Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT01447 (Fluorescein)
 2,705 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present five cases of severe retinal ischemia associated with gentamicin injection. In three of the cases massive doses of gentamicin were erroneously injected into the eye; in two of the cases the authors presume that gentamicin toxicity occurred. The sequence of clinical findings was similar in all five cases. The prominent findings included early superficial and intraretinal hemorrhages, opaque and edematous retina, cotton-wool infarcts, arteriolar narrowing, and venous beading. Fluorescein angiography revealed severe retinal vascular nonperfusion. Chronic findings included rubeosis irides, neovascular glaucoma, retinal pigmentary degeneration, and optic atrophy. Of the documented cases of massive intraocular gentamicin injection, two patients had no light perception (NLP) vision and one had bare light perception. Of the two cases of presumed gentamicin toxicity, one had 20/400 vision and one had count fingers vision. Strict precautions are necessary to prevent the catastrophic events resulting from inadvertent gentamicin injection; such precautions should include precise labeling of all injectable solutions on the surgical field, waiting to draw up injectable antibiotics until the time they are needed, and drawing up injectable antibiotics under direct physician observation. All intravitreal injections should be performed slowly, in the anterior vitreous, with the needle bevel up.
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PMID:Retinal toxicity secondary to intraocular gentamicin injection. 376 30

Pharmacologic alteration of the no-reflow phenomenon was determined based on increased tolerance to ischemia in ibuprofen-treated free flaps. Sprague-Dawley rats (N = 60) were divided into control (lactated Ringer's) and treated (ibuprofen) groups and subdivided into six groups of ischemia: 1 hour, 6 hours, 8 hours, 10 hours, 12 hours, and 14 hours of ischemia. Fluorescein uptake was measured after 10, 30, and 60 minutes following microrevascularization. Dye elimination studies were done for each ischemia group that demonstrated good fluorescein uptake. All free flaps in the 1-, 6-, and 8-hour groups survived. The ibuprofen-treated 10- and 12-hour flaps all survived, whereas the 10-hour control and 14-hour ibuprofen-treated free flaps failed to survive. Despite high fluorescein uptake, the 14-hour ibuprofen-treated flaps did not eliminate the fluorescein, whereas all surviving free flaps adequately eliminated the fluorescein. Failure to eliminate dye despite adequate uptake suggested a deranged microcirculation with increasing ischemia time. By inhibiting cyclo-oxygenase, nonsteroidal anti-inflammatory agents such as ibuprofen may block the untoward effects mediated by thromboxane A2, such as vasoconstriction, microvasculature thrombus formation, and intravascular sludging. These effects are theorized in part to be responsible for the failure of a free flap to survive despite revascularization.
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PMID:Beneficial effects of ibuprofen on experimental microvascular free flaps: pharmacologic alteration of the no-reflow phenomenon. 382 12

Periarteritis Nodosa (P.A.N.) is a systemic connective tissue disease with a variety of manifestations that includes ocular involvement in 20% of cases. The diagnosis of this condition is difficult due to the absence of any specific clinical signs or laboratory findings. However, histologic studies have demonstrated a segmental vasculitis that is often necrotic. Ocular findings frequently include choroidal involvement that is characteristic. Nevertheless, angiographic studies of this disease are extremely rare. The findings in three patients suspected of having P.A.N. are presented. Fluorescein angiography established the diagnosis of P.A.N. in two cases and ruled-out its presence in the third case. In the first case angiography demonstrated a retinal vasculitis with multiple arteriolar and capillary occlusions. There was also ischemic involvement of the choriocapillaris and a mild anterior optic nerve vasculitis. All findings resolved, leaving numerous Elschnig spots. In the second case the angiogram showed acute multifocal ischemia of the choriocapillaris. The ocular examination and fluorescein angiogram in the third case were entirely normal, thereby ruling-out P.A.N. on the basis of insufficient criteria. Acute multifocal choroidal ischemia is present in a variety of rare conditions: Toxemia of pregnancy, Disseminated Intravascular coagulopathy, Moskowitz Disease (T.T.P.), Leukemia and Malignant Hypertension. However, the presence of multifocal choroidal ischemia in the presence of a systemic connective tissue disorder strongly favors the diagnosis of P.A.N. The relative contributions of co-existent Malignant Hypertension and P.A.N. in producing choroidal ischemia are discussed. The spectrum of clinical manifestations and laboratory findings in P.A.N. as well as hypotheses concerning pathogenesis (immune-complex deposition) are described. Among all systemic vasculitis , only P.A.N., and rarely Scleroderma, feature choroidal involvement. This is possibly due to the fact that the degree of vasculitis in P.A.N. is sufficiently severe to cause clinically significant choroidal involvement.
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PMID:[Fluorescein angiography in the diagnosis of periarteritis nodosa]. 614 75

Fluorescein-isothiocyanate dextran (FITC-dextran; MW approximately 70,000) was used in isolated rat hearts to compare normal vascular perfusion of ventricular myocardium with the pattern and extent of reperfusion following 60 minutes of global ischemia. Its gross distribution in frozen transverse sections through the ventricles was similar to that of sodium fluorescein. However, unlike 0.1% sodium fluorescein, 6.7% FITC-dextran has a viscosity similar to that of blood, and its much higher molecular weight prevents its diffusion beyond the ischemically injured vessels. Furthermore, staining by the alcoholic periodic acid-Schiff technique enabled tracer distribution to be confirmed microscopically and distinguished competent from incompetent vessels in paraffin embedded material.
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PMID:A method for the gross and microscopic investigation of vascular reperfusion in ischemic myocardium. 618 58

Fluorescein angiography of the normal fundus reveals the segmental nature of the choroidal vascular bed. Despite the presence of anatomically demonstrable anastomoses, a segmental distribution is present in vivo up to the choriocapillaris level. Choroidal vascular diseases manifest by localized of diffuse delayed or incomplete filling of the choroid and by the involvement of the overlying retinal pigment epithelium. In the acute phase of choroidal arterial occlusive disease, ophthalmoscopy reveals localized or diffuse edema. Fluorescein angiography of such cases initially shows a delayed perfusion of the involved area followed later on by fluorescein leakage. This late diffusion of the dye is probably related to alterations of the retinal pigment epithelial barrier. The extent of the lesion after resolution of the edema mainly depends on the site and the extent of the occlusion, on the development of collaterals and possibly on the involvement of the choroidal venous circulation. Ophthalmoscopy and fluorescein angiography will reveal localized or diffuse pigmentary changes, sometimes of quite characteristic aspect. This may be associated with local destruction of the choriocapillaris, although normalization of choroidal blood flow may also be observed. Chronic choroidal vascular insufficiency is a possible cause for choroidal sclerosis. Chronic choroidal ischemia is also a possible explanation for peripheral pigmentary changes seen in the elderly.
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PMID:Fluorescein angiography of the choroid in health and disease. 683 97

Six cases of vascularly induced disc edema are described. Patients were all fairly young, with only slight and mostly transient visual decrease in spite of impaired pupillary reflexes (three cases) and altitudinal field defects. Bilateral, though asymmetric, involvement was detected in three cases. The fundus showed a usually pale disc; the emerging arteries always presented segmental constrictions and signs of inflammation (sheathing) or sclerosis (increased reflexes). The peripapillary retina showed splinter hemorrhages and cotton-wool spots. Fluorescein angiography typically showed slow retinal circulation times with arterial laminar flow often persisting well into the venous stages. The disc and peripapillary choroid showed patchy ischemia. Fluorescein leaked at the disc in all cases, often in an irregular fashion and with a tendency for dye to run along the initial arterial segments. History and medical workups were noncontributory. Three patients with evidence of inflammatory arterial disease (vitreous cells, periarterial cuffing, and fluorescein staining of the vessel walls) improved with systemic steroids. In the remaining three the papilloarterial ischemia was diagnosed as caused by premature arteriosclerosis. This vascular condition differs from ischemic optic neuropathy, in which retinal arteries are not obviously involved, and from papillophlebitis, in which the retinal vascular involvement, when present, is limited to the veins.
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PMID:Papilloarterial Ischemia. 729 38

Reperfusion injury and the no-reflow phenomenon are manifestations of a complex series of events that culminate in an acute inflammatory reaction within reperfused tissue. Antiinflammatory therapy attenuates ischemia-reperfusion injury. The purpose of this study is to evaluate the effects of dexamethasone on blood flow and viability of ischemic rat island groin flaps. Thirty-three mature male Sprague-Dawley rats were divided into 3 groups. The flaps were subjected to 8 hr of ischemia in the control and treatment groups. Fluorescein studies were performed, and flap viability was assessed. Twenty-four hour fluorescence (after reperfusion) correlated very closely with the percentage of eventual flap viability. The blood flow and viability of the treatment group flaps were significantly better than those in the ischemic control group. Dexamethasone significantly improved ischemic flap survival in the rat 8 hr ischemic island groin flap model in our study.
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PMID:Improved reflow and viability in reperfused ischemic rat island groin flaps using dexamethasone. 778 10

1. CRVO (central retinal vein occlusion) is of two types: ischemic (hemorrhagic retinopathy) and nonischemic (venous stasis retinopathy). 2. Retinal capillary obliteration is a hallmark of retinal ischemia. Fluorescein fundus angiography gives the most valuable information in the differentiation of CRVO into it two types. The ischemic type is in sharp contrast to the nonischemic because there is significant retinal capillary obliteration in ischemic CRVO. 3. The relative afferent pupillary defect (RAPD) is very helpful in separating the ischemic type from the nonischemic type, during both the early and the late stages of the disease. There is a positive RAPD in hemorrhagic retinopathy. 4. The most serious complication of CRVO is the development of various types of ocular neovascularization.
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PMID:Central retinal vein occlusion. 832 Jul 24

A 67-year-old diabetic man suffered from right neovascular glaucoma following the ipsilateral cataract surgery. Three years later, he underwent left cataract surgery and again developed left neovascular glaucoma after the operation. Fluorescein angiogram showed a marked delay in retinal circulation. Moreover, severe stenosis of bilateral carotid origins and reflux of bilateral ophthalmic arteries were ascertained by neurosonographical examination such as duplex cervical echography and transcranial Doppler, as well as an angiogram. Brain imaging demonstrated asymptomatic watershed infarction in the left parieto-occipital cortex. Chronic ocular ischemia caused by carotid stenosis is one of the decisive risk factors for secondary glaucoma after cataract surgery. Preoperative neurosonographical screening tests are required to decrease ocular surgery complications, especially in the aged, and diabetic patients.
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PMID:[A diabetic patient with bilateral carotid stenosis who developed neovascular glaucoma following cataract surgery]. 856 40

The ability of cardioplegia to protect against cardiac contractile dysfunction caused by ischemia and reperfusion is well established. The effects of cardioplegia on vascular injury and the no-reflow phenomenon, however, remain controversial. We used the blood-perfused rat heart to study the effect of St. Thomas' Hospital cardioplegic solution on postischemic endothelium-dependent and endothelium-independent vascular function, the extent of the no-reflow phenomenon, and the temporal relationship between postischemic vascular and contractile function. Isolated rat hearts (16 per group) perfused with blood from a support rat at 60 mm Hg were subjected to 10, 20, 30 or 40 minutes of global ischemia and 40 minutes of reperfusion at 37 degrees C. Eight hearts in each group also received cardioplegia (45 mm Hg for 2 minutes) before ischemia. Left ventricular developed pressure was measured with an intraventricular balloon. At the end of reperfusion, a bolus of 250 micrograms nitro-L-arginine methyl ester was infused to assess endothelium dependent vascular function. After a 20-minute washout, 25 micrograms sodium nitroprusside was infused to assess endothelium-independent vascular function. Fluorescein (1 ml, 1% weight/volume) was then infused to assess no-reflow; this involved freezing the hearts, cutting them into transverse sections (10 x 1 mm), video recording the sections under ultraviolet light, digitizing the images, and analyzing density of fluorescence. No-reflow was defined as a flow of less than 5%. Compared with nonischemic control responses, endothelium-independent vascular function was significantly decreased only after 30 and 40 minutes of ischemia (48.1% +/- 3.8% and 24.3% +/- 7.4%, p < 0.05), but it was significantly protected by cardioplegia (66.6% +/- 3.9% and 64.5% +/- 5.2%, p < 0.05). A significant reduction in endothelium-dependent vascular function was observed after 40 minutes of ischemia (-31.8% +/- 6.6% vs -50.4% +/- 1.6% in control hearts, p < 0.05), and again this was improved by cardioplegia (-45.0% +/- 3.4%, p < 0.05 vs ischemic group). Areas of no reflow were present after 30 and 40 minutes of ischemia (11.9% +/- 6.8% and 33.4% +/- 14.1% of left ventricular mass), and at each time period they were significantly decreased by cardioplegia (0.7% +/- 0.4% and 3.8% +/- 1.6%, p < 0.05). Postischemic contractile dysfunction was observed before any vascular alteration was apparent. After only 20 minutes of ischemia, the postischemic recovery of left ventricular developed pressure fell to 56.7% +/- 4.0%, but both endothelium-dependent vascular function and endothelium-independent vascular function were unaffected. In conclusion, vascular alterations are apparent only after prolonged periods of ischemia, longer than those required to observe contractile dysfunction, and cardioplegia protects against postischemic endothelium-dependent and endothelium-independent vascular dysfunction and reduces the extent of the no-reflow phenomenon.
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PMID:Effects of cardioplegia on vascular function and the "no-reflow" phenomenon after ischemia and reperfusion: studies in the isolated blood-perfused rat heart. 858 18


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