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A Ar'Rajab

Publications and source records attributed to A Ar'Rajab.

At least 19 recordsLinked to original sources
PubMed1999

Syngeneic renal transplantation increases the number of renal dendritic cells in the rat.

Dendritic cells participate in the regulation of CD4 and CD8 T cells during transplant rejection. Understanding what causes increased numbers of dendritic cells to appear in the renal transplant is therefore important. We performed syngeneic renal transplants between rats. We used the monoclonal antibody OX62 to detect dendritic cells, and OX6 to detect major histocompatability complex (MHC) Class II in the renal transplant. One week after transplant, dendritic cells appeared. This indicates that the injury of transplantation itself is sufficient to increase the number of dendritic cells in the kidney in a model where there is no alloreactivity.

Animals↗
PubMed1996

The role of neutrophils in peritoneal adhesion formation.

The most common cause of intraperitoneal adhesions is previous abdominal surgery. Postoperative adhesion formation results from a fibroproliferative inflammatory reaction that begins with an influx of polymorphonuclear leukocytes (PMNs) into the peritoneal cavity. Adherence of the PMNs to the endothelial cells (EC) is necessary for PMN migration into the tissue in response to a stimulus. Several receptor-counterreceptor pairs of ligands such as CD11/CD18 on the PMN and ICAM-1 (CD54) on EC have been identified. Monoclonal antibody against CD11/CD18 (R15.7) inhibits PMN adherence and migration and consequently protects against PMN-induced tissue injuries. We therefore studied the effect of preventing PMN-EC adherence, using anti-CD18 monoclonal antibody, on postoperative adhesion formation in rabbits. Group 1 was a control receiving physiologic saline, and group 2 received anti-CD18 antibody (R15.7, 2 mg/kg). The treatment was administered iv at the end of surgery and repeated on the first and second postoperative days. Peritoneal adhesions were induced at laparotomy by repairing two peritoneal defects, by oversewing the defect (model 1), and by resuturing the removed parietal peritoneum in its place as an ischemic graft (model 2). Adhesions were evaluated blindly at 10 days after operation by measuring the percentage of the suture line covered with adhesions (model 1) or by a scoring system (model 2). All control animals developed intraperitoneal adhesions and the percentage of the suture line covered with adhesions was 25 +/- 5.9% (mean +/- SEM) and the mean score in model 2 was 0.9 +/- 0.2. Anti-CD18 antibody, R15.7, increased the degree of postoperative adhesion formation in both models, but the results were significant only in model 2. Also, anti-CD18 antibody significantly decreased peritoneal neutrophils from 11.1 x 10(7) +/- 1.8 x 10(7) to 2.2 x 10(7) +/- 0.4 x 10(7) (P < 0.001) on the first postoperative day. It is concluded that inhibition of PMN-EC adherence does influence the postoperative adhesion formation. These results might suggest that PMNs have a role in modulating postoperative adhesion formation.

Animals↗
PubMed1996

The effect of preexisting long-term diabetes on the outcome after islet transplantation in rats.

Studies of islet transplantation conducted immediately following diabetes induction may not accurately reflect the clinical situation. Long term preexisting diabetes with generalized microvasculature complication might adversely affect the outcome after islet transplantation. The present study testing this hypothesis by evaluating the effect of long-term preexisting diabetes on glucose-induced insulin secretion up to 6 months after transplantation of two different quantities of islets. One thousand two hundred or 2,400 islets were isotransplanted into the left renal subcapsular space at 10 days (acute diabetes), 3 months (chronic diabetes), or 6 months (long-term diabetes) after diabetes induction by streptozotocin in the rat. In addition, one group of diabetic rats in which normoglycemia was maintained with exogenous insulin treatment for 6 months was then transplanted with 1,200 islets. Intravenous glucose tolerance tests were performed at 10, 90, and 180 days after islet transplantation. Islet transplantation normalized the basal blood glucose levels within 24-48 h in all transplanted groups that remained normal for the entire study period of 6 months, with no differences among acute, chronic, or long-term diabetes. Basal plasma insulin levels were also normalized in all transplanted groups. Diabetic (acute, chronic, or long-term) rats transplanted with 2,400 islets achieved normal glucose-induced insulin secretion at 10 and 90 days after transplantation. In contrast, glucose-induced insulin secretion was impaired in rats transplanted with only 1,200 islets, with no differences among acute, chronic, and long term diabetes. However, at 180 days after transplantation, long term diabetic rats transplanted with 2,400 islets had impaired insulin secretion compared to normal controls. Insulin-treated long-term diabetic rats transplanted with 1,200 islets had normal glucose-induced insulin secretion at 10 days after transplantation. However, at 90 and 180 days after transplantation, insulin-treated long-term diabetic rats had impaired glucose-induced insulin secretion which was not different from nontreated transplanted long-term diabetic rats. It is concluded that long-term preexisting diabetes has no impact on the early outcome after islet transplantation. However, it may adversely affect the long-term function of the transplanted islets. Also, transplantation of a sufficient islet mass is the critical factor in achieving complete glucose homeostasis.

Animals↗
PubMed1996

Early use of the Gore-Tex Stretch Graft.

This study reports firstly the overall outcome with the 4-7 mm tapered Gore-Tex Stretch Vascular Graft and secondly the feasibility of early (< 14 days) cannulation hemodialysis in 270 consecutive patients for first-time forearm loop placement. Ninety-six (36%) cases were cannulated within 14 days and 78 cases within 7 days. The overall results with the stretch graft are excellent. The statistically significantly worse outcome with early cannulation was mainly due to a select patient population (as determined by proportional hazards regression analysis) being more acutely ill, urgently needing hemodialysis and having no other options for needle puncture. A prospective randomized study, however, is warranted to fully resolve the safety issue of early cannulation.

Adolescent↗
PubMed1996

Reperfusion injury.

Reperfusion injury, precipitated by lack of oxygen, is likely to play a major role in many clinical conditions, including shock, coronary artery occlusion disease, and solid organ transplantation. Certain tissues, such as the intestinal mucosa, may be especially susceptible because of the specific microvascular anatomy. Structural changes include not only swelling of the organelles but also the entire cell due to the entry of water and electrolytes. Lysosomal ruptures precede cell death. Other key substances which either participate in or are part of oxygen free radical formation in tissue injury are calcium ions, leukocytes, and bacteria. Leukocyte adhesion has been implicated as a critical step in vascular endothelium injury, leading to increased microvascular permeability and thrombosis. Induction of neutropenia or the administration of antileukocyte adhesion monoclonal antibodies, preventing typical injuries, implies a central role of the white blood cells in reperfusion injury. Specifically, oxygen free radical formation in the intestines may trigger or cause injury in other distant organs, e.g., the heart and lungs, and affect overall vascular function. So-called "bacterial translocation" from the intestines to the lymphatic vessels and the bloodstream is a more recently discovered phenomenon whose role is largely unknown. Ischemic preconditioning is still another concept, mainly tested in the canine heart, that has potential clinical applications. Reperfusion of ischemic tissue occurs with solid organ transplantation, often after considerable cold ischemia time. Protective mechanisms include oxygen free radical scavengers, i.e., allopurinol and superoxide dismutase. Other measures proven to be effective during the implantation are blood volume expansion with colloid solutions and/or electrolyte solutions, and the administration of a calcium antagonist. The mechanisms of these measures are likely related to improved renal microcirculation and relief of vasospasm.

Animals↗
PubMed1995

Enhancement of peritoneal macrophages reduces postoperative peritoneal adhesion formation.

Postoperative adhesion formation results from a fibroproliferative inflammatory reaction. Macrophages are critical in the final resolution of the inflammatory process and tissue repair, including modulation of proliferation and differentiation of fibroblasts and secretion of neutral proteases like plasminogen activator. We, therefore, studied the influence of peritoneal macrophage enhancement on postoperative adhesion formation in five groups of rabbits. Group 1 was a control with normal peritoneum. Animals in group 2 had increased macrophage population in their peritoneum by intraperitoneal injection of protease peptone 3 days before adhesion induction. In group 3, animals were treated by protease peptone as in group 2 and then depleted of the increased macrophage population by peritoneal lavage before adhesion induction. In group 4 macrophages were transplanted from animals enriched as in group 2 into a nonenriched peritoneum at the time of adhesion induction. Group 5 had a normal peritoneum with peritoneal lavage before adhesion induction. Peritoneal adhesions were induced at laparotomy by repairing a peritoneal defect in two different models. It was found that enhancement of peritoneal macrophages by protease peptone reduced markedly the degree of postoperative adhesion formation. After depletion of the enhanced peritoneal macrophages by peritoneal lavage the degree of adhesion formation was equivalent to that of controls. Finally, macrophage transplantation into a nonenhanced macrophage peritoneum also reduced the degree of postoperative adhesion formation. It is concluded that enhancement of peritoneal macrophages reduces postoperative peritoneal adhesion formation.

Animals↗
PubMed1995

Exogenous phospholipid reduces postoperative peritoneal adhesions in rats.

OBJECTIVE: To find out if the previously described ability of phosphatidylcholine to reduce peritoneal adhesions is specific to it, or if other phospholipids such as phosphatidylinositol (PI) or DL-phosphatidylcholine dilauryl (DL-PC) have similar effects. DESIGN: Laboratory experiment. SETTING: University hospital, Sweden. MATERIALS: 160 rats which had had intraperitoneal adhesions induced at laparotomy by peritoneal defects repaired in one of two models. INTERVENTIONS: PI was given intraperitoneally either once in a dose of 20 or 40 mg/rat at the end of the operation, or at the end of the operation and repeated on the second and third postoperative days. DL-PC was given once at the end of the operation in a dose of either 20 or 40 mg/rat. MAIN OUTCOME MEASURES: Adhesions were assessed a week after operation by an observer who was unaware of the treatment given. RESULTS: PI given on three consecutive days significantly reduced adhesions formed postoperatively in both models (p < 0.05). Neither PI nor DL-PC given in a single dose of 20 mg/rat had any effect, whereas both PI and DL-PC given in single doses of 40 mg/rat significantly reduced adhesions (p < 0.05). CONCLUSION: Both PI and DL-PC are effective in the prevention and limiting of postoperative adhesions in rats.

Animals↗
PubMed1994

Temperature-dependent phospholipid degradation in the rat liver during preservation for transplantation. A comparison between different preservation solutions.

For the development of liver injury during preservation for transplantation, phospholipid degradation may be of importance. We therefore measured the degradation of [3H]-arachidonic acid (20:4)- and [14C]-linoleic acid (18:2)-labeled phospholipids during cold and warm preservation of rat livers in Eurocollins, University of Wisconsin, or a recently developed dextran-based solution. The amount of labeled phospholipids decreased with time during preservation at 37 degrees C with a concomitant increase in that of labeled fatty acids. The rate of degradation of [3H]-20:4-labeled phospholipids did not differ from that of [14C]-18:2-labeled phospholipids. The reduction of phosphatidylcholine and phosphatidylethanolamine radioactivity accounted for the major reduction of phospholipid radioactivity while there was no decrease in phosphatidylinositol radioactivity. In contrast, no phospholipid hydrolysis occurred during preservation at 4 degrees C or at 21 degrees C. The results were not different whether the livers were preserved in EC, UW, or the dextran-based preservation solution. During reperfusion of livers either immediately after removal or after cold storage at 4 degrees C in EC or UW solutions for 24 hr, a moderate increase in the [3H] and [14C] radioactivity of free fatty acids and triacylglycerol and in that of [3H] in PE occurred. There was, however, no difference between the three groups. Thus, during liver preservation at 37 degrees C, phospholipid degradation occurs, and its rate is independent of the preservation medium. In contrast, at the temperature used when preserving livers for transplantation, there is no phospholipid degradation. The cold storage in either EC or UW solution does not influence the net hydrolysis and the transesterification reaction that the phospholipids undergo during warm reperfusion of the isolated livers.

Adenosine↗
PubMed1994

Effect of the number of islets on the outcome after transplantation in streptozotocin-induced diabetic rats.

This study tested the hypothesis that normalization of glucose homeostasis after islet transplantation is correlated to the number of islets, and by increasing this number a complete normalization of glucose homeostasis could be achieved, 1,200 or 2,400 islets were transplanted into the left kidney subcapsular space in streptozotocin-induced diabetic rats. Intravenous glucose tolerance tests were performed at 10 days, 3 and 6 months after transplantation. Transplantation of both 1,200 and 2,400 islets normalized the basal blood glucose levels within 24-48 hours, which remained normal for the entire study period of 6 months. Basal plasma insulin levels and body weight were also normalized in both transplanted groups. Transplantation of 2,400 islets achieved normal glucose-induced insulin secretion at 10 days after transplantation and for the following 6 months. In contrast, glucose intolerance was present in rats transplanted with only 1,200 islets. It is concluded that complete glucose homeostasis after islet transplantation is dependent on the number of transplanted islets and can be achieved by increasing this number.

Animals↗
PubMed1994

Topical anticolitic efficacy and selectivity of the glucocorticoid budesonide in a new model of acetic acid-induced acute colitis in the rat.

AIMS: To study the effect of local or parenteral administration of the glucocorticoid budesonide in the acetic acid-induced colitis model in the rat. METHODS: Colitis was induced in an exteriorized colonic segment by administration of 4% acetic acid for 15 s. Four days later, this colonic segment with colitis was examined using a morphological scoring system, and measurements of myeloperoxidase activity and of plasma exudation into the colonic segment. The experimental colitis showed morphological similarities to human ulcerative colitis, with 3-fold increase in myeloperoxidase activity and 6-fold increase in the plasma exudation. Budesonide in different doses administered for 3 days, starting one day after acetic acid instillation, prevented the development of colitis in a dose-dependent manner. The best effect of budesonide on the morphological score was achieved after local treatment at a dose of 10(-5) M twice daily (76% reduction compared with a control colitis group) and parenteral treatment with 0.75 mg/kg (80% reduction). These doses also normalized myeloperoxidase activity and significantly reduced the plasma exudation. The systemic effects of the drug were most pronounced in the group treated with parenteral budesonide. This group showed the greatest reduction in body weight and a significant reduction of the weight of adrenal glands and spleen (as compared to controls). Thymus weight in animals treated systemically was significantly lower than in locally treated animals. In the group treated with local budesonide the weight of adrenals was reduced. However, the weights of spleen and thymus were not reduced and the reduction of the body weight was even less than in the control group. CONCLUSION: Local treatment with budesonide at a dose of 10(-5) M (0.17 mg/kg if completely absorbed, but only 0.03 mg/kg with 15% bioavailability on colonic application) was as effective as parenteral treatment at a dose of 0.75 mg/kg in the attenuation of acetic acid-induced colitis in the rat, but resulted in minor systemic side-effects.

Acetates↗
PubMed1994

Deleterious effect of cyclosporins on the ischemic kidney in the rat and the protection by the calcium antagonist verapamil.

Cyclosporine A (CsA) nephrotoxicity has been suggested to be aggravated in the presence of ischemia, as occurs after renal transplantation. Cyclosporine G (CsG) may be less nephrotoxic than CsA. This study evaluated in the rat (1) the effect of CsA and CsG on blood flow and the function of the kidney subjected to 60 min of warm ischemia and (2) the protective effect of the calcium antagonist verapamil (VP). After left nephrectomy, ischemia was induced in the right kidney by the clamping of the kidney pedicle for 60 min, which resulted in a significant increase in serum creatinine (SCr) to 2.30 +/- 0.25 mg/dL by Day 1 with 25% mortality by Day 7. The administration of CsA or CsG (20 mg/kg i.v. daily for 7 days) after 60 min of renal ischemia significantly increased SCr and mortality compared with ischemia alone. In another set of experiments, 60 min of warm ischemia was applied to the right kidney and RBF was measured in both kidneys with a laser Doppler flowmeter. Blood flow in the ischemic kidney returned to the preischemic level by 15 min after the removal of the vascular clamp in the control animals. In contrast, in animals treated with CsA, a significant decrease in RBF was seen in both kidneys; however, blood flow in the ischemic kidney was significantly lower than that in the nonischemic kidney. CsG also decreased RBF in both kidneys, although in the left (nonischemic) kidney, RBF remained significantly higher with CsG than with CsA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Phospholipids prevent enteric bacterial translocation in the early stage of experimental acute liver failure in the rat.

BACKGROUND: Bacterial infections and bacteremia in acute liver failure may at least partly be attributed to translocation of enteric bacteria. Attempts to prevent or treat such infections by the use of antibiotics may instead result in overgrowth of surviving microbes. METHODS: In the present study, normal saline (1.5 ml/100 g body weight), phosphatidylcholine (1.5 ml/100 g body weight), and phosphatidylinositol (1.5 ml/100 g body weight) were orally administered by means of a gastric tube both 12 h and 30 min before operation. Effects of enteric administration of phospholipids on the prevention of enteric bacterial translocation, intestinal and mucosal mass, and enterocyte protein contents in acute liver failure induced by subtotal liver resection in the rat were evaluated. RESULTS: The incidence of bacterial translocation increased significantly 2 and 4 h after 90% hepatectomy as compared with sham-operated animals. Enteric administration of phospholipids, however, significantly reduced the incidence of bacterial translocation after 90% hepatectomy. Phospholipid treatment prevented the postoperative decrease in intestinal mucosal mass and enterocyte protein content. CONCLUSIONS: Enteral administration of phospholipids thus seems to protect against translocation of enteric bacteria and prevent against a decrease in intestinal mucosal mass and enterocyte protein content after subtotal hepatectomy in the rat.

Animals↗