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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Survival of Lewis X Brown Norway F1 renal allografts was prolonged in Lewis recipients by pretreatment with small numbers of donor marrow cells and low dose antilymphocyte globulin(ALG)in combination. Either marrow cells or ALG alone were ineffective at these doses. It was also shown that pretreatment with marrow cells and antilymphocyte serum (ALS) considerably suppressed the local graft-versus-host reaction.
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PMID:Pretreatment with antilymphocyte globulin and donor cells on graft prolongation in an experimental model and some observations on graft-versus-host reaction. 1 54

Mercuric chloride induces anti-glomerular basement membrane antibodies in Brown Norway rats (Ag B3) and not in Lewis rats (Ag B1). Studies on (Lewis X BN) F1 and F2 and with back-crosses (Lewis X BN) F1 X Lewis demonstrate a genetic control for this immune response. This genetic control probably depends on two non-linked, autosomal and dominant genes. One of these genes is linked to the major histocompatibility locus.
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PMID:[Induction of anti-glomerular basement membrane antibodies in BN rats: genetic control]. 30 May 99

Lewis rats that were given injections of 10(6) to 10(8) (Lewis X Brown Norway) F1 hybrid bone marrow cells produce predominantly, if not exclusively, 19S lymphocytotoxic antibodies. A number of Lewis rats that received transplants of perfused renal allografts from bone marrow donors at, or near, the peak of IgM response survival for well over 200 days with good renal function and no histological evidence of chronic rejection. All long-surviving rats had detectable lymphocytotoxic antibodies up to 120 days after allografting; late enhancing antibodies had the restricted specificity possibly identical or similar to anti-I region antisera. All rats bearing prolonged renal allografts were unable to accept donor-specific skin grafts or to respond with specific lymphocytotoxic antibodies following skin grafting. The possible involvement of non-complement-fixing 19S alloantibodies in active enhancement of rat renal allografts is discussed.
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PMID:The alloantibody response and active enhancement of some rat renal allografts. 32 43

Five organs consisting of the liver, pancreas, duodenum, spleen, and kidney from (Lewis X Brown Norway)F1 rats were transplanted simultaneously as an en bloc graft to Lewis recipients. No immunosuppression was given postoperatively. Serial laporatomies were performed for macroscopic examination and biopsies of the grafts. Macroscopically, the first evidence of rejection was splenic enlargement followed by fatty metamorphotic change of the liver, dilation and loss of peristalsis of the duodenum, and injection of the pancreas. The kidney maintained normal color and consistency until late in the rejection process. Histological examination suggested that the liver and the spleen may be more vulnerable to immune attack, since in these organs cellular infiltration started earlier and was more extensive in comparison to other organs. While the pancreas exhibited a typical, although somewhat delayed rejection pattern, the kidney seemed to maintain a well preserved structure. Interestingly, the duodenum showed no significant cellular infiltration throughout the postoperative period of examination despite severe mucosal destruction.
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PMID:En bloc transplantation of the liver, pancreas, duodenum, spleen, and kidney in the rat. 33 83

The testis is an immunologically privileged site despite a normal lymphatic drainage, whereas the anterior chamber of the eye is a privileged site because it lacks normal lymphatics. Parathyroid grafts were transplanted between several strains of inbred rats (Buffalo leads to Lewis and Lewis X Brown Norway F1 leads to Lewis). Allografts were placed in the testis, thigh muscle, prostate, lymph nodes, anterior chamber of the eye and adrenal gland. The survival of intratesticular allografts also was tested in animals whose pituitary gonadotropins were suppressed by testosterone and estradiol implants. The effects of steroid implants were documented by measuring testosterone and progesterone concentrations in the serum and whole testis homogenates of these animals. Allograft survival was judged by fasting plasma calcium concentrations. The data show that 1) the adrenal is included among naturally occurring immunologically privileged sites, 2) the prolonged survival of intratesticular allografts may be related to the local production of steroid hormones, although allograft survival is not critically dependent on pituitary gonadotropins and 3) temperature differences and a high zinc concentration within the testis are not important to allograft survival.
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PMID:Intratesticular grafts: the testis as an exceptional immunologically privileged site. 75 27

Rejection of the cardiac allograft is often associated with reversible myocardial failure, the mechanism of which is not understood. We have examined this phenomenon in a small animal model that provides the opportunity for multimodality study of the rejection process. Heterotopic cardiac transplantation was performed in the Lewis rat with Lewis X Brown-Norway (allografts) or Lewis (isografts) donors. Without immunosuppression, allografts are completely rejected in 6 to 8 days. At 3 days cardiac grafts were explanted and mounted on a modified Langendorff apparatus for functional measurements or submitted for pathologic examination and biochemical determination of high-energy phosphates. Three-day isografts (n = 9) had minimal histologic changes. Pathologic examination of 3-day allografts (n = 13) showed lymphocytic infiltrate and myocyte necrosis, histologic features for which antirejection treatment is usually given clinically. For grafts subjected to functional studies (n = 11), heart rate, cardiac output, coronary flow, and stroke work were determined at baseline and in response to isoproterenol (3 x 10(-8) mol/ml). Three-day allografts (n = 6) and isografts (n = 5) had similar baseline function. The chronotropic response to isoproterenol was similar in allografts and isografts, but allografts had diminished cardiac output and stroke work after isoproterenol. Adenosine triphosphate levels were normal (41.9 nmol/mg) in 3-day allografts (n = 4). We have evaluated functional, biochemical, and pathologic changes associated with myocardial dysfunction during heterotopic cardiac transplant rejection in a small animal. This model reproducibly demonstrates diminished contractile reserve in 3-day allografts with normal baseline function and high-energy stores but histologically significant rejection.
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PMID:The mechanism of heart failure caused by cardiac allograft rejection. 199 37

Intestinal permeability was studied after accessory intestinal transplantation in Lewis rats. Five groups were evaluated: Group 1--isografts (N = 6); Group 2--Lewis X Brown Norway F1 (LBN-F1) allografts (N = 6); Group 3--isografts treated with CsA 2 mg/kg/day X 10 days (N = 6); Group 4--LBN-F1 allografts treated with CsA 2 mg/kg/day X 10 days (N = 6); Group 5--LBN-F1 allografts treated with CsA 4 mg/kg/day X 28 days (N = 6). Chromium-labeled ethylenedimianetetraacetate (51Cr-EDTA) was given through the proximal stoma of the graft. Renal clearance of 51Cr-EDTA and mucosal biopsies were followed post-transplant. The biopsies of the intestinal graft showed no rejection in Groups 1, 3, and 5; fulminant rejection in Group 2; and mild atypical rejection in Group 4. 51Cr-EDTA clearance was elevated in all groups during the first 7 days post-transplant. Thereafter, 51Cr-EDTA excretion fell to lower levels in the animals with histologically normal grafts (Groups 1, 3, and 5). 51Cr-EDTA excretion in Group 4 was increased with the first histological evidence of rejection on Day 14 and remained elevated until sacrifice (P less than 0.02 compared to Groups 3 and 5). A transient permeability defect occurs after intestinal grafting. Once the graft has recovered from this injury, 51Cr-EDTA is a sensitive marker for intestinal rejection.
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PMID:51Cr-EDTA: a marker of early intestinal rejection in the rat. 249 70

Three agents that significantly prolong cardiac allograft survival were tested in Lewis rats that were recipients of hearts from Lewis X Brown-Norway F1 hybrid donors. In the presence of azathioprine, the effects of daily administration of either the thromboxane antagonist (L 640,035), the platelet-activating factor (PAF) antagonist (BN 52021) or prednisolone were evaluated on the infiltration of cardiac allografts by syngeneic lymphocytes and platelets labeled with 111indium. As anticipated, platelet deposition was reduced by the thromboxane antagonist and unaffected by the PAF antagonist; the latter is likely due to the known absence of PAF receptors in rat platelets. In addition prednisolone had no effect. The increased accumulation of lymphocytes on days 4-5 was also unaffected by all three drugs. These experiments indicate that, in this model, graft survival is not necessarily related to lymphocyte and platelet infiltration of the graft. The data also provide evidence for the efficacy of the thromboxane receptor antagonist L 640,035 in preventing platelet deposition in vivo.
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PMID:The effect of prednisolone, thromboxane, and platelet-activating factor receptor antagonists on lymphocyte and platelet migration in experimental cardiac transplantation. 303 53

The purpose of these experiments was to evaluate the use of cyclosporine (CyS) in preventing accelerated rejection in donor-specific presensitized hosts by comparing its efficacy in donor-recipient strain combinations that were either haploidentical or completely mismatched at the major histocompatibility complex (MHC). Lewis X Brown Norway F1 (LBN) (Rt1(1)n) secondary heart allograft survival was prolonged indefinitely in CyS-treated Lewis (Rt1(1] recipients while ACI (Rt1a) grafts were ultimately rejected despite maintenance use of CyS. However, graft survival was significantly prolonged in these latter experiments with mean survival times (MSTs) of 29.4 +/- 32.1 days (CyS 10 mg/kg/day) and 19.4 +/- 21.1 days (CyS 15 mg/kg/day) compared to both untreated second-set controls (MST of 3.9 +/- 0.8 days, P less than 0.05), and untreated primary graft recipients (MST of 6.9 +/- 0.4 days, P less than 0.05). An attempt to identify suppressor cells in the long-term Lewis recipients of LBN hearts using an adoptive transfer experiment was unsuccessful when the spleen donors were still receiving CyS. Conversely, in a control experiment using spleens from CyS prolonged primary graft recipients in which splenectomy was performed after cessation of CyS, subsequent adoptive transfer did significantly prolong test heart graft survival in three of seven rats suggesting that suppressor cells may have been present. These data suggest that CyS is an effective immunosuppressant in presensitized hosts when MHC disparity is incomplete but that it cannot indefinitely prevent rejection in donor-recipient combinations that are completely mismatched at the MHC. Moreover, they suggest that splenic suppressor cells may not be present in animals concurrently receiving CyS.
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PMID:Cyclosporine abrogation of second-set rejection: dependence upon major histocompatibility complex disparity. 315 82

The relationship between the cyclosporine A (CSA) dose and rejection of varying lengths of small-bowel grafts was studied in a rat heterotopic microsurgical small-bowel transplantation model involving a haploidentical strain combination. When Lewis X Brown Norway F1 hybrid (LBN) small-bowel grafts were transplanted into Lewis (LEW) rats without CSA, all grafts in the proximal 10 cm, the proximal 40 cm, and the entire (approximately 80 cm) small bowel were rejected on days (mean +/- SEM) 6.6 +/- 0.2 (n = 11), 7.0 +/- 0.4 (n = 6), and 7.8 +/- 0.7 (n = 6), respectively. A 10-day course (days 0-9) of CSA 2 mg/kg significantly (p less than 0.05) prolonged the survival of the proximal 10 cm, the proximal 40 cm, and the entire small bowel allografts to days 18.8 +/- 1.7 (n = 5), 16.5 +2- 1.3 (n = 6), and 13.5 +/- 1.0 (n = 4), respectively. Similarly, the CSA 5 mg/kg regimen significantly (p less than 0.05) delayed the rejection of the 10 cm, the 40 cm, and the 80 cm small-bowel grafts to days 50.2 +/- 7.2 (n = 6), 47.7 +/- 2.6 (n = 3), and 40.3 +/- 5.8 (n = 3), respectively. However, 6 of 12 rats treated with CSA 5 mg/kg died of pneumonia, and these animals were all in groups with the 40 cm and 80 cm grafts. When these animals were included in calculations of rejection-free survival, the averages for the 40 and 80 cm groups treated with CSA 5 mg/kg were 34.2 +/- 6.4 and 28.7 +/- 6.1 days, respectively. CSA suppressed rejection of small-bowel allografts in a dose-related fashion. More important, significantly (p less than 0.05) lower doses of CSA were necessary for rats that received shorter intestinal grafts. In fact, the relationship between rejection and CSA dose in the 10 cm grafts was characterized by the formula: day of rejection = 9.3 [CSA dose]1.03. We conclude that the ideal small intestinal graft should be the smallest possible segment that maintains adequate nutrition and CSA doses should be matched for segment lengths.
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PMID:The effects of cyclosporine on varying segments of small-bowel grafts in the rat. 326 Apr 10


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