Development transitions of thin filament proteins in rat extraocular muscles.

Extraocular muscles are a unique subset of striated muscles. During postnatal development, the extraocular muscles undergo a number of myosin isoform transitions that occur between postnatal day P10 (P10) and P15. These include: (1) loss of embryonic myosin from the global layer resulting in the expression restricted to the orbital layer; (2) the onset of expression of extraocular myosin and the putative tonic myosin (myh 7b/14); and (3) the redistribution of nonmuscle myosin IIB from a subsarcolemmal position to a sarcomeric distribution in the slow fibers of the global layer. For this study, we examined the postnatal appearance and distribution of α-actinin, tropomyosin, and nebulin isoforms during postnatal development of the rat extraocular muscles. Although sarcomeric α-actinin is detectable from birth, α-actinin 3 appears around P15. Both tropomyosin-1 and -2 are present from birth in the same distribution as in the adult animal. The expression of nebulin was monitored by gel electrophoresis and western blots. At P5-10, nebulin exhibits a lower molecular mass than observed P15 and later during postnatal development. The changes in α-actinin 3 and nebulin expression between P10 and P15 coincide with transitions in myosin isoforms as detailed above. These data point to P10-P15 as the critical period for the maturation of the extraocular muscles, coinciding with eyelid opening.

Postnatal changes in the developing rat extraocular muscles.

PURPOSE: To examine the distribution and timing of expression of nonmuscle myosin IIB (nmMyH IIB) and the extraocular muscle (EOM)-specific myosin (EO-MyHC) during postnatal development of the rat extraocular muscles. METHODS: Whole orbits were collected from postnatal development day (P) 1 through P30 from Sprague-Dawley rats. Samples were analyzed by immunofluorescence microscopy and Western blot to examine the distribution and abundance of nmMyH IIB and EO-MyHC compared with other myosin isoforms and sarcomeric α-actinin. Polyclonal antibodies were produced to specifically detect EO-MyHC. Postnatal limb muscles were used as control. RESULTS: Analysis of EOM morphology in the developing orbits indicates that the global and orbital layers are not evident until day P15. The distribution of nmMyH IIB changes between days P10 and P15 from a subsarcolemma distribution to an intrafiber distribution in the global layer. EO-MyHC appears by day p15, primarily in the orbital layer of the EOMs. Sarcomeric α-actinin was equally abundant in the EOMs at all stages. Fetal MyHC was the predominant isoform at day P1 but slowly diminished in abundance with age in a layer-specific manner. CONCLUSIONS: These data demonstrate that significant changes occur in the EOMs from P10 to P15 and suggest that visual stimulation may play a role in the signals that regulate both nmMyH IIB and EO-MyHC developmental transitions. The pronounced distinctions of the orbital and global layers occurring by P15 establish the adult morphologic phenotype of the muscle.

Reconstruçäo arterial com tubo de pericárdio bovino corrugado / Arterial reconstruction with corrugated bovine pericardial conduit

No período de agosto de 1989 a fevereiro de 1992, 32 pacientes foram submetidos a reconstruçoes vasculares utilizando-se condutos de pericárdio bovino corrugado preservado em glutaraideído. A incorporaçao do principio crimping utilizado nas próteses vasculares sintéticas proporcionou tubos que mantêm sua forma cilíndrica, mesmo quando submetidos a curvaturas. Vinte e nove pacientes (Grupo I) eram portadores de doenças da aorta torácica e/ou abdominal, incluindo aneurismas, dissecçoes agudas, coarctaçao da aorta e lesao oclusiva aorto-ilíaca. A reconstruçao da aorta torácica foi realizada em 25 pacientes (incluindo a substituiçao da valva aórtica em 10), da aorta abdominal em 2 e aorto-ilíaca em 2. Três pacientes (Grupo II), portadores de cardiopatias congênitas complexas, foram submetidos a reconstruçao da via de saida do ventrículo direito em 2 e a operaçao de Fontan em 1. A mortalidade hospitalar no Grupo I foi 24 por cento (7 pacientes), causada por baixo débito cardíaco em 4, recidiva precoce da dissecçao em dois e infecçao respiratória em 1. Seis destes óbitos ocorreram em pacientes operados na fase aguda de dissecçao aórtica. Nao houve nenhum óbito no Grupo II. Houve um óbito tardio no Grupo I devido a complicaçoes metabólicas relacionadas a diabetes e insuficiência renal crônica. Esta experiência clínica inicial registrou um seguimento médico de 16 meses por paciente, com um máximo de 32 meses e nao se verificou nenhuma complicaçao tardia relacionada ao conduto de pericárdio bovino corrugado.