Estudo anatômico da via de acesso suprapatelar lateral para a haste intramedular bloqueada na fratura da tíbia

OBJETIVO: A haste intramedular (HIM) é o padrão ouro no tratamento das fraturas diafisárias da tíbia. Uma das complicações frequentes é a dor no joelho após o procedimento. MÉTODOS: Vias alternativas, como a suprapatelar para a introdução da haste como opção para evitar a dor no joelho no período pós-operatório tardio, têm sido estudadas. A questão é se nesta nova via ocorre alguma lesão às estruturas intra-articulares do joelho. RESULTADOS: Este estudo analisa a via suprapatelar e o risco para as estruturas adjacentes através da sua reprodução em 10 joelhos de cinco cadáveres. CONCLUSÃO: Foi visto facilidade para a localização do ponto de entrada por esta via, lesando apenas a gordura de Hoffa. Em três dos nossos casos houve lesão da superfície condral, sendo um obstáculo de difícil transposição e indicando necessidade de fabricação de material específico para minimizar a lesão das estruturas intra-articulares por essa via.

Influence of apical foramen lateral opening and file size on cemental canal instrumentation

Since instrumentation of the apical foramen has been suggested for cleaning and disinfection of the cemental canal, selection of the file size and position of the apical foramen have challenging steps. This study analyzed the influence of apical foramen lateral opening and file size can exert on cemental canal instrumentation. Thirty-four human maxillary central incisors were divided in two groups: Group 1 (n=17), without flaring, and Group 2 (n=17), with flaring with LA Axxess burs. K-files of increasing diameters were progressively inserted into the canal until binding at the apical foramen was achieved and tips were visible and bonded with ethyl cyanoacrylate adhesive. Roots/files set were cross-sectioned 5 mm from the apex. Apices were examined by scanning electron microscopy at ×140 and digital images were captured. Data were analyzed statistically by Student’s t test and Fisher’s exact test at 5% significance level. SEM micrographs showed that 19 (56%) apical foramina emerged laterally to the root apex, whereas 15 (44%) coincided with it. Significantly more difficulty to reach the apical foramen was noted in Group 2. Results suggest that the larger the foraminal file size, the more difficult the apical foramen instrumentation may be in laterally emerged cemental canals.

Facilitation of sodium intake by combining noradrenaline into the lateral parabrachial nucleus with prazosin peripherally

Injections of noradrenaline into the lateral parabrachial nucleus (LPBN) increase arterial pressure and 1.8% NaCl intake and decrease water intake in rats treated with the diuretic furosemide (FURO) combined with a low dose of the angiotensin converting enzyme inhibitor captopril (CAP). In the present study, we investigated the influence of the pressor response elicited by noradrenaline injected into the LPBN on FURO+CAP-induced water and 1.8% NaCl intake. Male Holtzman rats with bilateral stainless steel guide-cannulas implanted into LPBN were used. Bilateral injections of noradrenaline (40 nmol/0.2 μl) into the LPBN increased FURO+CAP-induced 1.8% NaCl intake (12.2±3.5, vs., saline: 4.2±0.8 ml/180 min), reduced water intake and strongly increased arterial pressure (50±7, vs. saline: 1±1 mmHg). The blockade of the α1 adrenoceptors with the prazosin injected intraperitoneally abolished the pressor response and increased 1.8% NaCl and water intake in rats treated with FURO+CAP combined with noradrenaline injected into the LPBN. The deactivation of baro and perhaps volume receptors due to the cardiovascular effects of prazosin is a mechanism that may facilitate water and NaCl intake in rats treated with FURO+CAP combined with noradrenaline injected into the LPBN. Therefore, the activation of α2 adrenoceptors with noradrenaline injected into the LPBN, at least in dose tested, may not completely remove the inhibitory signals produced by the activation of the cardiovascular receptors, particularly the signals that result from the extra activation of these receptors with the increase of arterial pressure.