Showing papers by "University of Arkansas for Medical Sciences published in 1975"
TL;DR: Experimental data suggest that the ointment globules are entrapped within the wound exudates and lodged below the plane of the corneal surface, and no treatment is necessary since the globules will be extruded within the next 24 to 48 hours even if the pressure dressing is continued.
Abstract: A previously unrecognized characteristic clinical entity, "pseudoentrapment of ointment in the cornea" may occur in corneal lesions that have (1) topical application of ointments to the corneal lesion, (2) application of a firm pressure dressing, and (3) stromal loss or distortion of its normal architecture that allows for ointment globules to lie below the corneal surface. The clinical picture is that of a cluster of large ointment globules lodged within the corneal defect. Experimental data suggest that the ointment globules are entrapped within the wound exudates and lodged below the plane of the corneal surface. No treatment is necessary since the globules are extruded within the next 24 to 48 hours even if the pressure dressing is continued. Pseudoentrapment of ointment in the cornea is compared with and differentiated from corneal ointment entrapment and corneal spheroidal degeneration.
6 citations
TL;DR: It is concluded that nicotine activates a viscerosomatic reflex by exciting sensory receptors in the cardiopulmonary region and that α motor depression results independent of the changes in γ activity.
Abstract: The effects of nicotine on the stretch reflex and on electrically induced monosynaptic and cutaneous polysynaptic reflex responses at a lumbosacral level were studied in lightly anesthetized (chloralose-urethane) cats in which the regional fusimotor-spindle loops had been interrupted by ventral rhizotomy. Doses of 15-40 mug/kg injected into the superior vena cava or the right atrium produced depression of the reflex responses in extensor and flexor alpha motoneurons after latent periods of 1-3 sec, while gamma activity was initially accelerated. The early phase of this alpha depression was abolished by bilateral vagotomy. Sebacylcholine (a nicotinic agent) and acetylcholine also caused depression of evoked alpha activity in the absence of spindle feedback. It is concluded that nicotine activates a viscerosomatic reflex by exciting sensory receptors in the cardiopulmonary region and that alpha motor depression results independent of the changes in gamma activity. However, alpha depression with delayed onset can still be elicited by nicotine after vagotomy and Renshaw blockade, and this effect is also duplicated by sebacylcholine and abolished by hexamethonium. In the doses used, spindle or skin afferents were not excited by nicotine. Thus, two more mechanisms are described by which nicotine can depress alpha activity. Both are reflex in nature, one implicating vagal, the other nonvagal peripheral receptors.
2 citations