ABSTRACT Luxation of the temporomandibular joint (TMJ) in horses, despite being an uncommon condition, is often associated with local trauma involving the head. Its clinical importance is mainly related to the painful injury and impairment of the multiple movements involved in chewing and breaking foods. The objective of the current work is to describe the manual reduction technique of TMJ dislocation in a 6-year-old Mangalarga Marchador stallion with a history of inability to close the oral cavity and lateral displacement of the mandible. In the radiographic and ultrasonographic evaluation of the region a rostral displacement of the mandibular condyle was observed. Manual reduction was effective with the patient under dissociative anesthesia, progressing to medical discharge within 12 days.

RESUMO A luxação da articulação temporomandibular (ATM) dos equinos, apesar de ser uma condição incomum, tem sua importância clínica principalmente relacionada à injúria dolorosa e ao prejuízo dos movimentos múltiplos envolvidos na mastigação e na quebra dos alimentos. Assim, o presente trabalho tem como objetivo descrever a técnica de redução manual da luxação de ATM em um equino. Foi atendido um garanhão Mangalarga Marchador, de 6 anos de idade, com histórico de incapacidade de fechamento da cavidade oral e de deslocamento lateral da mandíbula. Nas avaliações radiográfica e ultrassonográfica da região, observou-se deslocamento rostral do côndilo da mandíbula. A redução manual foi eficaz, com o paciente sob anestesia dissociativa, com progressão para a alta médica em 12 dias.

Previous studies have shown that exogenously generated nitric oxide (NO) inhibits smooth muscle cell proliferation. In the present study, we stimulated rabbit vascular smooth muscle cells (RVSMC) with E. coli lipopolysaccharide (LPS), a known inducer of NO synthase transcription, and established a connection between endogenous NO, phosphorylation/dephosphorylation-mediated signaling pathways, and DNA synthesis. Non-confluent RVSMC were cultured with 0, 5, 10, or 100 ng/ml of the endotoxin. NO release was increased by 86.6% (maximum effect) in low-density cell cultures stimulated with 10 ng/ml LPS as compared to non-stimulated controls. Conversely, LPS (5 to 100 ng/ml) did not lead to enhanced NO production in multilayered (high density) RVSMC. DNA synthesis measured by thymidine incorporation showed that LPS was mitogenic only to non-confluent RVSMC; furthermore, the effect was prevented statistically by aminoguanidine (AG), a potent inhibitor of the inducible NO synthase, and oxyhemoglobin, an NO scavenger. Finally, there was a cell density-dependent LPS effect on protein tyrosine phosphatase (PTP) and ERK1/ERK2 mitogen-activated protein (MAP) kinase activities. Short-term transient stimulation of ERK1/ERK2 MAP kinases was maximal at 12 min in non-confluent RVSMC and was prevented by preincubation with AG, whereas PTP activities were inhibited in these cells after 24-h LPS stimulation. Conversely, no significant LPS-mediated changes in kinase or phosphatase activities were observed in high-density cells. LPS-induced NO generation by RVSMC may switch on a cell density-dependent proliferative signaling cascade, which involves the participation of PTP and the ERK1/ERK2 MAP kinases.