Evolution of staples and clips for vascular anastomoses.

Because of the development of less invasive surgical techniques, there is an increasing demand for vascular anastomosing techniques that require less exposure of the operating field. This paper reviews the most important representatives of staples, clips, and other mechanical devices for vascular anastomosing described over the last five decades. This report is organized in three parts: (1) the history of clipping and stapling devices, (2) development of the Vessel Closure System (VCS) clips, and (3) current and potential status of mechanical vascular anastomotic devices. A Medline literature search was conducted and publications on the use of staples and/or clips for the creation of vascular anastomoses identified with extensive cross-referencing. The first literature description of a mechanical vascular stapling device was by Gudov in 1950. This and other reports from the Soviet Union stimulated brisk, competitive development of vascular anastomotic devices in Europe, North America, and Japan. Fasteners included staples, penetrating pin-rings, or toothed stainless steel clips, none of which gained acceptance because of their complexity and inability to facilitate end-to-side anastomoses. A more convenient and less traumatic anastomotic system (VCS Clip applier system) was introduced into clinical practice in 1995. This system differs from staples in that it is non-penetrating. A wide variety of reports have described the advantages, both technical and biological, that clips provide over conventional needle-and-suture, particularly for the construction of vascular access for hemodialysis. A steady evolution of mechanical vascular anastomotic devices has sought to eliminate the technical and biological disadvantages of conventional suturing. Although the conventional hand-sewn, overcast non-absorbable suture remains the "gold" standard, newer techniques such as the non-penetrating arcuate-legged VCS clips are gaining acceptance as a useful addition to the vascular surgeons' armamentarium.

Causes of limited survival of microencapsulated pancreatic islet grafts.

Successful transplantation of pancreatic tissue has been demonstrated to be an efficacious method of restoring glycemic control in type 1 diabetic patients. To establish graft acceptance patients require lifelong immunosuppression, which in turn is associated with severe deleterious side effects. Microencapsulation is a technique that enables the transplantation of pancreatic islets in the absence of immunosuppression by protecting the islet tissue through a mechanical barrier. This protection may even allow for the transplantation of animal tissue, which opens the perspective of using animal donors as a means to solve the problem of organ shortage. Microencapsulation is not yet applied in clinical practice, mainly because encapsulated islet graft survival is limited. In the present review we discuss the principal causes of microencapsulated islet graft failure, which are related to a lack of biocompatibility, limited immunoprotective properties, and hypoxia. Next to the causes of encapsulated islet graft failure we discuss possible improvements in the encapsulation technique and additional methods that could prolong encapsulated islet graft survival. Strategies that may well support encapsulated islet grafts include co-encapsulation of islets with Sertoli cells, the genetic modification of islet cells, the creation of an artificial implantation site, and the use of alternative donor sources. We conclude that encapsulation in combination with one or more of these additional strategies may well lead to a simple and safe transplantation therapy as a cure for diabetes.

Five years' world experience with nonpenetrating clips for vascular anastomoses.

BACKGROUND: A new sutureless technique has been introduced clinically to facilitate the process of vascular reconstruction and improve patency. The Vessel Closure System (VCS) is nonpenetrating, creates an elastomeric everted anastomosis, and is easily and reproducibly applied. The objective of this report is to review the published world experience that has accrued regarding these clips with attention to the assets, liabilities, and pitfalls associated with the new technology. DATA SOURCES: Medline search and manual cross-referencing were performed, after which 61 original articles were identified on the use of VCS clips for vascular anastomoses. RESULTS: Advantages of the clips compared with sutures include the technical ease of application, the reduced anastomotic time, the superior hemodynamics, and the improved healing pattern of the anastomosis. Disadvantages include the potential problems in atherosclerotic vessels, lack of prospective randomized long-term follow-up, and initial costs. The best clinical results have been achieved in microvascular repair, as well as with vascular access and transplantation surgery. CONCLUSIONS: The VCS clip technology has become an accepted vascular anastomosing technique, which in future could lead to the use of clips as a standard approach and the use of sutures only in case of severe atherosclerosis and other circumstances in which vessel edges are difficult to evert.

Macrophage overgrowth affects neighboring nonovergrown encapsulated islets.

BACKGROUND: Encapsulation significantly prolongs islet graft survival in the absence of immunosuppression. However, encapsulated islet graft survival is limited to periods of several months. Part of the encapsulated islet graft is affected by a nonprogressive pericapsular overgrowth. To investigate whether macrophages on overgrown capsules affect neighboring nonovergrown encapsulated islets, encapsulated islets were studied during coculture. MATERIALS AND METHODS: Encapsulated islet function, islet vitality, and islet cell replication were assessed, as well as the mRNA expression of Bcl-2, Bax, inducible nitric oxide synthase, and monocyte chemoattractant protein-1 in encapsulated islets after 48 h of culture together with microcapsules with macrophage overgrowth. Overgrown capsules were retrieved from the rat peritoneum, three weeks after implantation of an encapsulated islet graft. RESULTS: Coculture was associated with inhibition of the stimulated insulin secretion, with decreased cell replication, and with increased cell necrosis, but not with apoptosis of encapsulated islet cells. mRNA expression levels in encapsulated islets after coculture were not different from controls, except for a decrease in Bax mRNA. We found a high level of nitrite, as an indicator of nitric oxide production, but not an increase in inducible nitric oxide synthase mRNA in islets. This, in combination with the absence of increase in monocyte chemoattractant protein-1 mRNA and the lack of apoptosis, indicates that neither interleukin-1beta nor tumor necrosis factor-alpha was responsible for the deleterious effects of coculture on encapsulated islets. CONCLUSIONS: Nonovergrown encapsulated islets are affected by the overgrowth on encapsulated islets in their close proximity. This overgrowth contains macrophages that produce nitric oxide which, rather than cytokines, may be held responsible for the deleterious effect on the neighboring encapsulated islets.

Relationship between duration of brain death and hemodynamic (in)stability on progressive dysfunction and increased immunologic activation of donor kidneys.

BACKGROUND: Consistent difference in graft survival after renal transplantation has been shown when cadaveric transplants are compared to the living related donor situation, in favor of the latter. Recently, evidence has been put forward that brain death has significant effects on the donor organ quality. In this study, we aimed to assess the relation between brain death-induced hemodynamic instability in combination with the duration of brain death on the function and immunogenicity status of potential donor kidneys. METHODS: In Wistar rats, short-term (1 hour) or long-term (6 hours) brain death in the presence or absence of hemodynamic stability was applied. Sham-operated rats served as controls (1 hour and 6 hours). Organ function was studied by monitoring serum creatinine, lactate dehydrogenase (LDH), lactate, and total protein content. Expression of cell adhesion molecules [intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)] and the influx of leukocytes in the kidney assessed the immunologic status of the kidney. RESULTS: Progressive organ dysfunction was most pronounced in hemodynamically unstable brain-dead donors reflected by increased serum creatinine levels. Regardless of hemodynamic status, a progressive inflammatory activation by cell adhesion molecule expression and an influx of leukocytes could be observed in kidneys of brain-dead rats compared with nonbrain-dead controls. CONCLUSION: Brain death causes progressive kidney dysfunction. Also, inflammatory responses reflecting tissue injury are caused by brain death. When hemodynamic instability in the brain-dead donor is not corrected, kidney dysfunction is enhanced and immune activation occurs faster and is more profound. The observed changes may predispose the graft for additional ischemia/reperfusion injury during the transplant process and hence accelerate rejection of the graft after transplantation.

Effective removal of alginate-poly-L-lysine microcapsules from pancreatic islets by use of trypsin-EDTA.

Although the transplantation of alginate-poly-L-lysine-alginate encapsulated islets of Langerhans usually is successful, graft survival is still limited. Molecular analysis by RT-PCR of the encapsulated islets may provide insight into the mechanisms that affect islets during graft failure. However, RT-PCR on encapsulated islets is not possible because the poly-L-lysine of the capsule interferes with both cDNA synthesis and PCR amplification. We applied a method that mechanically removes the microcapsules from the islets after a short trypsin-EDTA treatment (decapsulation), thereby enabling RT-PCR analysis. The results of this study show that the decapsulation procedure does not affect islet vitality and has only minor effects on islet function and morphology. The decapsulation does not affect GAPDH, beta-actin, Bcl-2, or Bax gene expression. This method is an improvement over the time-consuming manual dissection of microcapsules because it allows for the rapid and relatively harmless removal of capsules on a larger scale. Decapsulation offers the possibility of applying RT-PCR, as well as other methods, which cannot be performed on encapsulated islets.

Brain death induces apoptosis in donor liver of the rat.

BACKGROUND: A difference in short- and long-term function between living-related and cadaveric donor organs is consistently shown in kidney- and liver-transplant studies. We hypothesize that this is caused by induction of apoptosis and inflammation of the potential graft because of the phase of brain death (BD) in the cadaveric donor that predisposes for additional transplant injury. Previously, we have shown inflammation in the liver of brain-dead donors by increased expression of cell adhesion molecules and influx of leukocytes. The key inflammatory mediator in inflammation is tumor necrosis factor (TNF)-alpha. In addition to being involved in inflammation, TNF-alpha also activates the potential detrimental process of apoptosis and, on the other hand, activates an antiapoptotic survival pathway by way of NF-kB. The aim of the present study was to investigate whether the inflammatory response in the liver of brain-dead donors is accompanied by changes in apoptosis and in expression of apoptosis-related proteins, in particular those regulated by NF-kB. METHODS: BD was induced by inflation of an intracranially placed balloon. Apoptosis was assessed by caspase-3 enzyme activity and terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) assay. Changes in expression of proteins involved in pathways leading to apoptosis were studied by determination of mRNA levels using semiquantitative reverse-transcriptase polymerase chain reaction followed by image analysis. TNF-receptor (TNFR), Fas, and Fas-ligand (FasL) were used as indicators for activation of the death receptor mediated pathway. Bcl-2, Bax, Bak, Bid, and A1 were used as indicators for activation of the mitochondrial pathway. RESULTS: After 6 hours of normotensive BD, the number of apoptotic cells and caspase-3 activity were significantly increased compared with non-brain-dead control rats. TUNEL staining revealed that the apoptotic cells were primarily hepatocytes. mRNA levels of all NF-kappaB induced activators (Fas, bid) and inhibitors (A1, BCl-xl, cIAP2) of both apoptotic pathways were significantly increased in liver tissue of BD donors versus non-BD controls. CONCLUSIONS: The phase of BD in the donor induces increased apoptosis of hepatocytes despite an enhanced expression of NF-kB-dependent antiapoptotic genes.

Factors predictive of failure of Brescia-Cimino arteriovenous fistulas.

OBJECTIVE: To evaluate patency rates of Brescia-Cimino fistulas and to find out which independent factors were predictors of failure. DESIGN: Retrospective clinical study. SETTING: University hospital, The Netherlands. SUBJECTS: 150 consecutive patients (mean age 56 years, range 17-80) who had 153 primary Brescia-Cimino fistulas created during the 5-year period January 1995-December 1999. MAIN OUTCOME MEASURES: Patency rates calculated by the Kaplan-Meier method and the possible predictive value of 20 different variables assessed by Cox's proportional hazard model. RESULTS: The primary patency rate was 70% at 3 months, and 7 distinct factors were significantly associated with failure of the fistula. The ones with a hazard ratio (HR) for failure greater than 2.5 were: the start of dialysis before creation of the fistula (HR 2.79, p < 0.01), moderate or poor quality of both the artery (HR 2.54, p < 0.01) and vein (HR 3.55, p < 0.001), and postoperative use of acenocoumarol instead of acetylsalicylic acid (HR 3.14. p < 0.01). CONCLUSION: The major determinants for a successfully created Brescia-Cimino fistula were creation of the fistula before the start of dialysis, as well as good quality of both the artery and the vein. This argues for timely creation of such fistulas in patients with end-stage renal disease and for accurate preoperative examination to establish the quality of the vessels.

Endovascular repair of acute AAAs under local anesthesia with bifurcated endografts: a feasibility study.

PURPOSE: To evaluate endovascular repair of abdominal aortic aneurysms (AAA) under local anesthesia in the acute setting. METHODS: Between 1998 and 2001, 47 patients with an acute AAA were evaluated for endovascular repair after informed consent, provided they were in a stable, albeit hypotensive condition. The patients underwent urgent computed tomography to assess suitability for endovascular repair; 16 were eligible for stent-graft repair: 9 were frank ruptures and 7 were symptomatic aneurysms. Complications and outcome of endovascular repair were evaluated; mortality was compared to a contemporaneous surgical cohort. RESULTS: Seven (23%) of 31 patients having a standard surgical procedure died in the study period compared to 1 (6%) of 16 patients undergoing endovascular repair (following conversion to surgery because of calcified access vessels). Twelve (75%) of the endovascular repairs were performed under local anesthesia; no complications with this mode of anesthesia were encountered. The median duration of the endovascular procedures was 110 minutes (range 75-240); median blood loss was 250 mL (range 100-2800 mL). Only 4 patients required blood transfusion, and only 8 patients required admission to the intensive care unit. There were 3 postoperative complications (1 ischemic colitis, 1 renal failure, 1 groin hematoma). During follow-up, 3 endograft patients received stent-graft extensions in uneventful procedures. Two patients died at 9 and 16 months from cardiac causes. CONCLUSIONS: This study demonstrates the feasibility and possible advantages of endovascular repair under local anesthesia in selected acute AAA patients. Further studies are needed to prove the advantages over open repair.