Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tenon plasty proved useful in eye burns, especially in cases involving corneoscleral ulceration. This surgical procedure was carried out in 24 severely burned eyes of 21 patients. A total of 75 Tenon flaps were prepared, each of them covering one quadrant of the anterior eye segment. In 13 cases the burns were fresh, showing necrotic and ischemic areas in the sclera. In seven eyes an extended corneoscleral ulceration had developed and was covered with Tenon plasty. In four cases, when highly inflamed tissue was removed from the limbus the proximal conjunctiva retracted and exposed large areas of the sclera. Again, Tenon plasty was carried out. In all cases, the damage was so extensive that no conjunctiva was available to form flaps for plastic repair. Besides, the extensive ischemia would not allow free transplants. The duration of postoperative observation after Tenon plasty ranged from 6 to 42 months. In 14 of 24 eyes the denuded corneal stroma was covered with an artificial epithelium. In 11 cases keratoplasty was performed. The conjunctival epithelium regenerated in 10 eyes within 10 days, in another 10 eyes within 20 days, and in 4 eyes within 50 days. In all cases, the corneoscleral ulceration healed. Although some symblephara formed, and in a number of cases the cornea became more turbid and vascularized, Tenon plasty was very helpful in shortening the period of intensive inpatient treatment and provided a sound foundation for further reconstructive surgery.
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PMID:[2 years experiences with Tenon-plasty]. 148 72

Removal of a rectus muscle results in permanent interruption of blood flow in the corresponding anterior ciliary artery, predisposing to anterior segment ischemia (ASI). A subhuman primate model of ASI was developed in order to study a novel muscle tuck procedure designed to preserve anterior ciliary artery circulation. Fluorescein angiograms were obtained before and after surgery to determine the effect of the muscle surgery on iris circulation. A total of 12 eyes from 12 cynomolgus monkeys underwent strabismus surgery consisting of tenectomy of all 4 rectus muscles in 3 eyes, tenectomy of 3 rectus muscles in 3 eyes, and tenectomy of 3 rectus muscles and muscle to sclera tuck of the remaining recti in 6 eyes. Postoperative angiograms documented preservation of perfusion in the distribution of the tucked muscle in all cases except one, in which there was iatrogenic trauma and disruption of anterior ciliary arteries. The modified tuck procedure thus appears to preserve anterior ciliary artery blood flow, and may be useful as a muscle strengthening procedure in patients predisposed to developing ASI.
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PMID:Effect of a modified rectus tuck on anterior segment circulation in monkeys. 205 Dec 93

Necrotizing scleritis with inflammation of the right eye developed after bilateral eye muscle surgery for thyroid ophthalmopathy. Debilitating pain, delay in onset, and involvement of the sclera distinguish this condition from anterior segment ischemia. The surgery may have acted as a nonspecific trigger in an eye at risk for scleritis. Necrotizing scleritis has occurred infrequently after other types of eye surgery but, to our knowledge, has not been previously reported as a complication of eye muscle surgery.
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PMID:Necrotizing scleritis following strabismus surgery for thyroid ophthalmopathy. 279 12

Glucose consumption and regional blood flow were determined using the [14C]-2-deoxyglucose (2-DG) method and microspheres in the optic nerve, the retina and different parts of the brain in monkeys. The relationship between the 2-DG accumulation and blood flow in the optic nerve head region was similar to that in grey matter of the brain under pentobarbital anaesthesia as well as under urethan anaesthesia. Pentobarbital anaesthesia resulted in lower values for blood flow and glucose metabolism in most regions. In the optic nerve the highest values were observed in the distal part; there was a fall in blood flow and metabolism along the nerve. There was a corresponding increase in myelin content. Artificial increments in intraocular pressure resulting in a perfusion pressure (mean arterial pressure minus intraocular pressure) of 40 cm H2O had no appreciable effect on the 2-DG accumulation. At a perfusion pressure of 20 cm H2O 2-DG accumulation in the retina and prelaminar part of the optic nerve was markedly increased indicating partial ischemia resulting in anaerobic glycolysis. At intraocular pressures higher than the systolic arterial blood pressure there was still some accumulation of 2-DG in the intraocular tissues, but no blood flow, which indicates that glucose could diffuse into the eye through the sclera. Behind the lamina cribrosa there was no indication of a reduction in blood flow or a metabolic disturbance. The results indicate that the blood flow and metabolism of the retina and prelaminar part of the optic nerve is disturbed only at very high intraocular pressures, and that even at extreme pressures there is no disturbance behind the lamina cribrosa in acute experiments. The 2-DG method will be useful in further studies on the nutritional status of the optic nerve head since it can detect abnormal glycolysis even in very discrete regions due to its high spatial resolution.
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PMID:Blood flow and glucose consumption in the optic nerve, retina and brain: effects of high intraocular pressure. 409 55

In severe burns of the anterior eye segment, including the cornea, limbus and adjacent conjunctiva, ischemia resulted from the necroses. While necrotic conjunctival and subconjunctival tissues may be removed to eliminate the toxic influence, the opaque cornea and ischemic sclera could not be removed. In the surrounding healthy tissues an inflammatory reaction developed, which brought about an infiltration of the damaged tissues by leukocytes and the release of lysosomal marker enzymes. N-Acetylglucosaminidase and cathepsin-D represent a number of other destructive enzymes involved with corneal and corneoscleral ulceration. Initially, their activities were low in the turbid, acellular cornea and increased 3 weeks after the burn. In the surrounding conjunctiva, these enzyme activities were normally higher than in the cornea and increased significantly after the burn. The elevated activities of N-acetylglucosaminidase and cathepsin-D in the conjunctiva and cornea were related clinically to corneal and corneoscleral ulceration.
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PMID:Investigation of enzyme activities in severe burns of the anterior eye segment. 831 22

In histological studies using retinas, eyes are commonly fixed with aldehyde derivatives administered by immersion or perfusion. However, the histology of rat retinas chemically fixed as a whole eye is typically inferior to the histology of retinas that are immediately fixed after acute dissection from the rest of the eye. Chemical fixation without dissection often results in neuronal swelling resembling excitotoxic damage induced by ischemia because the retina is protected by the sclera and is thus poorly accessible to immersion or perfusion fixation techniques. In order for the acute dissection technique to work properly, it must be completed in a timely manner, which may be difficult under some circumstances. Microwave irradiation is an alternative method for fixing tissues that are inaccessable to chemicals. We examined the effectiveness of microwave irradiation of the whole eye as a substitute for acute retinal dissection. To study the feasibility of microwave methods, we compared retinal morphology using microwave irradiation to morphology using conventional immersion fixation methods. Eyes were removed from rats, placed in a container with 2 or 20 ml artificial cerebrospinal fluid (aCSF) and irradiated with a household microwave oven. For morphological comparison, control eyes were immersed in a chemical fixative containing 1% paraformaldehyde and 1.5% glutaraldehyde. All eyes were embedded in araldite for evaluation by light microscopy. Retinal segments acutely isolated before immersion fixation revealed intact histology whereas retinal segments exposed to 60 min of simulated ischemia showed severe neuronal degeneration. Using an immersion technique, the retinas of chemically fixed whole eyes showed neuronal swelling similar to excitotoxic ischemic damage, suggesting that conventional immersion methods provide poor whole eye fixation. The neuronal degeneration observed with conventional immersion fixation was not found in retinas of whole eyes fixed with 20 sec of microwave irradiation. During microwave irradiation the temperature in the bathing aCSF rose to 55-72 degrees C. In some eyes, overcooking produced chromatin clumping and a small loss of contrast in staining. Although nuclear clumping and diminished staining occasionally result from overcooking, ischemic damage is well controlled with microwave fixation of enucleated eyes. When the optimal conditions are defined, microwave fixation may be preferable for retinal histology if chemical fixation following acute dissection is not feasible.
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PMID:Comparison of rat retinal fixation techniques: chemical fixation and microwave irradiation. 1065 44

A 52-year-old man had loss of vision and black discoloration of the lids of the right eye after a retrobulbar injection of 3 mL lidocaine hydrochloride 2% (Xylocaine). Examination of the right eye revealed no light perception with extensive necrosis of the lids. Anterior segment examination revealed conjunctival pallor, corneal edema, and necrosis of the sclera. This is a previously unreported complication of retrobulbar anesthesia comprising ophthalmic artery occlusion with scleral melt, ocular ischemia, and eyelid necrosis.
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PMID:Necrosis of the eyelids and sclera after retrobulbar anesthesia. 1268 60

In chronic glaucoma, there is a gradual painless loss of vision, early manifestation of arcuate field defect and typical atrophy of the optic disc known as 'cupping'. Chronic glaucoma is classified into high-tension glaucoma (HTG) and normal-tension glaucoma (NTG). Although both types manifest with the same typical visual field defect and cupping of the optic disc, high-tension glaucoma has elevated intraocular pressure whereas in normal-tension glaucoma the intraocular pressure (IOP) is within the normal range (10-21 mmHg). There are several theories about the pathogenesis of chronic glaucoma ranging from high intraocular pressure directly damaging the optic disc to programmed death(apoptosis) of the ganglion cells of the retina. But none of them satisfactorily explain the manifestation of the early arcuate field defect which is a pathognomonic feature of both types of chronic glaucoma. This article focuses on two main issues. First, how and why the arcuate field defects are produced in the early stages of glaucoma and secondly to find out the common ground in the pathogenesis of both high and normal tension glaucoma. The early arcuate field defects are an important lead in discovering the pathogenesis of glaucoma, therefore if any factor or site which could not possibly produce initial sharply defined arcuate field defects was ruled out. This article presents an unconventional approach to the pathogenesis of glaucoma. Instead of looking for various factors causing glaucoma, emphasis was placed on determining the primary site of injury which could produce the initial arcuate field defects. Keeping the arcuate visual field defects in mind, the primary site of injury appears to be at the scleral edge and not the optic disc or the retina in chronic glaucoma. The border tissue which separates the sclera and choroid from the nerve fibers would atrophy due to chronic ischemia as a result of high intraocular pressure in HTG, whereas due to poor systemic circulation in NTG. In both types of chronic glaucoma, the ciliary circulation supplying the prelaminar and border tissue is compromised. As a result of atrophy of the border tissue, the optic disc sinks as a whole beginning temporally due to its tilted position and causing nerve fibers to stretch, kink, and cut at the scleral edge. This process of optic disc sinking would accelerate due to loss of nerve fibers which also provides anchorage to the optic disc. This cycle would continue until all the nerve fibers are cut at the scleral edge and the optic disc is destroyed.
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PMID:Scleral edge, not optic disc or retina, is the primary site of injury in chronic glaucoma. 1682 94

Melatonin is a ubiquitous molecule and widely distributed in nature, with functional activity occurring in unicellular organisms, plants, fungi, and animals. Several studies have indicated that melatonin synthesis occurs in the retina of most vertebrates, including mammals. The retinal biosynthesis of melatonin and the mechanisms involved in the regulation of this process have been extensively studied. Circadian clocks located in the photoreceptors and retinal neurons regulate melatonin synthesis in the eye. Photoreceptors, dopaminergic amacrine neurons, and horizontal cells of the retina, corneal epithelium, stroma endothelium, and the sclera all have melatonin receptors, indicating a widespread ocular function for melatonin. In addition, melatonin is an effective antioxidant which scavenges free radicals and up-regulates several antioxidant enzymes. It also has a strong antiapoptotic signaling function, an effect that it exerts even during ischemia. Melatonin cytoprotective properties may have practical implications in the treatment of ocular diseases, like glaucoma and age-related macular degeneration.
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PMID:Role of melatonin in the eye and ocular dysfunctions. 1726 77

Previous RT-PCR experiments revealed the expression of gene transcripts for a variety of aquaporins in the neural retina, including aquaporin-0. We investigated by immunohistochemistry and Western blotting whether the aquaporin-0 protein is expressed in the retina of the rat. In addition to the lens, immunoreactivity for aquaporin-0 was expressed in the neural retina, but was absent in the pigment epithelium, choroidea, and sclera. In the neural retina, aquaporin-0 immunoreactivity was expressed by the nuclei and the synaptic terminals of protein kinase alpha- and beta-expressing bipolar and amacrine cells, and by the nuclei of neuronal cells in the ganglion cell layer. The immunoreactivity for aquaporin-0 did not co-localize with calbindin, a marker of horizontal cells, or with aquaporin-4, the glial water channel. Transient retinal ischemia caused a slight decrease in the retinal content of aquaporin-0, likely by degeneration of protein kinase alpha-expressing bipolar cells. It is concluded that aquaporin-0 may be involved in the regulation of the activity of retinal second order neurons.
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PMID:Localization of aquaporin-0 immunoreactivity in the rat retina. 1788 Nov 23


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