Effect of biogenic amine-receptor antagonists on paw edema induced by <i>Micrurus lemniscatus</i> venom.

<p>Groups of animals were treated with promethazine (5 mg/kg, i.p.) (an H₁ receptor antagonist), thioperamide (5 mg/kg, i.p.) (an H₃R/H₄R receptor antagonist) or methysergide (5 mg/kg, i.p.) (a nonselective 5-HT receptor antagonist) 30 min before intraplantar injection of MLV (5 μg/paw). The increase in volume of each paw (edema) was measured using a plethysmometer. Data were calculated as the difference between both paws and are expressed as a % increase in paw volume. Values are the mean ± SEM of five animals. * <i>p</i> < 0.05 compared with control group.</p

Participation of mast cells (MCs) in paw edema induced by <i>Micrurus lemniscatus</i> venom.

<p>(A) Groups of rats were treated with compound 48/80 (0.1 to 5.0 mg/mL i.p. twice a day for 5 consecutive days) or an equal volume of vehicle i.p. (control) before MLV injection (5 μg/paw). Edema was evaluated using a plethysmometer at the time points shown. Data are expressed as % increase in paw volume compared with the control paw. (B) Degranulation of mesenteric mast cells was assessed 15 min after venom injection by counting the percentage of cells with extruded granules in the histological preparation. (C, D) Toluidine blue staining of mesenteric mast cells treated with apyrogenic saline (C) or MLV (2.8 μg/g) (D). The mesentery had minimal mast cell degranulation after i.p. injection with apyrogenic saline and extensive mast cell degranulation after injection with MLV. Values are the mean ± SEM of five animals. * <i>p</i> < 0.05 compared with control group.</p

Effect of bradykinin BK₂-receptor antagonist (HOE 140) on paw edema induced by <i>Micrurus lemniscatus</i> venom.

<p>Groups of animals were treated with HOE 140 (5 μg/paw) concomitantly with MLV (5 μg/paw, i.pl.). The increase in volume of each paw (edema) was measured using a plethysmometer. Results were calculated as the difference between hind paws and are expressed as a % increase in paw volume. Values are the mean ± SEM of five animals. None of the results were statistically significant.</p

Time course of rat paw edema induced by selected doses of <i>Micrurus lemniscatus</i> venom.

<p>Increased paw volume was determined at various time points after intraplantar injection of MLV (1–10 μg/paw) into one paw and apyrogenic saline into the contralateral paw (control paw). The increase in volume of each paw (edema) was measured using a plethysmometer. Differences between paws were expressed as a % increase in paw volume. Values are the mean ± SEM of five animals. * <i>p</i> < 0.05 compared with MLV (1 μg/paw).</p

Effect of capsaicin and tachykinin NK₁- and NK₂-receptor antagonists (SR14033 and SR 48968, respectively) on edema induced by <i>Micrurus lemniscatus</i> venom.

<p>Groups of animals were treated with capsaicin (15, 30 and 50 mg/kg, s.c.) for 4 consecutive days to deplete substance P from sensitive primary afferent neurons or NK₁- or NK₂ receptor antagonists. Both SR 140333 (1 nmol/paw) and SR 48968 (10 nmol/paw) were co-injected i.pl. with MLV (5 μg/paw). The increase in volume of each paw (edema) was measured using a plethysmometer. Results were calculated as the difference between hind paws and are expressed as a % increase in paw volume. Values are the mean ± SEM of five animals. * p < 0.05 compared with control group.</p

Participation of mast cells (MCs) in paw edema induced by <i>Micrurus lemniscatus</i> venom.

<p>(A) Groups of rats were treated with compound 48/80 (0.1 to 5.0 mg/mL i.p. twice a day for 5 consecutive days) or an equal volume of vehicle i.p. (control) before MLV injection (5 μg/paw). Edema was evaluated using a plethysmometer at the time points shown. Data are expressed as % increase in paw volume compared with the control paw. (B) Degranulation of mesenteric mast cells was assessed 15 min after venom injection by counting the percentage of cells with extruded granules in the histological preparation. (C, D) Toluidine blue staining of mesenteric mast cells treated with apyrogenic saline (C) or MLV (2.8 μg/g) (D). The mesentery had minimal mast cell degranulation after i.p. injection with apyrogenic saline and extensive mast cell degranulation after injection with MLV. Values are the mean ± SEM of five animals. * <i>p</i> < 0.05 compared with control group.</p

Mechanisms involved in hearing disorders of thyroid ontogeny: a literature review

<div><p>ABSTRACT Endocochlear, retrocochlear and/or central origin hearing damage may be related to the absence of appropriate levels of thyroid hormone during morphogenesis and/or auditory system development. Hearing disorders related to the thyroid are not well studied, despite speculation on the pathophysiological mechanisms. The objective of this review was to characterize the main pathophysiological mechanisms of congenital hypothyroidism and to evaluate the relationship with central and peripheral hearing disorders. We conducted a literature review using the databases MedLine, LILACS, Cochrane Library, SciELO, Institute for Scientific Information (ISI), Embase, and Science Direct between July and September on 2016. We identified the studies that address hearing disorder mechanisms on the congenital hypothyroidism. Congenital hypothyroidism may have clinical and subclinical manifestations that affect the auditory system and may be a potential risk factor for hearing impairment. Hearing impairment can severely impact quality-of-life, which emphasizes the importance of monitoring and evaluating hearing during the clinical routine of these patients.</p></div