed integrates four elements: a) force sensors mounted on surgical appliances, b) a feedback control mechanism utilizing the intrinsic mechanical properties of the blood vessel, c) feedback of the force applied on the tissue back to the surgeon through a haptic feedback device, and d) visual feedback by a graphical computer model of the vessel. Finally, we evaluate the performance of MEMSurgery by testing the hypothesis that the combination of haptic feedback, feedback control based on vascular mechanical properties, and real-time visual representation of the vessel will help the surgeon decrease the probability of applying excess force while occluding the blood vessel. To this end, we designed a rodent experimental model to obtain the ideal minimum occlusion force (MOF). After a series of human performance studies, and subsequent comparison to direct application of force on the forceps (without feedback), the results show that the probability of applying reasonable MOF increases from 35.5% to 80%. After a brief training period, the probability increases to 90%.     

Minimum vascular occlusive force.

A mathematical analysis of the minimum occlusion force necessary to occlude small vessels based on the parametric influence of blood pressure, vessel diameter, clamp width, and vessel shape after clamping was performed. The results were confirmed by in vivo experimentation with 60 rat aortas (of 1.8 to 2.4 mm caliber) using a variable-force clamp gauge developed in our laboratory. Experimental and theoretical results differed by only 3 gm. Scanning electron microscopy revealed that the initial changes in the endothelium occurred in smaller radii of curvature. Increased pressure resulted in gross morphological changes across the vessel. The minimum occlusion force (as determined by the variable-force clamp gauge) produced only minimal endothelial damage.     

组织工程小血管摩擦力测量方法的研究与应用

目的设计一套用于组织工程小血管内壁摩擦力测量的装置并对组织工程血管的材料进行初步的测量,以验证装置的可靠性和相关结论。方法根据血液动力学的原理,对血管的力学模型进行分析,确定组织工程血管内皮细胞摩擦力的测量方法,从而设计完成整套装置并对弹性元件进行测量,并进行组织工程降解材料聚羟基乙酸PGA构成的管状支架进行摩擦力的测量。结果设计完成了测量组织工程血管内壁摩擦力的实验装置,弹性元件的牵拉力与位移的关系呈良好的线性关系。聚羟基乙酸PGA管状支架的摩擦力随流速的增加而增加。结论测量组织工程血管内壁摩擦力的实验装置是可行的,聚羟基乙酸PGA管状支架的摩擦力与流速基本呈现线性关系。     

The influence of force feedback and visual feedback in grasping tissue laparoscopically

BACKGROUND: Due to the limited force feedback provided by laparoscopic instruments, surgeons may have difficulty in applying the appropriate force on the tissue. The aim of this study was to determine the influence of force feedback and visual feedback on the exerted pinch force. METHODS: A grasper with a force sensor in the jaws was developed. Subjects with and without laparoscopic experience grasped and pulled pig bowel with a force of 5 N. The applied pinch force was measured during tasks of 1-s and 1-min duration. Visual feedback was provided in half the measurements. Force feedback was adjusted by changing the mechanical efficiency of the forceps from 30% to 90%. RESULTS: The mean pinch force applied was 6.8 N (+/-0.5), whereas the force to prevent slippage was 3.0 N (+/-0.4). Improving the mechanical efficiency had no effect on the pinch force for the 1-s measurements. The amount of excessive pinch force when holding tissue for 1 min was lower at 30% mechanical efficiency compared with 90% (105% vs 131%, p = 0.04). The tissue slipped more often when the subject had no visual feedback (2% vs 8%, p = 0.02). CONCLUSION: Force feedback and visual feedback play a more limited role than expected in the task of grasping tissue with laparoscopic forceps.     

Tissue antioxidant capacity during anesthesia: propofol enhances in vivo red cell and tissue antioxidant capacity in a rat model.

The effects of anesthesia on ischemia-reperfusion injury are of considerable scientific and clinical interest. We examined the effects of propofol (known to possess antioxidant activity) and halothane (devoid of antioxidant activity in vitro) on tissue and red blood cell (RBC) antioxidant capacity. Adult male Wistar rats were anesthetized with halothane 0.5%-1.0% (n = 7), propofol 500 microg x kg(-1) x min(-1) with halothane 0.25%-0.5% (small-dose propofol; n = 9), or propofol 2000 microg x kg(-1) x min(-1) (large-dose propofol; n = 8) for 45 min. Blood and tissue samples of liver, kidney, heart, and lung were then harvested for in vitro exposure to a peroxidizing agent. Red cell malondialdehyde and tissue thiobarbituric acid reactive substances were determined spectrophotometrically. Antioxidant capacities of blood and tissues in the Large-Dose Propofol group, and of blood and all tissues except lung in the Small-Dose Propofol group, were increased significantly compared with halothane (P < 0.003). The increases in tissue antioxidant capacities varied in their magnitude: RBC > liver > kidney > heart > lung. There was a high correlation between changes in RBC susceptibility to oxidative damage and corresponding changes in tissues. These findings demonstrate that large-dose propofol significantly enhances tissue antioxidant capacity, and RBC antioxidant capacity can serve as a functional measure of tissue activity, in vivo. IMPLICATIONS: We designed this study to investigate the antioxidant effects of propofol in various tissues in a rat model. Pretreatment of animals with propofol led to a reduction in the susceptibility to an in vitro oxidative stress of five different tissues investigated, demonstrating the drug's ability to limit oxidative injury. This may have future application in limiting organ dysfunction after periods of tissue ischemia (which results in oxidative damage).     

Investigation on radiofrequency and laser (980 nm) effects after endoluminal treatment of saphenous vein insufficiency in an ex-vivo model.

OBJECTIVES: An ex-vivo model for the experimental evaluation of endoluminal thermal procedures for occlusion of saphenous veins was developed. Radiofrequency obliteration (RFO) and endovenous laser therapy (ELT) were compared using this model. DESIGN: Experimental ex-vivo treatment study. MATERIALS AND METHODS: The model consists of the subcutaneous foot veins from freshly slaughtered cows which were reperfused in situ with heparinised bovine blood. The veins were treated with either radiofrequency (RFO n=5) or with endoluminal 980 nm laser light (ELT n=5) using a continuous pull-back for RFO and a stepwise illumination and pull-back protocol for ELT. Immediately after treatment perivenous tissue and veins were examined macroscopically. In a second study the same treatment parameters were used in four further vein segments with RFO (n=2) and ELT (n=2). These vein segments were examined microscopically in HE-stained histological sections. RESULTS: Induration of the vessel wall and contraction of the vessel lumen were observed after RFO. Laser treatment produced carbonised lesions of the vein wall. After 12-24 laser exposures these lesions often became transmural, causing complete perforation of the vessel wall. Histological evaluation after radiofrequency treatment demonstrated homogenous circular thermal tissue alteration with disintegration of intima and media structures. Histological evaluation after endovenous laser treatment showed large variations of thermal tissue effects. Tissue effects ranged from major tissue ablation and vessel wall disruption to minor effects located between laser exposures and on the opposite vessel wall. CONCLUSIONS: Our model is suitable for systematic scientific evaluation of endovenous thermal occlusion procedures. Our first results and theoretical considerations indicate that endovenous laser treatment should be modified in order to ensure controlled homogenous circular thermal damage, avoiding vessel wall perforation and damage to perivascular structures.     

Titration of postischemic cerebral hypoperfusion by variation of ischemic severity in a murine model of stroke.

OBJECTIVE: Murine models using intraluminal occluding sutures to establish transient focal cerebral ischemia are becoming increasingly widespread, because of advances in transgenic technology and the advent of cerebroprotective strategies to ameliorate postischemic cerebrovascular no-reflow. We hypothesize that the degree of postischemic hypoperfusion is directly related to the severity of the initial ischemic insult. METHODS: Transient ischemia of 45-minute duration was produced using middle cerebral artery occlusion with 10-0 (n = 5), 9-0 (n = 5), 8-0 (n = 6), 7-0 (n = 8), 6-0 (n = 30), or 5-0 (n = 5) sutures. In separate experiments, transient vessel occlusion with 6-0 sutures was performed for 15 (n = 17), 30 (n = 16), or 45 (n = 30) minutes. Sequential laser Doppler measurements of relative cerebral blood flow were obtained, and stroke severity was assessed using neurological deficit scores and infarction volumes. RESULTS: Although relative cerebral blood flow at the time of occlusion and 24 hours thereafter was diminished in parallel with increasing suture diameters, only the use of larger sutures resulted in postischemic no-reflow. As the suture diameter was increased, the resultant reflow was decreased and the stroke outcome worsened. A more than twofold increase in infarction volume (8.0 +/- 3 versus 19.7 +/- 3%, P < 0.05) resulted when ischemia duration was increased from 30 to 45 minutes. CONCLUSION: Titration of the initial ischemic insult leads to corresponding variations in the magnitude of postischemic no-reflow and tissue damage. Therefore, critical control of the severity of the initial injury in studies using intraluminal suture occlusion is warranted.     

Role of myocardial temperature measurement in monitoring the adequacy of myocardial protection during cardiac surgery.

Inadequate myocardial protection continues to be encountered despite improved methods of cardioplegia delivery. Although myocardial temperature is commonly monitored to assess the adequacy of cardioplegia delivery, its relationship to the metabolic status of the myocardium has not been investigated. We prospectively reviewed patients who underwent valvular heart surgery with blood (n = 47) or crystalloid (n = 48) cardioplegia and continuous measurement of intraoperative myocardial tissue pH and temperature. We previously demonstrated a high correlation (r = 0.99) between extracellular myocardial pH, levels of intracellular hydrogen ion concentration, and a lowering of tissue ATP during coronary occlusion. Clinically, optimal metabolic protection was defined as the absence of myocardial tissue acidosis during the period of aortic occlusion as quantified by a temperature-corrected integrated mean pH of 6.8 or greater, which has been shown to be predictive of a favorable postoperative outcome. Age, bypass time, myocardial temperature, myocardial tissue pH at the onset of aortic occlusion, cross-clamp time, and volume of cardioplegia were not significantly different between blood and crystalloid groups. Linear regression analysis demonstrated no significant correlation between mean myocardial tissue pH and the corresponding mean myocardial temperature in either group during aortic occlusion. There was also no correlation between the mean myocardial tissue pH and volume of cardioplegia delivered in both groups. These data demonstrate wide intercardiac and intracardiac variability in the degree of regional tissue acidosis encountered during of hypothermic cardioplegia. Cardioplegia delivery guided by measurement of myocardial temperature or by standardized protocol did not prevent the occurrence of tissue acidosis and thus, did not ensure optimal metabolic protection of the heart. In 95 patients undergoing valvular heart surgery with cold blood or crystalloid cardioplegia, there was no correlation between myocardial tissue pH and mycardial temperature or between myocardial tissue pH and volume of cardioplegia administered. Temperature is a poor indicator of the metabolic state of the myocardium.     

alpha4beta1-integrin blockade and cyclosporine decreases the prevalence and severity of transplant vasculopathy in a rat transplant model.

BACKGROUND: Transplant vasculopathy leads to neointimal proliferation of allograft arteries, and alpha4beta1-integrin (very late antigen-4 [VLA-4]) seems to play an important role in the pathogenesis. This study evaluates the effect of a new, synthetic, VLA-4 blocker (S3429) on transplant vasculopathy in a rat cardiac transplant model. METHODS: After transplantation (Lewis to Fisher), rats were divided randomly into 6 therapy groups: Group 1, n = 14, saline solution (vehicle); Group 2, n = 14, 3 mg/kg/day cyclosporine; Group 3, n = 21, 10 mg/kg/day S3429 + 3 mg/kg/day cyclosporine; Group 4, n = 21, 5 mg/kg/day S3429 + 3 mg/kg/day cyclosporine; Group 5: n = 21, 10 mg/kg/day S3429; Group 6, n = 21, 5 mg/kg/day S3429. Cyclosporine was given continuously until rats were killed. S3429 was either given for the entire study time or was discontinued after 20 days and animals were killed at Day 80. Twenty-eighty days after grafting, we assessed vasculopathy prevalence and mean vessel occlusion in coronary arteries. RESULTS: Cyclosporine decreased the prevalence of vasculopathy and mean vessel occlusion compared with controls. We observed a further decrease in prevalence and mean vessel occlusion with 80 days of therapy with S3429 and cyclosporine. After discontinuing S3429 therapy at Day 20, prevalence and mean vessel occlusion increased to values seen in cyclosporine-treated animals at Day 80. S3429 alone decreased mean vessel occlusion only within the first 20 days compared with controls but had no effect on the prevalence of vasculopathy. CONCLUSION: Because of the further decrease with S3429 therapy and the dramatic increase after discontinuation of S3429 therapy, we conclude that blocking VLA-4 receptors may prevent the development of transplant vasculopathy.     

Experimental ischemic colitis in dogs

Experimental ischemic colitis was produced in 42 dogs by either ligation (ligation group, n=18) or temporary occlusion of the mesenteric vessels (temporary occlusion group, n=24) and changes in the local blood flow in the bowel were measured by the hydrogen clearance method. Tissue damage similar to damage seen in patients with ischemic colitis were produced in both of these groups. There was a close correlation between the severity of the ischemia and the ensuing tissue damages. In the ligation group, the tissue damages ranging from erosions or minute ulcerations to diffuse ulcerations occurred when the local blood flow was measured at 30 minutes after the ligation and was below 50 per cent of the basal flow. In the temporary occlusion group, the tissue damages were observed when the local blood flow was below 40 per cent of the basal flow and the occlusion was maintained for over two hours.     

Can varying flow velocity across an arterial anastomosis prevent thromboembolic injury?

In this study, simulated “poor” repairs applied to transverse incisions in the iliac arteries of 40 rats were the basis for comparing the effect of variations in blood flow on throm-boembolism. Using vital microscopy and digital image processing, we performed 2 experiments. In the first experiment (n = 20), the reduction of post-repair blood flow by approximately 50% resulted in an 83% reduction in the total number of emboli appearing in the microcirculation of the cremaster muscle distal to the repair. In the second experiment (n = 20), the same reduction in blood flow typically resulted in larger repair-site thrombi which required significantly more time to grow to their maximum size. We conclude that reducing pedicle artery blood flow to approximately half in our rat model during reperfusion can protect the downstream micro-circulation from embolic injury without increasing the incidence of thrombotic occlusion. © 1995 Wiley-Liss, Inc.     

Dynamic measurement of bone blood perfusion with modified laser Doppler imaging.

Although the mechanisms are not clearly defined, blood flow may play an important role in moderating skeletal adaptation. Most techniques currently available to measure blood flow in bone are time-consuming and require destruction of the tissue, but laser Doppler technology offers a less invasive method. The present study assessed whether laser Doppler perfusion imaging could detect changes in perfusion in cortical bone. By use of modified laser Doppler perfusion imaging with an adjustable, incorporated, near infrared-laser gain photodetection system, perfusion of blood in the mid-diaphyseal tibial cortex of New Zealand White rabbits (n = 5) was measured before, during, and after occlusion of the femoral artery. During occlusion, perfusion decreased 69% compared with control levels; removal of the arterial clip caused flux values to return to near normal. Laser Doppler perfusion imaging provides a two-dimensional image related to blood flow, and the results of this pilot study suggest that it may be an effective technique for imaging in vivo dynamic changes in perfusion in cortical bone.     

In-vivo evaluation of a novel bipolar radiofrequency device for interstitial thermotherapy of liver tumors during normal and interrupted hepatic perfusion

BACKGROUND: Only monopolar systems have thus far been available for radiofrequency ablation of liver tumors, whose application is restricted because of the incalculable energy flow, reduction of electrical tissue conduction, and limited lesion size. The aim of this study was to evaluate a novel internally cooled bipolar radiofrequency application device under in vivo conditions and to compare the effect of this system on lesion size when combined with hepatic arterial microembolization or complete hepatic blood flow occlusion. MATERIALS AND METHODS: In a porcine liver model, RFA (60 W, 12 min) was performed with either normal (n = 12), partially interrupted (arterial microembolization via a hepatic artery catheter n = 12) or completely interrupted hepatic perfusion (Pringle's maneuver, n = 12). RFA parameters (impedance, power output, temperature, applied energy) were determined continuously during therapy. RFA lesions were macroscopically assessed after liver dissection. RESULTS: Bipolar RFA induced clinical relevant ellipsoid thermal lesions without complications. Hepatic inflow occlusion led to a 4.3-fold increase in lesion volume after arterial microembolization and a 5.8-fold increase after complete interruption (7.4 cm(3)versus 31.9 cm(3)versus 42.6 cm(3), P < 0.01). CONCLUSIONS: The novel bipolar RFA device is a safe and effective alternative to monopolar RFA-systems. Interrupting hepatic perfusion significantly increases lesion volumes in bipolar RFA. This beneficial effect can also be achieved in the percutaneous application mode by RFA combined with arterial microembolization via a hepatic artery catheter.     

Microcirculatory hemodynamics after acute blood loss followed by fresh and banked blood transfusion

BACKGROUND: Red blood cell (RBC) conformational changes occur when blood is stored. This study was designed to be a preliminary evaluation to assess how these changes affect the microcirculation. METHODS: The rat cremaster muscle flap model was used to evaluate in vivo microcirculatory changes after withdrawal of 1 mL blood with subsequent administration of fresh blood (group I, n=6) and banked blood (group II, n=6). Each group underwent a 3-stage evaluation: baseline, after blood withdrawal, and after transfusion. Using intravital microscopy, RBC velocity, vessel diameter, functional capillary perfusion, and leukocyte-endothelial interactions were noted. RESULTS: After blood withdrawal, changes in RBC velocity, vessel diameter, functional capillary perfusion, and number of activated leukocytes were observed in both groups, but these changes were more significant in stored blood compared with fresh blood (P相似文献   

Influence of mild metabolic acidosis on cardiac contractility and isoprenaline response in isolated ovine myocardium

The postoperative course after major surgical procedures such as cardiothoracic operations is often accompanied by acute metabolic abnormalities due to large volume and temperature shifts. In general, those intervention-induced trauma might cause the use of catecholamines to stabilize hemodynamics. Within the cardiac community, there are still controversial discussions about standardized medical therapy to treat postoperative acidosis, for example, buffering versus nonbuffering for improving catecholaminergic response of myocardial contractility. The aim of this study was to investigate the influence of mild (and thus clinically relevant) acidosis on myocardial contractility and catecholamine response in explanted trabeculae of ovine hearts. Intact trabeculae (n = 24) were isolated from the right ventricle of healthy sheep hearts. Two different groups (group 1: pH = 7.40, n = 9 and group 2: pH = 7.20, n = 13) were investigated, and force amplitudes were measured at frequencies between 30 and 180 beats per minute and increasing catecholamine concentrations (isoprenaline 0-3 × 10(-6) mM). Force-frequency relation experiments in the presence of a physiological and/or mild acidotic pH solution showed no significant differences. Mean force amplitudes normalized to the lowest frequency showing no significant differences in force development between 0.5 and 3 Hz (n = 9 vs. 13, P = n.s.) (0.5 Hz absolute values 3.1 ± 2.6 for pH = 7.40 vs. 3.8 ± 2.6 mN/mm(2) for pH = 7.20, P = n.s.). Moreover, there was no significant difference in relaxation kinetics between the two groups. Furthermore, the experiments showed similar catecholamine responses in both groups. Force amplitudes normalized to baseline and maximum force showed no significant differences in force development between baseline and maximum isoprenaline concentrations (n = 6 vs. 9, P = n.s.) (baseline absolute values 4.3 ± 4.0 for pH = 7.40 vs. 3.9 ± 1.2 mN/mm(2) for pH = 7.20, P = n.s.). Additionally, relaxation kinetics did not show differences after catecholamine stimulation. The presented experiments revealed no significant negative inotropic effects on isometrically contracting ovine trabeculae with mild metabolic acidosis (pH = 7.2) compared with physiological pH (7.4). Additionally, similar catecholamine responses were seen in both groups. Further investigations (e.g., in vivo and/or in failing hearts with reduced compensatory reserves) will be necessary to examine optimal medical treatment for metabolic abnormalities after cardiac surgery.     

Effects of nitric oxide on reactive oxygen species production and infarction size after brain reperfusion injury

OBJECTIVE: Deleterious effects of strokes may be ameliorated when thrombolysis (i.e., with recombinant tissue plasminogen activator) restores circulation. However, reperfusion injury, mediated by oxygen free radicals (reactive oxygen species [ROS]), may limit the benefits of recombinant tissue plasminogen activator treatment. We hypothesized that, during reperfusion, exogenous nitric oxide (NO) would reduce stroke size by quenching ROS. METHODS: To investigate this hypothesis, we used two in vivo ischemia-reperfusion models, i.e., autologous cerebral embolism in rabbits and filament middle cerebral artery occlusion in rats. Using these models, we measured ROS levels (rabbit model) and stroke volumes (rat model) in response to transient ischemia, with and without intracarotid administration of ultrafast NO donor proline NO (proliNO). RESULTS: In the rabbit cerebral embolism model, intracarotid administration of proliNO (10(-6) mol/L) (n = 6) during reperfusion decreased free radical levels from 538 +/- 86 nmol/L in the vehicle-treated group (n = 7) to 186 +/- 31 nmol/L (2,3'-dihydroxybenzoic acid; P < 0.001) and from 521 +/- 86 nmol/L (n = 7) to 201 +/- 39 nmol/L (2,5'-dihydroxybenzoic acid; P < 0.002). In the rat middle cerebral artery occlusion model, intracarotid administration of proliNO (10(-5) mol/L) (n = 10) during reperfusion reduced the brain infarction volume from 256 +/- 48 mm3 in the vehicle-treated group (n = 8) to 187 +/- 41 mm3 (P < 0.005). In both experimental groups, intracarotid infusion of proliNO did not affect regional cerebral blood flow, mean arterial blood pressure, or brain and body temperatures. CONCLUSION: The beneficial effects of early restoration of cerebral circulation after cerebral ischemia were enhanced by intracarotid infusion of proliNO, most likely because of ROS scavenging by NO. These findings suggest the possibility of preventive treatment of reperfusion injury using NO donors.     

Pharmacological preconditioning of rat liver by up-regulation of heme oxygenase 1

PURPOSE: We investigated whether pharmacologically induced up-regulation of heme oxygenase 1 by pyrrolidine dithiocarbamate (PDTC) conferred protection against subsequent ischemia-reperfusion injury (IRI) to the rat liver after temporary vascular occlusion of 70% of the organ. METHODS: Female Wistar rats (200 to 250 g body weight) anesthetized with pentobarbitone were cannulated in the carotid artery and jugular vein. After laparotomy, a rubber band was applied around the entire vascular supply to the median and left lateral lobes, enabling vascular occlusion of 70% of the liver. A laser Doppler miniprobe was placed on the left lateral lobe to monitor peripheral liver blood flow (PLBF). Immediately upon completion of the surgery, the rats were administered either PDTC (50 mg/kg intravenously; n = 8) or its solvent (isotonic NaCl; n = 8). After 60 minutes, regional ischemia was induced for 30 minutes. The animals were then monitored for 2 hours of reperfusion. Blood samples for alanine transferase (ALT) estimation (as a measure of parenchymal injury) were drawn immediately prior to ischemia and reperfusion, as well as 60 and 120 minutes after reperfusion; PLBF was calculated at these times. RESULTS: ALT increased in the course of the experiments but there was no difference between the groups. The reduction in PBLF due to ischemia-reperfusion was significantly lower in the PDTC group: about 16% versus 40%, after 2 hours of reperfusion. CONCLUSION: Pretreatment with PDTC attenuated the disturbance of hepatic microcirculation, but not parenchymal injury, in the early phase of IRI.     

Impact of gradual blood flow increase on ischaemia-reperfusion injury in the rat cremaster microcirculation model.

INTRODUCTION: We aimed to evaluate the impact of gradual blood reperfusion on ischaemia-reperfusion injury and to explain the pathophysiology of reperfusion injury in a rat cremaster muscle microcirculation model. MATERIALS AND METHODS: Twenty-four Sprague-Dawley rats weighing 150-200 g were evaluated in three groups. Cremaster muscles were prepared for microcirculatory observations. Group I (n=8, control): no ischemia was induced. Group II (n=8, acute reperfusion): microclamps were applied to the right external iliac vessels for 150 min, then venous and arterial clamps were released at once. Group III (n=8, gradual reperfusion): microclamps were applied to the right external iliac vessels for 150 min, and then the first venous clamp was released; the arterial clamp was opened gradually by a specially designed microclamp holder (Sheey ossicle holding clamp). In all groups, following a wait of 150 min blood flow velocity was measured for 15 min and then the animals were reperfused freely for 1h. Next, red blood cell velocity, vessel diameters, functional capillary perfusion and endothelial oedema index were analysed, and rolling, migrating and adhesing leukocytes and lymphocytes were counted. All observations were videotaped for slow-motion replay. Muscle damage was evaluated histologically. RESULTS: In the acute clamp release group, blood velocities increased up to 600% of their pre-ischaemic values during the post-ischaemia-reperfusion period. The numbers of rolling, adhering and transmigrating leukocytes were significantly higher and histological evaluation revealed more tissue damage in the acute reperfusion group. CONCLUSION: Depending on histological and microcirculatory findings, gradual reperfusion was confirmed to reduce the intensity of reperfusion injury.     

利用脱细胞基质预构小口径组织工程血管的实验研究

目的 在犬腹腔内预置脱细胞基质后形成结缔组织管,观察将其作为血管替代物的力学特征及移植于自体股动脉后的组织结构变化.方法 在犬腹腔内埋置长8～12 cm用硅胶棒支撑的制备好的脱细胞基质,3周后将硅胶棒周围形成的管状物作为血管替代物移植于自体股动脉,同时对此管状物作力学、组织学检测及与颈动脉、股静脉的对比分析.在移植术后6个月观察血管通畅情况.光镜、透射及扫描电镜观察替代物的组织结构.结果 ①血管替代物的力学性能弱于正常动脉而强于正常静脉.②组织学观察:形成的管状物内腔有少量的间皮细胞黏附;弹性纤维、胶原纤维结构较完整;纤维网中充满成纤维母细胞.6个月后内皮细胞在替代物内壁覆盖连续,平滑肌细胞与对照组相近.③移植6个月后脱细胞基质组血管全部通畅.结论 ①用脱细胞基质预构的血管替代物力学性能符合血管移植、血运重建的需要.②所形成的血管替代物移植6个月后组织相容性良好,替代物管壁厚度及组织结构已接近正常血管.     

Increases in clitoral and vaginal blood flow following clitoral and pelvic plexus nerve stimulations in the female rat

The objective of this present study is to establish a model in the rat for the study of female clitoral and vaginal vascular changes during sexual excitation. A laser Doppler was used to measure blood flow changes following clitoral and pelvic plexus nerve stimulations. Results show an increase in clitoral blood flow following clitoral nerve (df1 = 12, df2 = 108, F = 21.4, P < 0.001) and pelvic plexus nerve stimulations (n = 3). A vaginal blood flow increase is also observed following pelvic plexus nerve stimulations (df1 = 12, df2 = 108, F = 4.75, P < 0.001). The female rat can therefore be used as a model for the study of the physiology, pharmacology and sexual dysfunction relating to blood flow in clitoral and vaginal tissue.