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

Peridural anesthesia is believed to be a complicated kind of analgesia yielding grave complications (syncope, apnoe, collapse, persistant and pronounced hypotension, nematomyelia, paraplegia of the lower extremities, Brown--Seguard syndrome and many others). This king od anesthesia is permissible only in an anesthesiological or reanimatological department. The frequency of complications depends on a level of injecting the anesthetic, patient's status and age. The former is the greater the higher the level of the peridural space puncture. To combat against complications occurring while using this kind of analgesia everything necessary for reanimation provision (intubation of the trachea, closed and open heart massage, etc.) should be ready at hand.
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PMID:[Complications of peridural anesthesia]. 122 52

The immunologic consequences of transplantation of vascularized bone allografts have not been previously characterized. In this study, knee allografts, both vascularized and nonvascularized, were transplanted from Lewis rats to Brown Norway rats across a strong histocompatibility barrier. A total of 66 transplants and 8 control animals were evaluated. The vascularized knee grafts consisted of 1 cm of proximal tibia and distal femur with a minimal muscular cuff isolated on the femoral vessels, and these were transplanted to a heterotopic, subcutaneous position on the abdominal wall of the recipient rat. Nonvascularized allografts (identical but without anastomoses) were transplanted for comparison. The cell-mediated response was measured by lymphocytotoxicity assay, and the humoral response was measured by cytotoxic antibody assay, both employing 51Cr-labeled target cells. The timing and intensity of the immune response differed according to the type of graft. The vascularized bone allografts generated significant cell-mediated and humoral responses as early as 5 days posttransplant. A significant humoral response in nonvascularized bone allografts was not apparent until day 14, while cell-mediated response in these grafts was variable. These findings were correlated with the histologic appearance of the grafted tissue. Cyclosporine, which was administered to one group of vascularized bone allografts, resulted in the suppression of both types of immune responses. The histologic appearance of this group resembled that of isografts transplanted as controls. The clinical application of vascularized bone allografts may offer significant advantages over nonvascularized allografts in the reconstruction of massive bone defects. Complications such as nonunion, fracture, and collapse of articular segments seen in nonvascularized allograft transplantation may be avoided by preservation of the blood supply to the graft. Characterization of the immune response to vascularized bone allografts may subsequently allow the manipulation of the host and/or graft tissue and promote graft incorporation.
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PMID:Vascularized bone allografts: in vitro assessment of cell-mediated and humoral responses. 198 24

Brown Norway rats have been actively sensitized against hen ovalbumine mixed with anti Bordella pertussis vaccine. After ten to twelve days, IgE are detected in the blood, but no precipitins. Anaphylactic shock induced by i.v. injection of 1 mg.100 g-1 body weight of ovalbumine is caracterized by a vascular collapse, the animal dying in about 15 minutes. This collapse is identical with the same general anaphylactic reaction as observed in the Wistar rats, which have large amounts of precipitins in the blood.
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PMID:[Anaphylactic shock in brown Norway rats with reagins and no precipitins in the blood (author's transl)]. 700 96

Cardiac allografts of (Lewis x Brown Norway) F1 rats are rejected by Lewis recipients at 7.5 days after engrafting. When recipients are presensitized with Brown Norway skin grafts at 7 days before engrafting, the cardiac grafts are rejected between 24 and 36 h (accelerated rejection, ACR). We previously demonstrated that the number of thymocytes in recipients showing ACR is decreased to approximately one eighth at 24 h after engrafting, and the thymocytes remaining in the thymus are phenotypically and functionally more mature. In the present study, flow cytometric analysis of the thymocytes in the sensitized recipient at 24 h after engraftment demonstrated that the frequency of single positive cells (CD4+CD8- and CD4-CD8+) was increased and that of double positive cells (CD4+CD8+) was decreased, indicating that immature thymocytes preferentially disappeared during the ACR episode. Thymocytes of the recipients undergoing ACR suffered from extensive apoptosis, characterized by chromatin condensation in the nuclei, cell shrinkage, nuclear collapse, and DNA fragmentation. Serum levels of corticosterone were elevated but were within a similar range among the transplant recipients destined for acute rejection, those undergoing ACR, and isografted controls, suggesting the participation of mediator(s) other than glucocorticoid in the induction of extensive apoptosis in the transplant recipients with ACR. We propose that thymocyte apoptosis is accelerated during the allograft rejection episode.
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PMID:Extensive apoptosis occurring in the thymus during accelerated rejection of cardiac allografts in presensitized rats. 833 6

Oxytocin, the most powerful uterotonic agent known, is released from the pituitary gland in large amounts during parturition in all placental mammals studied so far, including humans. Although parturition can proceed in its absence, oxytocin is thought to play an important role (see Russell & Leng, 1998). In the rat, pregnancy normally lasts for 21 days. About 24 h before the pups are born, increased production of prostaglandins by the uterus induces luteolysis, and ovarian progesterone production falls dramatically. This fall is an essential prelude to parturition; if prevented, then the rat pups will remain unborn. The fall leads to a further increase in prostaglandin production, and, directly or indirectly, to a host of changes that prepare the uterus and birth canal for parturition. In the last few hours of pregnancy, oxytocin receptors appear in high concentrations in the uterus, and establish a positive-feedback loop between the uterus and the hypothalamic oxytocin system. Uterine contractions, triggered by prostaglandins, excite the oxytocin cells, and oxytocin release triggers further prostaglandin production and further uterine contraction. Thus progesterone plays a critical role in the timing of parturition through its peripheral actions (see Leng & Brown, 1997). A paper in this issue of The Journal of Physiology (Brussaard et al. 1999) suggests that actions of progesterone at the oxytocin cells in the hypothalamus may also be important for parturition. Classically, progesterone acts through specific intracellular receptors to regulate gene expression. However, metabolites of progesterone can also have membrane actions, and in particular, allopregnanolone can act at GABAA receptors to potentiate the actions of GABA, depending upon the particular subunit composition of the receptor. GABA is an important neurotransmitter for oxytocin cells about 45 % of all synapses onto them contain GABA, and the total number of GABA synapses in the supraoptic nucleus is substantially higher in lactating animals than in virgins (El Majdoubi et al. 1997). The GABA innervation appears to play a role in patterning the pulsatile discharge of oxytocin cells that is observed both during parturition and during suckling-induced reflex milk ejection (Moos, 1995; Voisin et al. 1995). Brussaard et al. (1999) recorded GABAA receptor-mediated spontaneous monoquantal inhibitory postsynaptic currents (sIPSCs) from rat supraoptic neurones in hypothalamic slices in vitro. They found a higher incidence of sIPSCs in pregnant rats than in virgin rats, consistent with the observations of an increase in the density of GABA-containing synaptic boutons. Importantly, the sIPSCs were markedly prolonged in the presence of allopregnanolone. Taking into account the frequency and amplitude of sIPSCs, the action of allopregnanolone and the hypertrophy of oxytocin neurones in lactation (reflected in increased capacitance), Brussaard et al. (1999) inferred that the effective GABAA receptor-mediated synaptic current density was much greater in pregnant rats than in virgin or lactating rats. Thus the collapse of progesterone production at term may abruptly reduce the effectiveness of GABA inhibition, and thereby enhance the excitability of oxytocin cells. Clearly this may be important during parturition, but the effect may not persist for long. Indeed, within a day the duration of sIPSCs is significantly longer in the absence of allopregnanolone, which now has no significant effect. This seems to be due to a rapid switch in the types of a subunits inserted into the GABAA receptors. By mid-lactation, a massive change in expression of GABAA receptor subunit mRNAs is apparent. With competitive polymerase chain reaction Brussaard and colleagues found that, while the expression of both a1 and a2 subunit mRNAs was increased, the ratio of a1 : a2 subunit mRNA expression was changed 8-fold in favour of a2 subunit mRNA. (ABSTRACT TRUNCATED)
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PMID:Coming to term with GABA 1008 58

Tropical Australia has an amazing diversity of venomous fauna, from "the world's most venomous creature," the multi-tentacled (chirodropid) box jellyfish Chironex fleckeri, to aggressive spiders whose venom remains to be characterized. All genera of highly venomous Australasian elapid snakes are present, except for tiger snakes. Most notable is the taipan (Oxyuranus scutellatus), with the most efficient "snap-release" biting mechanism of any snake and venom components causing the full constellation of clinical envenoming features: coagulopathy from fibrinogen depletion (procoagulant), neurotoxicity (predominantly presynaptic neurotoxin) and rhabdomyolysis (myotoxin). Brown snakes (Pseudonaja textilis and P. nuchalis) now account for most snake bite fatalities in Australia, as a result of severe coagulopathy and a poorly defined early scenario of collapse, postulated to be caused by profound hypotension caused by transient myocardial dysfunction associated with prothrombin activation. Other venomous entities include paralyzing ticks, the blue-ringed octopus, stone fish and other marine animals with venomous spines, paralyzing cone shells, and a wide range of jellyfish including Carukia barnesi and possibly other four-tentacled (carybdeid) box jellyfish causing the Irukandji syndrome.
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PMID:Clinical toxicology: a tropical Australian perspective. 1068 64

Anaphylactic shock accidents after allergen exposure are frequent. After immunization with ovalbumin (OVA), a common dietary constituent, we evaluated the efficacy of pretreatment with histamine-receptor or serotonin-receptor blockers administered alone or in combination with a nitric oxide synthase inhibitor (L-NAME) on OVA-induced anaphylactic shock in Brown Norway rats. Animals were allocated to the following groups (n = 6 each): control (0.9% saline); diphenydramine (15 mg kg(-1)); cimetidine (20 mg kg(-1)); diphenydramine + cimetidine; dihydroergotamine (50 microg kg(-1)); diphenydramine + cimetidine + dihydroergotamine; L-NAME (100 mg/kg) alone or associated with diphenydramine, cimetidine, diphenydramine + cimetidine, dihydroergotamine, or diphenydramine + cimetidine + dihydroergotamine. Mean arterial blood pressure (MABP), heart rate (HR), and survival time were monitored for 60 min following treatment. The shock was initiated with i.v. OVA. The MABP drop after i.v. OVA was worsened by diphenydramine and was modestly attenuated by cimetidine, dihydroergotamine, or both together. L-NAME potentiated slightly the effects of cimetidine and dihydroergotamine by lessening the initial MABP decrease, but this transient effect was not sufficient to prevent the final collapse or to improve survival time. Decreased vasodilatory (prostaglandins E2), increased vasoconstrictory (thromboxane B2) prostaglandins, and unchanged leukotriene C4 concentrations were contributory to the overall hemodynamic changes. Thus, the combined blockade of vasodilator mediators (histamine, serotonin, and nitric oxide) slowed the MABP drop in anaphylactic shock, but did not improve survival. More studies are needed to understand these discordant effects.
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PMID:Constitutive nitric oxide synthase inhibition combined with histamine and serotonin receptor blockade improves the initial ovalbumin-induced arterial hypotension but decreases the survival time in brown norway rats anaphylactic shock. 1255 48

Quantitative structure toxicity relationship (QSTR) equations were obtained to predict and describe the cytotoxicity of 31 phenols using logLD(50) as a concentration to induce 50% cytotoxicity of isolated rat hepatocytes in 2 h and logP as octanol/water partitioning: logLD(50) (microM)=-0.588(+/-0.059)logP+4.652(+/-0.153) (n=27, r(2)=0.801, s=0.261, P<1 x 10(-9)). Hydroquinone, catechol, 4-nitrophenol, and 2,4-dinitrophenol were outliers for this equation. When the ionization constant pK(a) was considered as a contributing factor a two-parameter QSTR equation was derived: logLD(50) (microM)=-0.595(+/-0.051)logP+0.197(+/-0.029)pK(a)+2.665(+/-0.281) (n=28, r(2)=0.859, s=0.218, P<1 x 10(-6)). Using sigma+, the Brown variation of the Hammet electronic constant, as a contributing parameter, the cytotoxicity of phenols towards hepatocytes were defined by logLD(50) (microM)=-0.594(+/-0.052)logP-0.552(+/-0.085)sigma+ +4.540(+/-0.132) (n=28, r(2)=0.853, s=0.223, P<1 x 10(-6)). Replacing sigma+ with the homolytic bond dissociation energy (BDE) for (X-PhOH+PhO.-->X-PhO.+PhOH) led to logLD(50) (microM)=-0.601(+/-0.066)logP-0.040(+/-0.018)BDE+4.611(+/-0.166) (n=23, r(2)=0.827, s=0.223, P<0.05). Hydroquinone, catechol and 2-nitrophenol were outliers for the above equations. Using redox potential and logP led to a new correlation: logLD(50) (microM)=-0.529(+/-0.135)logP+2.077(+/-0.892)E(p/2)+2.806(+/-0.592) (n=15, r(2)=0.561, s=0.383, P<0.05) with 4-nitrophenol as an outlier. Our findings indicate that phenols with higher lipophilicity, BDE, or sigma+ values or with lower pK(a) and redox potential were more toxic towards hepatocytes. We also showed that a collapse of hepatocyte mitochondrial membrane potential preceded the cytotoxicity of most phenols. Our study indicates that one or a combination of mechanisms; i.e. mitochondrial uncoupling, phenoxy radicals, or phenol metabolism to quinone methides and quinones, contribute to phenol cytotoxicity towards hepatocytes depending on the phenol chemical structure.
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PMID:Quantitative structure toxicity relationships for phenols in isolated rat hepatocytes. 1268 97

Brown spider (Loxosceles genus) venom causes necrotic lesions often accompanied by fever, hemolysis, thrombocytopenia, and acute renal failure. Using mice exposed to Loxosceles intermedia venom, we aimed to show whether the venom directly induces renal damage. The experimental groups were composed of 50 mice as controls and 50 mice that received the venom. Light microscopic analysis of renal biopsy specimens showed alterations including hyalinization of proximal and distal tubules, erythrocytes in Bowman's space, glomerular collapse, tubule epithelial cell blebs and vacuoles, interstitial edema, and deposition of eosinophilic material in the tubule lumen. Electron microscopic findings indicated changes including glomerular epithelial and endothelial cell cytotoxicity as well as disorders of the basement membrane. Tubule alterations include epithelial cell cytotoxicity with cytoplasmic membrane blebs, mitochondrial changes, increase in smooth endoplasmic reticulum, presence of autophagosomes, and deposits of amorphous material in the tubules. We also found that the venom caused azotemia with elevation of blood urea levels but did not decrease C3 complement concentration or cause hemolysis in vivo. Confocal microscopy with antibodies against venom proteins showed direct binding of toxins to renal structures, confirmed by competition assays. Double-staining immunofluorescence reactions with antibodies against type IV collagen or laminin, antibodies to venom toxins, and fluorescent cytochemistry with DAPI revealed deposition of toxins in glomerular and tubule epithelial cells and in renal basement membranes. Two-dimensional electrophoresis showed venom rich in low molecular mass and cationic toxins. By immunoblotting with antibodies to venom toxins on renal extracts from venom-treated mice, we detected a renal binding toxin at 30 kD. The data provide experimental evidence that L. intermedia venom is directly involved in nephrotoxicity.
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PMID:Experimental evidence for a direct cytotoxicity of Loxosceles intermedia (brown spider) venom in renal tissue. 1503 97

In this study we addressed initial laboratory observations of enhanced cardiovascular sensitivity to sodium pentobarbital (PTB) in normotensive Dahl Salt Sensitive rats (SS) compared to Brown Norway (BN) rats. We also used unique consomic (chromosomal substitution) strains to confirm preliminary observations that such differences were related to chromosome 13. Increasing concentrations of PTB were administered sequentially to SS, BN, and SS strains with BN chromosomal substitutions until the point of cardiovascular collapse. Both spontaneous and controlled ventilation were studied. The effect of large (450 microg/mL) and small (35 microg/mL) concentrations of PTB on in situ transmembrane potential of mesenteric arterial vascular smooth muscle (VSM) cells was also measured in these animals with local sympathetic innervation both intact and eliminated. An analysis of variance was used to identify significant differences among groups. Despite virtually identical plasma clearance of PTB, cardiovascular collapse occurred at approximately 35%-45% smaller cumulative doses of administered PTB in SS and other strains compared with BN and SS.13BN (introgression of BN chromosome 13 into an SS) in both spontaneous and controlled ventilation. In neurally intact preparations, large dose PTB-induced VSM hyperpolarization was 4-5 times greater than the small dose in SS and SS.16BN but not in BN and SS.13BN strains. Denervation eliminated this strain difference. These results suggest that enhanced cardiovascular sensitivity to PTB in SS rats is related to greater hyperpolarization of VSM transmembrane potential in resistance vessels and this effect is associated with chromosome 13.
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PMID:Chromosomal substitution-dependent differences in cardiovascular responses to sodium pentobarbital. 1649 31


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