ABSTRACT
It has been established that beyond middle age, mice are slower to recover inner retinal function following an acute intraocular pressure (IOP) injury. While 3 month old animals exhibit near-complete recovery 1 week following injury, 12 and 18 month old animals demonstrate prolonged inner retinal dysfunction. In this study we aim to determine whether age-related differences in functional recovery of the inner retina are due to differences in retinal ganglion cell (RGC) axonal transport. C57BL/6J mice at 3 (n = 8) and 18 months (n = 8) of age were used. At day 0, right eyes were cannulated and the IOP was maintained at 50 mmHg for 30 min. At day 5, mice received bilateral intravitreal injections of choleratoxin subunit B (CTB) conjugated to Alexafluor 488. At day 7, mice were euthanized and tissue was collected. Axonal transport of CTB was quantified in retinas and superior colliculi (SC) using fluorescent microscopy. In response to IOP elevation, the overall degree of axonal transport was comparable between young and old mice. Furthermore, no differences in axonal transport were detected between control eyes and injured in mice at any age. In conclusion, impaired recovery of inner retinal function 1 week following acute IOP injury in old mice is not associated with changes in active axonal transport in RGCs at this time.
Subject(s)
Aging/physiology , Axonal Transport/physiology , Optic Nerve Injuries/physiopathology , Recovery of Function/physiology , Retinal Diseases/physiopathology , Retinal Ganglion Cells/physiology , Animals , Disease Models, Animal , Electroretinography , Intraocular Pressure/physiology , Mice , Mice, Inbred C57BLABSTRACT
This paper follows up a previous paper reported in this journal. This study was a single-blind parallel comparison of naproxen sodium ("Synflex") and a paracetamol/dextropropoxyphene combination ("Distalgesic"). It was carried out in 184 patients suffering from soft-tissue disorders recruited from four centres. More patients were considered cured and the pain score was significantly lower after seven days' treatment in the naproxen sodium ("NS") group. For those patients who received 14 days' treatment the total symptom score was significantly lower in the naproxen sodium group at the end of treatment. Two patients in the NS treatment group withdrew from the study due to lack of efficacy. Fewer side-effects were reported in the NS group. Of the eight patients stopping treatment due to side-effects, two were in the naproxen sodium group and six in the paracetamol/dextropropoxyphene ("control") group. The results suggest that a better clinical response to treatment and fewer side-effects may be obtained with naproxen sodium than with paracetamol/dextropropoxyphene in the treatment of soft-tissue injuries.
Subject(s)
Acetaminophen/therapeutic use , Athletic Injuries/drug therapy , Bone Diseases/drug therapy , Dextropropoxyphene/therapeutic use , Muscular Diseases/drug therapy , Naproxen/therapeutic use , Acetaminophen/adverse effects , Acute Disease , Adult , Dextropropoxyphene/adverse effects , Drug Combinations , Female , Humans , Male , Naproxen/adverse effectsABSTRACT
Ninety-eight patients were admitted to a single-blind parallel study comparing the efficacy of naproxen sodium with a paracetamol/dextropropoxyphene combination in the treatment of soft-tissue disorders. The two study groups were well matched in all respects. After seven days of treatment patients in the naproxen sodium group had less residual symptoms and more of them were considered cured. These patients also had a significantly lower mean-pain-score, tended to have less daily symptoms and recorded a significantly greater initial improvement in their condition. Fewer side-effects were recorded by the naproxen sodium-treated patients. One patient from each group withdrew from the study because of side-effects. It was concluded that in the treatment of non-articular soft-tissue disorders the use of a rapidly-acting withdrew anti-inflammatory drug, naproxen sodium, gave a better clinical response than did treatment with a simple analgesic combination.
Subject(s)
Acetaminophen/administration & dosage , Athletic Injuries/drug therapy , Contusions/drug therapy , Dextropropoxyphene/administration & dosage , Naproxen/therapeutic use , Sprains and Strains/drug therapy , Adult , Clinical Trials as Topic , Drug Combinations , Female , Humans , Male , Tendinopathy/drug therapy , Tenosynovitis/drug therapyABSTRACT
Vasoconstriction occuring a unventilated or hypoxic lung was studied in dogs and cats to elucidate mechanisms which both cause and reverse it. Lungs were perfused in vivo at constant pressure or constant blood flow; alternatively blood flow and pressure were measured with minimal operative interference. Stimulus-response curves of lung vessels to hypoxia showed a large response within the physiological range of P02 values. Vasoconstriction in unventilated lung caused by bronchial occlusion sometimes matched that caused by an equal degree of ventilation hypoxia but was sometimes greater. Responses to both stimuli varied widely between animals and in one animal at different times. This could be due to variable availability of a transmitter or variable presence of vasodilator substances. Both histamine and beta-adrenoreceptor stimulants caused pulmonary vasodilatation in unventilated lung. Histamine caused pulmonary vasoconstriction and vasodilatation in different circumstances which could be blocked respectively by H1 and H2 antihistamine drugs. Potent alpha- and beta-adrenoreceptor action on pulmonary vessels was demonstrated in both species. Alpha-adrenoreceptor blocking drugs caused dilatation and beta-adrenoreceptor blocking drugs caused vasoconstriction. The possible role of histamine and catecholamines in causing or reversing hypoxic vasoconstriction or in maintaining pulmonary vascular tone is discussed.