Cilostazol attenuates gentamicin-induced nephrotoxicity in rats.

In this issue of the Journal of Neuro-Ophthalmology, Almog et al (1) present the results of their review of 52 adults referred for outpatient or inpatient consultation to a neuro-ophthalmologist for evaluation of Horner syndrome. They found that in two-thirds of patients, the cause of the Horner syndrome will already be known at the time of the first neuro-ophthalmic consultation (usually surgery or trauma to the head, neck, or chest, dorsolateral medullary stroke, or carotid dissection). Among one-sixth of the patients in whom the cause of Horner syndrome is not yet known, there will be clinical clues to allow localization of the lesion, such as acute neck or face pain (cervical region), arm pain or weakness (brachial plexus or paraspinal region), or sixth cranial nerve palsy (cavernous sinus); in those patients, targeted imaging will usually find the lesion. In the remaining one-sixth of patients, there will be no localizing clues for the Horner syndrome; in those patients, nontargeted imaging of the head, neck, and chest will rarely find a responsible lesion (only 1 case of thyroid carcinoma). This ‘‘real world’’ study, together with previous studies, provides valuable guidance in the evaluation of Horner syndrome in adults and suggests the following approach: Step 1. Confirm that there really is a Horner syndrome. The clinical features—ptosis and miosis—are calling cards, but they may be exceedingly subtle or transient (2). (The report of anhydrosis or absent facial flushing is helpful but rarely elicited.) Because there are other causes of miosis and ptosis (3), topical pharmacologic testing should be used—and results may be positive even if signs are equivocal or completely absent (2)! Cocaine has been the traditional agent, but it is a weak pupil dilator and, as a controlled substance, often is not readily available. It has been supplanted by topical 0.5% apraclonidine (4) (except in children younger than 1 year of age, in whom it may cause serious acute dysautonomia [5,6]), although wider experience will be needed to establish how reliable it is, especially in an acute Horner syndrome (7,8). The traditional use of pharmacologic agents such as topical hydroxyamphetamine to assist in localization is a waste of time. These agents are difficult to obtain and do not provide information reliable enough to allow targeted imaging (9). Step 2. Determine whether there has been previous accidental or surgical trauma to the neck, upper spine, or chest that will explain the Horner syndrome. (Include carotid endarterectomy/stenting and epidural anesthesia among legitimate causes [10,11].) If so, no further diagnostic work-up is necessary. Move to. . . Step 3. Determine whether there are localizing clinical features for the Horner syndrome. For example, ataxia and nystagmus would suggest a medullary lesion. Arm pain/weakness/numbness or myelopathic features would direct attention to the lung apex, brachial plexus, and cervical spine. Acute neck or face pain would direct attention to the cervical carotid artery. (The oculosympathetic fibers crawling up the outside of the cervical carotid artery are exquisitely vulnerable to compression, trauma, dissection, and inflammation, including arteritis.) Beware of attributing persistent Horner syndrome to trigeminal autonomic syndromes such as cluster headache; carotid artery dissection can perfectly mimic these syndromes (12). Ear pain or hearing loss would direct attention to the temporal bone and carotid canal (13). Ipsilateral sixth cranial nerve palsy would direct attention to the cavernous sinus. Perform targeted (selective) imaging on the basis of this kind of information. If there are no localizing features, then the Horner syndrome is considered ‘‘isolated,’’ and you move to. . . Step 4. Perform nontargeted (nonselective) imaging of the upper chest and neck as far up as the skull base to encompass the second (preganglionic) segment and the extracranial part of the third (postganglionic) segment of the oculosympathetic pathway. If the Horner syndrome is truly ‘‘isolated,’’

The evaluation of horner syndrome.

Cilostazol attenuates indices of liver damage induced by thioacetamide in albino rats through regulating inflammatory cytokines and apoptotic biomarkers.

PURPOSE: To evaluate effects of ischemic preconditioning and Cilostazol on muscle ischemia-reperfusion injury. METHODS: Male Wistar rats were submitted to muscle ischemic and reperfusion injury (4h of the left common iliac artery occlusion followed by 1h of reperfusion). Five experimental groups were constituted: Control group (n=4); Ischemia-Reperfusion (IR, n=5); Ischemic preconditioning group (IP, n=6); Ischemia-Reperfusion group treated with cilostazol (IRCi, n=6) and Ischemic preconditioning group treated with cilostazol (IPCi, n=6). At the end, left gracile muscle was removed and embedded in paraffin. Histopathology, neutrophil infiltration, myocyte necrosis and edema were analyzed. RESULTS: When compared with the control group, IR group showed increased neutrophil infiltration, severe necrosis and edema. There was significant difference between myocytes necrosis of IR group and IP group. There was no difference between the histopathological changes between IP, IRCi and IPCi groups. CONCLUSIONS: The model of IR caused severe muscle injury in the rat hind limb and ischemic preconditioning has a protective effect, reducing myocyte necrosis, however, treatment with cilostazol and also the association between cilostazol and preconditioning has no protective effect on the skeletal muscle subjected to ischemia and reperfusion injury.

/pdf/effects-of-ischemic-preconditioning-and-cilostazol-on-muscle-3fi28remoj.pdf

Effects of ischemic preconditioning and cilostazol on muscle ischemia-reperfusion injury in rats

Hydrogen sulphide as a novel therapy to ameliorate cyclosporine nephrotoxicity.

Objective: To present a case with nonalcoholic Wernicke’s encephalopathy (WE) developing astasia and optic neuropathy as major sequelae. Clinical Presentation and Intervent

/pdf/nonalcoholic-wernicke-s-encephalopathy-with-prominent-3uic4wqqof.pdf

Nonalcoholic Wernicke's encephalopathy with prominent astasia and optic neuropathy.

Aim Cyclosporine (CsA), an important agent used in organ transplantation to prevent rejection, displays nephrotoxicity as the most important side effect limiting usage. In this study, we sought to evaluate the effects of cilostazol and diltiazem to counter the nephrotoxicity induced by the calcineurin inhibitor CsA. Materials and methods Animals were randomly divided into seven groups, each consisting of eight animals: sham, controls, cilostazol, diltiazem, CsA, CsA plus diltiazem, and CsA plus cilostazol treatment. At the end of a 60-minute ischemic period, we administered the drugs after reperfusion for 7 days thereafter. CsA (10 mg/kg/d) was intraperitoneally for 7 days; cilostazol (10 mg/kg/d) orally by catheter for 7 days; diltiazem (5 mg/kg/d) intraperitoneally for 7 days. At the end of the 7-day treatment period, blood and tissue samples were harvested for biochemical, and serological evaluation. Results Ischemia-reperfusion injury significantly increased malondialdehyde (MDA) levels as well as decreased catalase (CAT) activities and superoxide dysmutase (SOD) content. The lowest MDA mean level was observed in the diltiazem and, the highest in the control group. The lowest CAT mean levels were noted in the CsA and diltiazem groups with highest CAT content was in the CsA and cilostazol groups. The lowest SOD mean level occurred in the sham group; the highest, in the CsA group. Conclusion Cilostazol and especially diltiazem were effective to mitigate renal ischemia-reperfusion injury.

Cilostazol and Diltiazem Attenuate Cyclosporine-Induced Nephrotoxicity in Rats

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Nonalcoholic Wernicke's encephalopathy with prominent astasia and optic neuropathy.

Cilostazol and Diltiazem Attenuate Cyclosporine-Induced Nephrotoxicity in Rats