[Changes in urodynamic parameters following cystourethropexy].
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Female↗
Biomedical subjects
E Wight
Publications and source records attributed to E Wight.
Induction of specific transplantation tolerance via immunization with donor-specific idiotypes.
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Animals↗
Induction of specific transplantation tolerance via immunisation with donor-directed idiotype(s).
We have re-explored the efficiency of anti-idiotypic immunisation on the generation of transplantation tolerance to cardiac allografts in the rat. Recipient Lewis rats were immunised using 13 different protocols with different doses of anti-DA or anti-BN idiotype(s) and different adjuvants. Four protocols proved successful. Immunisation with Lewis anti-BN blasts either in complete Freund's adjuvant or in muramyl dipeptide (MDP) prolonged the survival of a congeneic AgB incompatible L.BN cardiac allograft from 6.7 +/- 0.3 to 26.8 +/- 5.1 and to greater than 30 +/- 0.0 days, respectively. Immunisation with Lewis anti-T cell 'receptor' in complete Freund's and in MDP increased the survival of a DA heart allograft in Lewis recipients from 6.0 +/- 0.0 days to 13.2 +/- 0.8 and 10.0 +/- 4.0 days, respectively, indicating that most of the MHC effect was also overcome here. The prolongations of survival were immunologically specific, and accompanied by a specific deletion of the relevant alloantibody response. So far no generation of anti-idiotypic antibody in the immunised recipient has been detected; instead, a successful immunisation seems to be accompanied by the generation of immunising idiotype-directed cytotoxic (T?) lymphocytes in the recipient.
Animals↗
Induction of specific immune unresponsiveness with purified mixed leukocyte culture-activated T lymphoblasts as autoimmunogen. II. An analysis of the effects measured at the cellular and serological levels.
T lymphoblasts specific for foreign histocompatibility antigens and purified via mixed leukocyte culture (MLC) and 1 g velocity sedimentation procedures can be used as autoimmunogen to produce specific immunological unresponsiveness in adult animals. This unresponsiveness is positively correlated to the production of autoanti-idiotypic antibodies in the blast immunized animals and no evidence of coexisting alloimmunity was found. We consider this autoanti-idiotypic immunity to be the specific inducing agent of the immune tolerance. The blast immunization procedure will lead to selective reduction in T-cell reactivity against the relevant alloantigens as measured by MLC, cell-mediated lympholysis, or graft-versus-host assays. However, in individual animals, dichtomy in suppression between two T-cell assays could sometimes be observed indicating elimination of only a select group of idiotypic functionally distinct population of T cells in these blast-immunized animals. Attempts to abrogate already immune animals by the autoblast procedure were successful, in part suggesting the use of the present procedure when trying to induce in accelerated reversion of such immunity.
Animals↗
Induction of specific immune unresponsiveness using purified mixed leukocyte culture-activated T lymphoblasts as autoimmunogen. I. Demonstration of general validity as to species and histocompatibility barriers.
Normal immunocompetent T lymphocytes can be induced into specific proliferation if confronted with the relevant alloantigen in vitro. Such mixed leuko-cyteculture-activated T lymphoblasts carring idiotypic receptors on their surface can be purified using velocity sedimentation and serve as immunogen if administered in adjuvant to the autologous host. Autoblast immunization can be shown to lead to specific, long-lasting unresponsiveness against the relevant alloantigens, while leaving reactivity against third-party antigens intact. When tested as to general validity, it could be shown to function in all species analyzed (mouse, rat, and guinea pig) as well as across both major and minor histocompatibility barriers. No negative side effects have been noted so far. It would thus seem clear that autoblast immunization using the above described scheme may serve as a general tool in inducing long-lasting, specific unresponsiveness in any species and across any histocompatibility barrier.
Animals↗
Specific suppression of MLC and CML by anti-idiotypic antibodies in the mouse.
Rabbit antisera directed against idiotypic determinants of alloreactive mouse CBA anti-C57BL/6 T blasts were raised in the following manner: first, a rabbit serum directed against nonspecific CBA blasts cells was prepared by injecting CBA concanavalin A blasts three times at monthly intervals into a rabbit. Second, specific CBA anti-C57BL/6 T lymphoblasts were induced in a mixed lymphocyte culture (MLC), were purified by gravity sedimentation through a fetal calf serum gradient, and, finally, were incubated with the anti-blast serum from the first step. During this incubation, presumably all epitopes of the blast cell population were blocked by anti-blast antibodies, except for the greatly amplified set of CBA anti-C57BL/6 alloreactive idiotypes. The mixture was then injected into fresh rabbits, which were boosted with similar mixtures after 3 and 6 weeks. Blood samples were removed 10 days after each injection. Such sera, when used together with complement, inhibited specifically the stimulation of CBA cells by C57BL/6 antigens in MLC and the CBA anti-C57BL/6 killer cells.
Animals↗
Oral superparamagnetic contrast agent (ferumoxsil): tolerance and efficacy in MR imaging of gynecologic diseases.
The purpose of this study was to determine the tolerance and the efficacy of the oral contrast agent ferumoxsil in the assessment of gynecologic diseases. Twenty patients underwent MR imaging at 1.5 T. T1-weighted spin-echo (SE) and T2-weighted fast SE images were obtained before and after ingestion of 600-900 mL of the superparamagnetic negative contrast agent ferumoxsil. No side effects were observed. No statistically significant increase in artifact generation was present in the postcontrast images. The efficacy in bowel marking was significant for the small bowel (P = .0001) and the cecum (P < .01), but not significant in all sequences for the sigmoid. In the postcontrast images, delineation of the uterus, the right-sided adnexa, the lymph nodes, and the pathologic lesions was significantly better (P < .01), but not all sequences showed an improvement in delineation of the other pelvic organs. After administration of ferumoxsil, the level of confidence in diagnosis was significantly higher (P = .0001), but no change in diagnosis was made from the pre- to the postcontrast images. We found the oral contrast agent ferumoxsil to be well tolerated and effective in marking the bowel and in delineating the normal organs as well as the pathologic lesions on pelvic MR images.
Administration, Oral↗
Chronic blockade of nitric oxide-synthase and endothelin receptors during pregnancy in the rat: effect on pregnancy outcome.
OBJECTIVES: To investigate the effects of endothelin-1 (ET-1) receptor antagonism and/or chronic blockade of nitric oxide (NO) production on pregnancy outcome in the rat. METHODS: Pregnant or nonpregnant Wistar rats were either treated orally for up to 18 days with the NO-synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), the ETA-/ETB-receptor antagonist bosentan (Roche Basel, Switzerland) or both, or received no treatment (controls). Blood pressure, body weight, and drug intake were measured at regular intervals. Pregnancy outcome and proteinurea were also determined. Analysis of variance and paired Student t test were used for statistical analysis. RESULTS: Chronic L-NAME treatment increased systolic blood pressure by 69 and 64 mmHg in pregnant and virgin rats respectively (P < .05). Bosentan-blunted, L-NAME-induced hypertension at the beginning (P < .05), but not at the end of the treatment period in all rats examined. N omega-nitro-L-arginine methyl ester-treatment in pregnancy reduced the number of living fetuses at term (P < .05) and caused proteinurea (P < .05). Bosentan tended to reverse the effects of L-NAME on fetus number and proteinurea, but both effects failed to reach statistical significance. CONCLUSIONS: The effects of chronic, NO-synthase-blockade on blood pressure in gravid rats can be reversed only temporarily by ETA-/ETB-antagonism, suggesting an involvement of endothelin-1 in the early phase of the L-NAME-induced, preeclampsia-like syndrome during pregnancy, although at later stages other mechanisms may come into play.
Animals↗
Chronic blockade of nitric oxide synthase and endothelin receptors during pregnancy in the rat: effect on reactivity of the uterine artery in vitro.
OBJECTIVE: To investigate the effects of chronic blockade of nitric oxide (NO) production and endothelin (ET-1) receptor antagonism on endothelial and vascular smooth muscle function of the uterine artery in vitro obtained from nonpregnant and pregnant rats. METHODS: Pregnant or nonpregnant Wistar rats were either treated orally for up to 18 days with the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME), the ETA-/ET beta-receptor antagonist bosentan, or both, or they received no treatment (controls). Absolute contractile force as well as endothelium-dependent and -independent vascular reactivity of uterine arteries were determined in vitro. Isometric tension was recorded. ANOVA and the Mann-Whitney U test were used for statistical analysis. RESULTS: Pregnancy increased absolute tension (mN/mm) elicited in uterine arteries by ET-1 (P < .01), serotonin (P < .05), norepinephrine (P < .02), and KCl (P < .0001). Chronic treatment with L-NAME or L-NAME plus bosentan, but not with bosentan alone, reduced contractions to KCl in pregnant and nonpregnant rats (P < .005-.0001), while pregnancy-induced enhancement in tension development remained unchanged in all groups (P < .005). After exposure of uterine arteries to L-NAME in vitro, vascular sensitivity to ET-1 was augmented in uterine arteries of pregnant but not of nonpregnant animals (P < .05). L-NAME-pretreatment did not influence the pregnancy-induced increase of vascular sensitivity to acetylcholine but reduced maximal relaxation in nonpregnant animals (P < .05). In addition, pregnancy diminished sensitivity of uterine arteries to sodium nitroprusside (P < .002), which was abolished by chronically administered L-NAME. Bosentan had no influence on vasodilation in vitro. CONCLUSION: Neither endothelin-1 nor nitric oxide seem to contribute to the augmented tension to depolarization and receptor-operated stimulation of vascular smooth muscle cells in rat uterine arteries during pregnancy. In addition, pregnancy is associated with increased NO production in uterine arteries, as evidenced by augmented endothelium-dependent relaxations, increased NO release by endothelin-1, and decreased sensitivity to sodium nitroprusside.
Acetylcholine↗
Aging, serum estradiol levels, and pregnancy differentially affect vascular reactivity of the rat uterine artery.
OBJECTIVES: To investigate the effects of aging, ovarian ablation, and pregnancy on vascular reactivity of the rat uterine artery. METHODS: Segments of uterine artery from 3-month-old pregnant and nonpregnant Wistar rats and from aged and ovariectomized animals, both 9 months of age, were exposed in vitro to vasoactive mediators. Absolute contractile force as well as endothelium-dependent and -independent vascular reactivity were determined. Isometric tension was recorded using a modified Mulvany myograph system. Results were compared with analysis of variance and Bonferroni-Dunn post hoc analysis and correlated with serum estradiol levels. RESULTS: Aging up to 9 months decreased absolute tension of uterine arteries in vitro elicited by KCl (P < .0001), while not affecting receptor-operated responses to norepinephrine, endothelin-1, and angiotensin II. After ovarian ablation maximal contraction to norepinephrine was selectively reduced in the aged animal (P = .0053). Pregnancy increased absolute tension to KCl (P < .0001), norepinephrine (P < .008), and endothelin-1 (P = .0003), whereas relative contractile force (percentage of KCl) induced by norepinephrine and endothelin-1 remained unchanged and that induced by angiotension II decreased (P = .0001) in pregnant animals. In addition, pregnancy increased sensitivity to the endothelium-dependent vasodilator acetylcholine (P = .0022) but decreased that to the endothelium-independent vasodilator sodium nitroprusside (P = .0062). Endothelium-dependent relaxation correlated with serum estrogen levels remained unchanged in 9-month-old Wistar rats, which physiologically exhibited high serum estrogen concentrations but was impaired with regard to both maximum relaxation (P < .0001) and sensitivity in aged rats (P = .0007) after ovariectomy. CONCLUSIONS: Vascular contractility is impaired in the uterine artery of the aged rat as evidenced by reduced responses to KCl, whereas responses to receptor-operated agonists remain unchanged. Functional ovaries are essential to preserve endothelium-dependent relaxation in aging animals. During pregnancy, contractile machinery and endothelium-dependent relaxation are enhanced. In contrast, contractions to angiotensin II and endothelium-independent relaxation to sodium nitroprusside are reduced in late pregnancy. These changes in reactivity of the uterine artery may be important for the regulation of blood flow in the uterus according to physiologic needs.
Acetylcholine↗
Pulmonary atresia with ventricular septal defect: a case for central venous pressure and oxygen saturation monitoring.
A 21-year-old patient with pulmonary atresia and ventricular septal defect (PA-VSD) was admitted to the hospital for tubal ligation. Invasive arterial and central venous (CVP) pressure, pulse oximetric oxygen saturation (SpO2), and (from the tip of oximetric central venous catheter) central venous oxygen saturation (ScvO2) and oxygen extraction rate (ExO2) were continuously monitored. Heart rate (range: 68-75 beat/min), mean arterial pressure (80-90 mmHg), CVP (7-10 mmHg), SpO2 (79-90 percent), ScvO2 (57-70 percent), and ExO2 (21-30 percent) remained stable during epidural anesthesia and transvaginal sterilization. Following an overnight stay (peak SpO2 92 percent; peak ScvO2 71 percent; through ExO2 21 percent), the oxygen data returned to baseline on awakening (SpO2 < 80 percent, ScvO2 < 55 percent, ExO2 > 35 percent), and the patient was discharged. In PA-VSD, a single-outlet double-ventricle anomaly, CVP reflects the preload of systemic ventricle. As the mixed venous oxygen saturation cannot be defined, ScvO2 is the best available indicator of the whole body oxygen consumption. Continuous monitoring of CVP, ScvO2 and ExO2 in the superior vena cava may provide more insight into the response to anesthesia and surgery in patients with PA-VSD.
Abnormalities, Multiple↗