Is there any role for minimally invasive surgery in NET?

Neuroendocrine tumors (NET) represent the variability of almost benign lesions either secreting hormones occurring as a single lesion up to malignant lesions with metastatic potential. Treatment of NET is usually performed by surgical resection. Due to the rarity of NET, surgical treatment is mainly based on the experience and recommendations of experts and less on the basis of prospective randomized studies. In addition, the development and establishment of new surgical procedures is made more difficult by their rarity. The development of laparoscopic-assisted surgery has significantly improved the treatment of many diseases. Due to the well-known advantages of laparoscopic surgery, this method has also been increasingly used to treat NET. However, due to limited comparative data, the assumed superiority of laparoscopic surgery in the area NET remains often unclear or not yet proven. This review focuses on the present usage of laparoscopic techniques in the area of NET. Relating to the current literature, this review presents the evidence of various laparoscopic procedures for treatment of adrenal, pancreatic and intestine NET as well as extraadrenal pheochromocytoma and neuroendocrine liver metastases. Further, this review focuses on recent new developments of minimally invasive surgery in the area of NET. Here, robotic-assisted surgery and single-port surgery are promising approaches.

A new liposomal formulation of Gemcitabine is active in an orthotopic mouse model of pancreatic cancer accessible to bioluminescence imaging.

Despite its rapid enzymatic inactivation and therefore limited activity in vivo, Gemcitabine is the standard drug for pancreatic cancer treatment. To protect the drug, and achieve passive tumor targeting, we developed a liposomal formulation of Gemcitabine, GemLip (Ø: 36 nm: 47% entrapment). Its anti-tumoral activity was tested on MIA PaCa-2 cells growing orthotopically in nude mice. Bioluminescence measurement mediated by the stable integration of the luciferase gene was employed to randomize the mice, and monitor tumor growth. GemLip (4 and 8 mg/kg), Gemcitabine (240 mg/kg), and empty liposomes (equivalent to 8 mg/kg GemLip) were injected intravenously once weekly for 5 weeks. GemLip (8 mg/kg) stopped tumor growth, as measured via in vivo bioluminescence, reducing the primary tumor size by 68% (SD +/- 8%; p < 0.02), whereas Gemcitabine hardly affected tumor size (-7%; +/- 1.5%). In 80% of animals, luciferase activity in the liver indicated the presence of metastases. All treatments, including the empty liposomes, reduced the metastatic burden. Thus, GemLip shows promising antitumoral activity in this model. Surprisingly, empty liposomes attenuate the spread of metastases similar to Gemcitabine and GemLip. Further, luciferase marked tumor cells are a powerful tool to observe tumor growth in vivo, and to detect and quantify metastases.

Nonoperative treatment of four esophageal perforations with hemostatic clips.

Spontaneous or iatrogenic esophageal perforations are despite advances of modern surgery and intensive care medicine still potentially life-threatening events with a considerable mortality rate. Recently, encouraging results on the sealing of esophageal perforations by placement of endoluminal prostheses were reported. However, if the perforation is very proximal (close to the larynx) or very distal (involving the cardia), the situation is to our experience unsuitable for stent therapy. In these special cases non-operative treatment is still possible by application of hemostatic metal clips. We present four cases unsuitable for stent therapy where the perforation was sealed by endoscopic clip application. All patients had an uneventful recovery. Non-operative treatment of esophageal perforations with hemostatic metal clips is feasible and safe in cases not treatable with self-expanding metal stents.

Evaluation of preservation solutions by ESR-spectroscopy: superior effects of University of Wisconsin over Histidine-Tryptophan-Ketoglutarate in reducing renal reactive oxygen species.

Despite the causative role of oxidative stress in renal ischemia-reperfusion (I-R) injury effects of preservation solutions on reactive oxygen species (ROS) release have not been sufficiently evaluated. We compared the effects of most common solutions in kidney transplantation, University of Wisconsin (UW) and Histidine-Tryptophan-Ketoglutarate (HTK). ROS formation in isolated perfused rat kidney was detected by electron spin resonance spectroscopy using spin label 1-hydroxy-3-methoxycarbonyl-2,2,5,5-tetramethyl-pyrrolidine. Donor kidneys from Lewis rats were pretreated with saline (controls), in therapeutic groups, kidneys underwent 18 h of cold storage (CS) preserved by HTK or UW solution. Experimental protocol included a stabilization period followed by additional I-R. Kidneys preserved by HTK produced highest ROS values in the control period after CS, whereas levels in UW and control group did not vary significantly. A peak release induced by additional I-R was also significantly highest in HTK kidneys, and UW did not differ from controls. During reperfusion, levels in HTK exceeded control and UW values. Renal vascular resistance, caspase-3-activity, and tissue hydration were enhanced in HTK compared with UW group, whereas ATP concentration was less reduced in UW-preserved tissue. These data show the greater antioxidative potential of UW solution, which also attenuated organ impairment after CS in the early reperfusion period.

Effect of liver regeneration after partial hepatectomy and ischemia-reperfusion on expression of growth factor receptors.

AIM: To investigate the effects of experimental partial hepatectomy and normothermic ischemia-reperfusion damage on the time course of the expression of four different growth factor receptors in liver regeneration. This is relevant due to the potential therapeutic use of growth factors in stimulating liver regeneration. METHODS: For partial hepatectomy (PH) 80% of the liver mass was resected in Sprague Dawley rats. Ischemia and reperfusion (I/R) were induced by occlusion of the portal vein and the hepatic artery for 15 min. The epidermal growth factor receptor, hepatic growth factor receptor, fibroblast growth factor receptor and tumour necrosis factor receptor-1 were analysed by immunohistochemistry up to 72 h after injury. Quantitative RT-PCR was performed at the time point of minimal receptor expression (24 h). RESULTS: In immunohistochemistry, EGFR, HGFR, FGFR and TNFR1 showed biphasic kinetics after partial hepatectomy with a peak up to 12 h, a nadir after 24 h and another weak increase up to 72 h. During liver regeneration, after ischemia and reperfusion, the receptor expression was lower; the nadir at 24 h after reperfusion was the same. To evaluate whether this nadir was caused by a lack of mRNA transcription, or due to a posttranslational regulation, RT-PCR was performed at 24 h and compared to resting liver. In every probe there was specific mRNA for the receptors. EGFR, FGFR and TNFR1 mRNA expression was equal or lower than in resting liver, HGFR expression after I/R was stronger than in the control. CONCLUSION: At least partially due to a post-transcriptional process, there is a nadir in the expression of the analysed receptors 24 h after liver injury. Therefore, a therapeutic use of growth factors to stimulate liver regeneration 24 h after the damage might be not successful.

Kupffer cells infiltrate liver tissue early after ischemia-reperfusion and partial hepatectomy.

Kupffer cells, ED2+macrophages of the liver, play an important role in liver damage and regeneration. It is proposed that Kupffer cells are stationary and regenerate after acute liver trauma by local proliferation. We analyzed their kinetics in three surgically relevant murine models of acute liver injury: partial liver resection, ischemia with reperfusion and sepsis. We found an early increase in ED2+cells after 0.5 h and a maximum after 12 h. These results suggest an infiltration of the cells early after the injury and a later local proliferation. These ED2+macrophages are localized predominantly periportally; nearly no macrophages are found pericentrally, except in the sepsis model. Therefore, a shifting of macrophages from portal to central seems to be unlikely, suggesting a hepatic zonation of homing factors.

Laparoscopically assisted colorectal resection in Hirschsprung's disease.

BACKGROUND: Minimally invasive surgery (MIS) has been adapted to virtually every kind of abdominal operation. Colorectal resections of any extent are possible. The reduction in local and systemic surgical trauma in MIS suggests this method could be valuable for rectal resection for Hirschsprung's disease. - METHOD: Diagnostic work-up is similar to that in open surgery. Three trocars are sufficient, and a fourth may be helpful. Dissection encompasses the entire aganglionic segment and is extended orally to normal bowel.. After complete dissection down to the pelvic floor the bowel is everted transanally, resected in due length and the coloanal anastomosis sutured from outside. Since 1996 four children out of nine (age 11 weeks - 18 years) have been operated laparoscopically at our institution. - RESULTS: There were no intraoperative complications. Recovery time is impressively rapid. Oral intake may be begun on the first postoperative day and physical activity is rapidly restored. There are however problems typical to this method: anastomotic leakage, stricture formation, and the necessity of continuing dilation. - CONCLUSIONS: The feasibility of laparoscopic colorectal resections of any extent is unquestionable. Benefits for the patient seem evident. Prospective randomized studies to provide a higher level of evidence for the benefit of laparoscopy as compared to open technique are difficult to perform due to the small number of patients.

Protective effect of endotoxin preconditioning in pancreas: analysis with DNA chip arrays.

Recently we demonstrated a protective effect of endotoxin preconditioning 24 hours before pancreatic ischemia-reperfusion injury, which has also been described for other organs. The mechanisms underlying this phenomenon, such as differential gene expression, are poorly investigated. We chose to approach this question by investigating differential gene expression in the rat pancreas over the time course of endotoxin pretreatment. Male Wistar rats (5 groups, 5 animals per group) were pretreated with endotoxin intraperitoneally (1 mg/kg of body weight). After treatment at 30 minutes, and at 3 and 24 hours the pancreas was removed. Untreated animals and animals with injection of saline solution served as controls. After RNA isolation, RNA was pooled and hybridized to Affymetrix chips to measure the relative mRNA levels of 7000 genes and 1000 expression sequence tags. Three hours after administration of endotoxin there was an activation of proinflammatory transcription factors and other proinflammatory genes. After 24 hours there was a clear decrease of these proinflammatory genes, but a remaining and increasing upregulation of important antiapoptotic genes, antiproteases, and other probably protective genes. There was also a significant upregulation of complement factors. It was surprising that heat-shock proteins and other typical immediate early genes of the AP-1 complex were not upregulated. Our data show that 24 hours after endotoxin stress there is a regulation of a network of genes that represents a multifaceted preconditioning. As most important factors, inhibition of apoptosis and antiproteatic strategies are identified. Heat-shock proteins seem to play no important role in the mechanism of endotoxin preconditioning.

[Surgical therapy of inflammatory and malignant strictures of the common bile duct]. / Chirurgische Therapie entzündlicher und maligner Stenosen der distalen Gallenwege.

Although there are growing possibilities of interventional endoscopic treatment of benign and malignant stenosis of the distal common bile duct the definitive operative drainage by terminolateral hepaticojejunostomy is in many cases the therapy of choice. In patients with chronic pancreatitis and bile duct stricture the modified duodenum preserving pancreatic head resection ("Beger operation") enables a resection of the inflammatory mass together with a drainage of the bile. Of 391 patients from our clinic being operated due to a bile duct stricture 337 underwent a biliary drainage together with a pancreatic head resection. Early postoperative biliary complications were in 0.3 % strictures of the duct and 1.5 % bile fistulas. Half of those complications could be managed conservatively. In high volume centers the operative therapy of distal common bile duct stenosis is a safe procedure with high patency rate.

[The non-healing wound]. / Diabetischer Fuss, ischämisches Ulkus, Druckgeschwür. So bringen Sie chronische Wunden zum Verschluss.

The most common chronic wounds are pressure ulcers, diabetic ulcers, arterial occlusive disease and venous ulcers. The therapeutic aim after appropriate diagnostic work-up is causal treatment. Pressure relief, revascularisation or compression head the list of potential measures. Apart from local factors such as infection or necrosis, systemic factors such as patient compliance, renal insufficiency and immunosuppression are of relevance. If there is a chance of healing, wound management comprises repeated debridement and wet dressings. In the presence of an infection, local antiseptic treatment is indicated. In the individual case, wound stimulation can be supported by protease inhibitors, growth factors or tissue engineering. Definitive wound closure is achieved by epithelial migration from the margins of the wound, or by plastic surgery. Regular documentation of the course and success of wound healing is mandatory. In the wound care center, surgical disciplines, diabetology, dermatology and diagnostic work-up are coordinated, and liaison with the family doctor and home care providers practiced. This wound healing concept successfully heals approximately 80% of the cases of chronic wounds in 18.8 months (mean healing duration 4.8 months).

Organ procurement in experimental pancreas transplantation with minimal microcirculatory impairment.

BACKGROUND: Ischemia-reperfusion injury has been shown to deteriorate microcirculation in experimental pancreas transplantation. However, minor concern was taken on the impact of organ procurement in this condition. We examined the impact of a standardized technique of organ procurement on microcirculation and apoptosis in experimental pancreas transplantation. METHODS: Male Lewis rats were divided into three groups: sham-operated animals without dissection of the pancreas served as controls (n = 5); animals undergoing nearly total process of organ procurement with the pancreas pedunculated on the aorta and the hepatoduodenal ligament (n = 7), and animals receiving pancreaticoduodenal transplantation. Pancreatic grafts were preserved for 6 h in cold University of Wisconsin solution (n = 7). At 1 and 2 h reperfusion and in time-matched controls, microcirculation was assessed by means of intravital fluorescence microscopy. Tissue samples were obtained after 2 h measurement and DNA breaks of acinar cells were detected by in situ nick end-labeling (TUNEL assay). The apoptotic index (apoptotic cells per high- power fields; hpf) was quantified by microscopic counting of at least 50 hpf. RESULTS: Assessment of functional capillary density (FCD) in animals undergoing subtotal process of organ procurement revealed a slight non-significant decrease at 1 and 2 h compared with controls. In addition, leukocyte sticking to postcapillary venules (LAV) as well as the apoptotic index were found slightly increased after organ procurement compared with controls (p > 0.05). However, after pancreas transplantation the apoptotic index and the LAV were significantly increased and the FCD significantly decreased compared with both groups of non-transplanted animals (p < 0.01). CONCLUSIONS: Our validated technique of organ procurement does not negatively impact microcirculation and apoptosis in experimental pancreas transplantation.

Exogenous and endogenous nitric oxide donors improve post-ischemic tissue oxygenation in early pancreatic ischemia/reperfusion injury in the rat.

INTRODUCTION: In pancreatic ischemia/reperfusion (IR) injury (IRI) the role of nitric oxide (NO) is not completely understood. Using a rat model of normothermic in situ IRI, the effect of endogenous and exogenous NO donors on post-ischemic tissue oxygenation and tissue damage was investigated. METHODS: IR was induced by 2-hour normothermic in situ ischemia of a pancreatic tail segment pedunculated on the splenic vessels with 2 h of reperfusion in an untreated, an L-arginine- and a sodium-nitroprusside-treated group (Wistar rats, n = 7/group). Animals without ischemia served as controls. Tissue oxygenation (pO(2ti)) was monitored using a pO2-sensitive Clark-type electrode. Histological investigation was performed following a semiquantitative score (edema, vacuolization, PMN infiltration, necrosis). Plasma lipase was another marker of organ damage. RESULTS: The administration of L-arginine and sodium nitroprusside caused a significant amelioration of the decrease in pO2i) after reperfusion compared to IR animals (p < 0.05). Histological damage was also reduced in the NO donor groups (p < 0.05). After reperfusion, plasma lipase in the L-arginine-treated animals was significantly lower compared to IR and sodium nitroprusside (p < 0.05). CONCLUSIONS: The administration of both endogenous and exogenous NO donors is protective in IRI of the rat pancreas which can be seen by an improvement in post-ischemic tissue oxygenation which indicates better nutritive tissue perfusion, amelioration of the histological tissue injury and, in L-arginine animals, lower lipase levels. NO donors could be useful in the prevention and reduction of the pancreatic IRI.

Heterotopic pancreatitis with obstruction of the major duodenal papill--a rare trigger of obstructive orthotopic pancreatitis.

BACKGROUND: Heterotopic pancreas appears in 0.5 to 13% of autopsies. The most frequent locations are stomach, duodenum or upper jejunum. Pancreatitis in heterotopic pancreas is rarely described, and clinical symptoms caused by this heterotopic inflammation are uncommon. METHOD: We report a case of heterotopic pancreatitis localized in the major duodenal papilla causing biliary obstruction and mimicking a pancreatic head tumor. Clinically and radiologically, malignancy was suspected. Preoperative biopsies showed only fibrosis. A pylorus preserving resection of the pancreatic head was performed followed by an uneventful postoperative course. RESULT: Macroscopically, in the periampullary region on the pancreatic side a thickened duodenal wall with multiple lobules and cysts was found, compressing the common bile duct. Microscopic examination showed heterotopic pancreas with inflammatory lesions surrounding the ampulla. In the orthotopic pancreas a diffuse chronic pancreatitis with marked inflammation, fibrosis and atrophy of exocrine tissue was found. CONCLUSION: In our case it was impossible to differentiate between chronic pancreatitis and pancreas carcinoma preoperatively. Radiological findings and endoscopic biopsies were not sufficient to distinguish heterotopic pancreatitis from other tumors of the pancreatic head. Clear diagnosis could only be made by complete histological examinations after pancreatic head resection, being the treatment of choice for pancreatic head tumors of unclear dignity. The differential diagnosis of heterotopic pancreatitis as trigger of unclear enlargement of the pancreatic head is very seldom.

Influence of nitric oxide on microcirculation in pancreatic ischemia/reperfusion injury: an intravital microscopic study.

Recently, protective effects of nitric oxide donors in pancreatic ischemia/reperfusion (IRI) injury have been described. Their role in post-ischemic microcirculation was previously not investigated. Ischemia reperfusion was induced in an isolated pancreatic tail segment in situ. Animals were randomized to four experimental groups (n=7 animals/group), the control group (CO) received saline as placebo. Treatment groups received either sodium nitroprusside (SN) 5 min before until 2 h after reperfusion, L-arginine (LA) 30 min before reperfusion until 2 h after reperfusion or sodium nitroprusside and L-arginine (SNLA) together. After induction of ischemia (2 h) post-ischemic microcirculation was observed for 2 h by intravital-fluorescence microscopy. Functional-capillary density (FCD), leukocyte adherence in post-capillary venules (LAV) and histological damage were analysed. After reperfusion FCD decreased in all groups (P<0.05). FCD was significantly restored in all groups with administration of nitric oxide donors after reperfusion (P<0.05) as compared to CO without significant difference between the individual nitric oxide donor groups. Leukocyte adherence was significantly increased 1 h and 2 h after reperfusion (P<0.001) as compared to baseline, which was lower in all nitric oxide donor groups. Histological damage in the pancreatic tail-segment was significantly reduced in nitric oxide donor groups (P<0.01). Administration of nitric oxide donors might be useful in ischemia-reperfusion injury of the pancreas by its protective effect on microcirculation and inflammatory reaction.

Ischemic preconditioning attenuates capillary no-reflow and leukocyte adherence in postischemic pancreatitis.

BACKGROUND AND AIMS: Ischemic preconditioning (IPC) has been shown to protect several organs from ischemia-reperfusion injury. Postischemic microvascular dysfunction is considered to be the key mechanism of early graft pancreatitis after transplantation. The aim of the study was to determine whether brief ischemia and reperfusion before prolonged ischemia followed by reperfusion is protective in respect to microcirculatory derangement in postischemic pancreatitis. METHODS: In an in-situ model of ischemia-reperfusion was induced in the isolated pancreatic tail segment. Wistar rats were randomized to one group ( n=7/group) with 2-h ischemia and reperfusion (I/R) and another group with 10-min ischemia and 10-min reperfusion (IPC) before the prolonged ischemia time. Microcirculation was observed for 2 h by intravital-fluorescence microscopy that analyzed functional capillary density and leukocyte adherence in postcapillary venules. Histological damage was quantified by a semiquantitative score (edema, vacuolization, PMN infiltration, necrosis). RESULTS: IPC resulted in a significant improvement of functional capillary density (248+/-20 vs 372+/-8 cm(-1), P<0.001), a significant reduction in leukocyte adherence in postcapillary venules (476+/-79 vs 179+/-15 cells/mm(2), P<0.001) and in significantly lower histological damage (score 9+/-0.8 vs 5+/-1.4, P<0.001), when compared with the ischemia-reperfusion group. CONCLUSION: IPC reduces pancreatic inflammatory reaction by preservation of postischemic microcirculation. Therefore, it might become a useful procedure before organ procurement in pancreas transplantation.

Soluble complement receptor 1 preserves endothelial barrier function and microcirculation in postischemic pancreatitis in the rat.

Components of the activated complement cascade are considered to play a pivotal role in ischemia-reperfusion-induced organ injury. With the use of intravital epifluorescence microscopy, we investigated the effect of complement inhibition by the recombinant soluble complement receptor 1 (sCR1; TP10) on the effect of macromolecular microvascular permeability, functional capillary perfusion, and leukocyte endothelium interaction in postischemic pancreatitis. Anaesthetized Sprague-Dawley rats were subjected to 60 min of normothermic pancreatic ischemia induced by microclipping of the blood-supplying arteries of the organ. Rats who received sCR1 (15 mg/kg body wt iv; n = 7) during reperfusion showed a significant reduction of permeability (1.77 +/- 1.34 x 10(-8) cm/s; n = 7) of tetramethylrhodamine isothiocyanate-labeled albumin injected 90 min after the onset of reperfusion compared with vehicle-treated animals (6.95 +/- 1.56 x 10(-8) cm/s; n = 7). At 120 min after the onset of reperfusion, the length of red blood cell-perfused capillaries (functional capillary density) was significantly improved (from 279 +/- 15.7 to 330 +/- 3.7 cm(-1); n = 7) and the number of leukocytes adherent to postcapillary venules was significantly reduced (from 314 +/- 87 to 163 +/- 71 mm(-2); n = 7) by sCR1 compared with vehicle treatment. Complement inhibition by sCR1 effectively ameliorates pancreatic ischemia-reperfusion-induced microcirculatory disturbances and might be considered for treatment of postischemic pancreatitis.

Noninvasive in vivo assessment of the pancreatic microcirculation: orthogonal polarization spectral imaging.

INTRODUCTION: Capillary perfusion failure of the pancreatic microcirculation is characteristic in the pathogenesis of acute pancreatitis and ischemia-reperfusion damage after pancreas transplantation. Up to now, no logistic suitable method for analyzing pancreatic capillary perfusion during operations in humans has been established without the use of fluorescent dyes. AIM: To compare the well-established technique of intravital epifluorescence microscopy with the novel noninvasive method of orthogonal polarization spectral (OPS) imaging for measurement of the pancreatic functional capillary density. METHODOLOGY: In eight anesthetized rats, six identical capillary regions of interest per animal were measured by both methods, and the results were compared. RESULTS: Absolute values from the capillary perfusion data were not significantly different between the two methods (fluorescence microscopy: 394 +/- 44 cm/cm2; OPS imaging: 385 +/- 45 cm/cm2). Correlation parameters were significant, and Bland-Altman analyses showed good agreement with a mean difference (bias) between the two methods of 6.9 cm/cm2, indicating that slightly smaller values are measured with OPS imaging. CONCLUSION: OPS imaging is a valid noninvasive method that analyzes the pancreatic microcirculation as accurately as the established intravital microscopy technique and therefore could be useful for clinical research and diagnosis during transplantation and operations.

Characterization of microcirculatory disturbance in a novel model of pancreatic ischemia-reperfusion using intravital fluorescence-microscopy.

INTRODUCTION: Microcirculatory disturbances caused by ischemia-reperfusion injury (IRI) are the crucial hallmarks of pancreatitis following pancreas transplantation. AIMS: To develop a novel rodent model of normothermic in situ ischemia of a pancreatic tail-segment that simulates the clinical situation of pancreas transplantation by flushing the organ via an inserted microcatheter and thus enables selective treatment of the organ via this access. METHODOLOGY: Four experimental groups were investigated (n = 7 Wistar rats/group): sham animals without ischemia and dissection of the pancreas; control animals with dissection of a pancreatic tail segment pedunculated on the splenic vessels and flushing od this segment with saline via a microcatheter; and two groups of animals treated like controls with a pancreatic ischemia time of 1 hour or 2 hours. With use of intravital epifluorescence microscopy, the microcirculatory damage was characterized by investigation of functional capillary density (FCD) and leukocyte adherence in postcapillary venules (LAV) before ischemia and during a reperfusion time of 2 hours. Dry:wet ratio determinations, light microscopy, and electron microscopic investigations were performed to characterize the histologic organ damage. RESULTS: FCD decreased significantly (p < 0.05) 2 hours after reperfusion in the groups of 1-hour (-29.21%) and 2-hour ischemia (-42.73%), in comparison with baseline values. LAV increased significantly (p < 0.05), 4.3- and 5.8-fold, after 1-hour and 2-hour ischemia during the observation time. The histologic damage was similar to posttransplantation pancreatitis in humans 1 hour after reperfusion. In sham and control animals these alterations were not significant. CONCLUSIONS: The rodent in situ model of pancreatic IRI showed standardized microcirculatory damage dependent on the ischemia time. Offering the possibility of selective treatment by the direct artery access to the ischemic pancreatic area, the model enables investigations of questions related to human pancreas transplantation.

Orthogonal polarization spectral imaging as a tool for the assessment of hepatic microcirculation: a validation study.

BACKGROUND: Quantitative analysis of liver microcirculation using intravital fluorescence microscopy in animals has increased our knowledge about ischemia-reperfusion injury. However, because of the size of the instrumentation and the necessity of fluochromes for contrast enhancement, human liver microcirculation cannot be observed. Orthogonal Polarization Spectral (OPS) imaging is a recently introduced technique that can be used to visualize the microcirculation without the need for fluorescent dyes. It is a small, hand-held device and could potentially be used to study the microcirculation of the human liver in a clinical setting. However, before implementation into clinical use its ability to quantitatively measure microcirculatory parameters must be validated. METHODS: The livers of Spraque-Dawley rats (n=9) were exteriorized, and images were obtained using OPS imaging and intravital fluorescence microscopy of the identical microvascular regions before and after the induction of a 20-min warm lobar ischemia. Images were videotaped for later computer-assisted off-line analysis. RESULTS: OPS imaging can be used to accurately quantify the sinusoidal perfusion rate, vessel diameter, and venular red blood cell velocity. Correlation parameters were significant and Bland-Altman analyses showed good agreement for data obtained from the two methods at baseline as well as during reperfusion. CONCLUSION: OPS imaging can be used to quantitatively measure microcirculatory parameters in the rat liver under both physiological and pathophysiological conditions. Thus, OPS imaging has the potential to be used to make quantitative measurements of the microcirculation in the human liver.