Traumatic blepharoptosis, although considered relatively rare, is an entity which demands recognition if one is to achieve optimal results. Reports of levator injury following orbital, ocular, and adnexal surgery, as well as in cataract and blepharoplasty procedures, are well described. In most cases eventuating in complete ptosis, levator disinsertion is the anatomic correlate, the ptosis is usually permanent, and surgical intervention is often indicated. We have observed two cases of transient, complete post-traumatic ptosis which have recovered by 6 weeks with expectant management. We believe this entity to be more pervasive than the current literature seems to reflect and emphasis is placed on nonoperative therapy. This paper reviews the anatomical considerations relevant to the function of the levator complex as well as the possible mechanisms for its injury.
A porcine myocutaneous flap model was utilized to assess the development of denervation adrenergic hypersensitivity and to determine the effects of the alpha-adrenergic blocking agent--phenoxybenzamine--on flap blood perfusion. During intravenous administration of norepinephrine, blood flow to the flaps and control skin was monitored simultaneously, using laser Doppler velocimetry and dermofluorometry. A relative decrease in myocutaneous flap blood flow, as compared to control skin in response to norepinephrine infusion, was observed at between 2 and 7 days following flap elevation. This is the same time period during which norepinephrine content of skin flaps is diminished, and suggests development of an increased sensitivity to adrenergic stimulation. Administration of phenoxybenzamine blunted norepinephrine-induced pressor responses and blocked development of adrenergic hypersensitivity in the porcine myocutaneous flap model. Phenoxybenzamine significantly increased flap blood perfusion (as measured by dermofluorometry).
In anesthetized dogs, the diuretic furosemide has been shown to increase renal blood flow, an effect which can be blocked by the prostaglandin synthetase inhibitor, indomethacin (1, 2). Furosemide also caused an increase in PGE2 release into renal venous blood and this increase was inhibited by indomethacin (2). These data suggest a relationship between the hemodynamic effect of furosemide and the renal prostaglandins.PGE2 is a vasodilator in the dog kidney; however, Malik and MgGiff (3) demonstrated that this prostaglandin increases renal vascular resistance in the rat. This apparent species difference between the rat and other mammals (4) offers a potential tool for elucidating the relationship between furosemide and PGE2 on renal hemodynamics. If the action of furosemide to dilate the renal vasculature in dogs is dependent on release of PGE2, and if PGE2 is a vasoconstrictor in rats, then furosemide would be expected to decrease renal blood flow in the rat. Alternatively, if the primary effect of furosemide is to produce hemodynamic changes which secondarily influence prostaglandin synthesis, furosemide might increase renal blood flow in rats as it does in dogs.The purpose of this investigation was to determine the effect of furosemide on renal vascular resistance and to elucidate the interactions between this diuretic and PGE2 in isolated perfused rat kidneys. Since the reninangiotensin system may also influence the renal vasculature, experiments were performed to evaluate interactions between this system and PGE2 and furosemide.Methods. All experiments were performed on kidneys obtained from male, Sprague-Dawley rats (Spartan Research Animals, Inc., Haslett, MI) weighing 300-375 g. Rats were ' Supported in part by USPHS Grant Nos. AM 10913 Medical Student Research Fellow of the Michigan and HD 06290. Heart Association.anesthetized with 50 mg/kg sodium pentobarbital, intraperitoneally. The abdomen was opened by a midline incision and the right kidney, the right renal artery, and the abdominal aorta were exposed. All rats received 3 mg of heparin via the femoral vein five minutes prior to cannulation of the inferior vena cava. The right ureter and the inferior vena cava were cannulated for collection of urine and venous effluent, respectively. Following cannulation of the right renal artery, perfusion with modified Tyrode's solution containing 1% inulin and saturated with a 95% 02-5% C02 mixture was immediately initiated using a Harvard Apparatus Peristaltic Pump, Model 1203. Tyrode's solution was modified as follows: 124 mM NaC1, 2.7 mM KC1, 1.8 mM CaC12, 1.1 mM MgC12, 25 mM NaHC03, 0.42 mM NaHP04, and 5.6 mM D-glucose. The kidney was excised from the animal, placed on a nylon covered ring and covered with cotton gauze moistened with modified Tyrode's solution. Temperature of the perfusate and kidney was maintained at 35-39' with a heat lamp. The perfusate did not recirculate.An equilibrium period followed attachment of the isolated kidney to the perfusion apparatus. During this time the flow rate was adjuste...
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