Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The accumulated data on combined OC (oral contraceptive) use makes it possible to assess with accuracy the longterm risk associated with such use. The risks for young women are low. Risks rise with age and such factors as smoking, hypertension, diabetes, and hyperlipidemia. Women over 35, especially smokers, are at considerable risk of vascular disease. There are small risks of liver, endometrial, and cervical neoplasms, increasing with use and other risk factors. Diabetes may be accelerated. There is also a risk of depression in susceptible patients. For oral and injectable progestagen-only contraceptives, the risks are reasonably well documented in the short- but not the longterm. With progestagen-only minipills, the risks other than that of pregnancy are low. Injectable progestagen may cause anaphylaxis at the time of injection.
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PMID:The long term safety of hormonal steroid contraceptives. 724 46

We studied the effects of a nitric oxide synthase (NOS) inhibitor, N omega-nitro-L-arginine-methyl ester (L-NAME), on cardiac depression and bronchospasm provoked by systemic anaphylaxis in vivo in rabbits. Animals pretreated with L-NAME showed lower survival rates than control animals pretreated with normal saline. The survival rate in L-NAME-pretreated animals was increased by the administration of L-arginine after initiation of anaphylaxis. Cardiac output fell significantly in animals pretreated with L-NAME compared with controls, although venous return was increased. In animals pretreated with L-NAME, pulmonary resistance was significantly increased, and administration of arginine attenuated the bronchospasm. In conclusion, these results, along with the low survival rates in the L-NAME-treated animals, suggest that NO production may be beneficial to cardiac depression and bronchospasm in anaphylaxis in vivo.
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PMID:Nitric oxide synthase inhibition is detrimental to cardiac function and promotes bronchospasm in anaphylaxis in rabbits. 749

We investigated whether a nitric oxide synthase (NOS) inhibitor improves cardiovascular depression associated with anaphylaxis. After induction of anaphylactic circulatory depression, one group received an NOS inhibitor (Group I, n = 6) and the other received saline solution (Group II, n = 5). Mean arterial pressure and right atrial pressure were significantly higher in Group I than in Group II. Hematocrit was significantly lower in Group I than in Group II. Cardiac output, stroke volume, mean pulmonary arterial pressure, the maximum rate of increase in left ventricular pressure, and the time constant of the fall in isovolumic left ventricular pressure did not differ between the groups. In conclusion, L-NAME attenuates hypotension, but does not improve cardiac depression in anaphylaxis in dogs. Our finding that NOS inhibitor did not improve cardiac function implies that the production of NO in anaphylaxis may have a protective effect with regard to cardiac performance.
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PMID:An inhibitor of nitric oxide synthase, N omega-nitro-L-arginine-methyl ester, attenuates hypotension but does not improve cardiac depression in anaphylaxis in dogs. 765 70

Nitric oxide, synthesized from the guanidino group of L-arginine by nitric oxide synthase, has an important role in pathophysiological changes associated with anaphylaxis. Nitric oxide production due to activation of constitutive nitric oxide synthase is detected using a nitric oxide-selective electrode in anaphylactic rabbits in vivo. A nitric oxide synthase inhibitor attenuates hypotension and hemoconcentration and decreases venous return but does not improve cardiac depression. Nitric oxide functionally antagonizes the effects of vasoconstrictors released by anaphylaxis in vitro. In animals pretreated with a nitric oxide synthase inhibitor, the cardiac output falls significantly, although venous return is increased. Pulmonary resistance is significantly increased with a nitric oxide synthase inhibitor, and L-arginine attenuates the bronchospasm. These findings suggest that production of nitric oxide may reduce the pathophysiologic changes, except for vasodilatation, associated with anaphylaxis.
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PMID:Role of nitric oxide in anaphylactic shock. 857 13

Rats of the Flinders sensitive line (FSL, selectively bred for their increased cholinergic activity and used as a genetic animal model of depression) were compared with their control counterparts, the Flinders resistant line, for their susceptibility to anaphylaxis and the response of small intestinal tissues to the muscarinic agonist, bethanechol. Following sensitization to ovalbumin (OA), rats of both lines were challenged in vivo either with 3 mg OA i.p. or with saline. In spite of the absence of line-related differences in IgE titers, FSL rats were more susceptible to the induction of anaphylactic shock as evidenced by (1) more pronounced mast cell degranulation; (2) a greater drop in rectal temperature; (3) higher hematocrit values; and (4) changes in gut function characterized by an elevation of basal short-circuit current and increased conductance (indicating increases in transport tone and permeability) of the tissues mounted in Ussing chambers. Thus, this study provides further evidence for a common cholinergic mechanisms in susceptibility to both allergies and depression.
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PMID:Immediate hypersensitivity in the Flinders rat: further evidence for a possible link between susceptibility to allergies and depression. 859 Aug 17

Echinococcosis is a human disease caused by the larval form of Taenia echinococcus, which lives in the gut of the dog, wild canides and other carnivorous animals which represent the definitive hosts and involves as intermediate hosts both domestic and wild animals. Humans become accidental intermediate hosts by ingesting Taenia eggs. The main species pathogenic for man are E granulosus causing cystic echinococcosis with worldwide distribution and endemic in sheep and cattle breeding countries, and E multilocularis causing alveolar echinococcosis, with preferential distribution in the northern hemisphere. After ingestion of contaminated food, hexacanth embryos migrate by the portal system to liver and later lung, brain and other tissues. Symptoms are related to both cyst location and size. E granulosus infection of the central nervous system (CNS) may be primary or secondary and has been estimated to be low (2%). Sharply demarcated, spherical and intraparenchymal, cysts may reach a large size causing neurological symptoms. Spilling of cyst fluid due to trauma or surgery may trigger anaphylaxis as well as disseminated infection. Host reaction is minimal in the brain but a foreign giant cell reaction may develop. E multilocularis develops within the liver as a rapid invasive pseudomalignant growth and may metastasize to the CNS, where estimated incidence reaches 5%. Hydatid antigens induce an immune reaction in the host which is helpful for the diagnosis. DNA probes and PCR may be applied to differentiate between Echinococcus spp. Although the host develops an immunological protection from reinfection, the parasite evades host immune attack. A wide range of evasion mechanisms have been advanced, including a barrier for host cells due to hydatid cyst laminated cuticle, polyclonal activation of lymphocytes by parasite soluble antigens, and depression of host cell immune responses. Chronic stimulation of the host by cyst fluid antigens leads to increased specific IgG4 production, which might act as blocking antibodies against anaphlaxis suggestive of host response immunomodulation.
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PMID:Echinococcosis. 903 73

We investigated whether an inhibitor of poly(adenosine 5'-diphosphoribose) synthetase (PARS) is beneficial in anaphylaxis. Twenty-eight rabbits were randomly allocated to three groups: Group I (control) received .9% NaCl solution 10 min before antigen challenge followed by the infusion of the same solution. Group II (3-aminobenzamide 20 mg.kg-1) received 20 mg.kg-1 of 3-aminobenzamide (a PARS inhibitor) 10 min before antigen challenge followed by the continuous infusion of 20 mg.kg-1 of 3-aminobenzamide. Group III received 40 mg.kg-1 10 min before antigen challenge followed by the continuous infusion of 20 mg.kg-1 of 3-aminobenzamide. Survival were similar between three groups. Heart rate, mean arterial pressure (MAP), central various pressure, and pulmonary resistance did not differ between three groups. Dynamic pulmonary compliance did not differ in the early phase after the antigen challenge; however, it was significantly lower in Group III than in Groups I and II 15 min after the initiation of anaphylaxis. 3-aminobenzamide per se did not affect heart rate, MAP, central venous pressure, pulmonary resistance, or dynamic pulmonary compliance in animals without systemic anaphylaxis. In conclusion, this PARS inhibitor did not improve cardiovascular depression or bronchospasm in the early phase of systemic aggregated anaphylaxis in rabbits in vivo, implying that the pathophysiological changes associated with systemic anaphylaxis may not be related to activation of an energy-consuming DNA repair cycle triggered by PARS.
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PMID:An inhibitor of poly(adenosine 5'-diphosphoribose) synthetase, 3-aminobenzamide, does not improve cardiovascular depression, bronchospasm, or survival associated with systemic anaphylaxis in rabbits in vivo. 926 9

In anaphylactic shock (AS), the relative effects of the autacoids including histamine, prostaglandins, and leukotrienes on causing cardiovascular collapse and the extent to which receptor blocking agents and pathway inhibitors may prevent this collapse are not clear. In a ragweed model of anaphylaxis, we examined whether pretreatment with H1, H2, H3 receptor blockers, and cyclooxygenase and leukotriene pathway inhibitors was useful in preventing the depression in left ventricular (LV) contractility known to occur in this model. The dose of allergen was varied to produce similar degrees of shock between treatments. The animals were studied under pentobarbital anesthesia in which the treatment studies were approximately 3 wk apart. LV volumes were measured by sonomicrometric techniques. During challenge, mean arterial blood pressure (Pa), cardiac output (Q), and LV end-diastolic pressure (LVEDP) decreased approximately 50% compared with preshock values in all treatments. Histamine H3 receptor blockade was associated with higher heart rates (HR) and higher stroke work (SW) (p < 0.05) as compared with the other treatment studies. We conclude that histamine H3 activation by inhibiting adrenergic neural norepinephrine release contributes to cardiovascular collapse in AS.
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PMID:Histamine H3 receptor blockade improves cardiac function in canine anaphylaxis. 1050

A generalized allergic reaction to or anaphylaxis from honeybee sting may involve the skin with erythema, puritus, urticaria, or angioedema; the respiratory tract with laryngeal edema, and brochospasm; the cardiovascular system with myocardial depression, hypotension, and shock; and the gastrointestinal system with nausea, vomiting, and incontinence. Acute pulmonary hemorrhage following a honeybee sting has never been reported. We describe a previously healthy 14-year-old girl who developed acute pulmonary hemorrhage, hypotension, and generalized skin rash after a single honeybee sting on her right fourth finger. Her serum immunoglobulin E (IgE) was high (360 IU/mL). Chest X-ray revealed perihilar alveolar infiltrative lesions. Metabolic acidosis and hypoxemia were also found. After treatment with antihistamines, dopamine, corticosteroids, bronchodilaters, fluid replacement, and mechanical ventilation, her condition improved dramatically. A hypersensitivity reaction to honeybee venom is the most likely explanation for this unusual case of acute pulmonary hemorrhage.
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PMID:Acute pulmonary hemorrhage following a honeybee sting: a case report. 1059 91

Recent studies demonstrate that vasopressin is useful when treating hemorrhagic and septic shock. The effect of vasopressin on systemic anaphylaxis has not been investigated except in clinical case reports. Vasopressin increases blood pressure because of vasoconstriction through the V1 receptor. Thus, we evaluated the effect of vasopressin on circulatory depression and bronchoconstriction provoked by systemic anaphylaxis and survival rates in rabbits. In the first set of experiments, 15 nonsensitized rabbits received normal saline (control) and vasopressin at 0.8 or 0.08 U/kg. In the second set, 40 sensitized rabbits received horse serum to induce anaphylaxis, and then received the same drugs as in the first set. In the first set, mean arterial pressure (MAP) in vasopressin groups increased by 18% to 24% compared with the control. Vasopressin at 0.8 U/kg decreased MAP insignificantly before the increases of MAP occurred. In the second set, vasopressin at 0.08 U/kg improved the survival rate. At 45 min after antigen challenge, 69% of the rabbits that received vasopressin at 0.08 U/kg were alive, whereas 29% of the control rabbits and 23% of the rabbits that received vasopressin at 0.8 U/kg were alive. Vasopressin increased MAP by 36% to 109% compared with the control within 5 min, however, at 2 min, vasopressin at 0.8 U/kg had no effect on MAP. Pulmonary dynamics were similar. In conclusion, vasopressin at 0.08 U/kg improved survival rates and severe hypotension provoked by systemic anaphylaxis, suggesting that this agent may be useful in the treatment of systemic anaphylaxis.
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PMID:Vasopressin may be useful in the treatment of systemic anaphylaxis in rabbits. 1613 66


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