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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The stability of sensory conduction and evoked potentials during ischemia has been used in the evaluation of diabetic neuropathy and diabetic control (Hgb A1C). Six newly diagnosed juvenile diabetics were studied at diagnosis and 3 to 12 months later. In three patients in good control, ischemic "resistance" became normal. In three patients in poor control, resistance remained increased; two of these three experienced a 10%-20% slowing in conduction velocity. Similar relationships between control and ischemic resistance are found in long-term diabetics. These data suggest that abnormal ischemic resistance may herald the onset of an electrical and clinical neuropathic state.
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PMID:Peripheral nerve responses during ischemia in the evaluation of diabetic neuropathy. 26 77

On the basis of vascular involvement, an open clinical trial was performed to determine whether or not the antithrombotic drug cilostazol (6-[4-(1-cyclohexyl-1H-tetrazol-5-yl) butoxy]-3,4-dihydro-2(1H)-quinolinone, OPC-13013, Pletaal, CAS 73963-72-1) applied as a single 100 mg tablet increases peripheral blood flow and prevents diabetic neuropathy in 30 patients with non-insulin dependent diabetes mellitus. The hemodynamic effects of this drug on the a. dorsalis pedis were examined using a new real-time two-dimensional Doppler echography. 1 h after oral administration of cilostazol, the cross-sectional area of the a. dorsalis pedis significantly increased from 2.2 +/- 0.2 to 2.9 +/- 0.3 mm2 (p less than 0.05). Also, the a. dorsalis pedis blood flow index significantly increased from 16 +/- 1 to 31 +/- 4 (p less than 0.05). Cilostazol did not affect plasma glucose level (from 213 +/- 14 to 198 +/- 15 mg/dl), but slightly plasma ratio of 6-keto PGF1a to TXB2 (from 0.71 +/- 0.09 to 0.83 +/- 0.12). These effects of cilostazol might ameliorate diabetic neuropathy by improving blood flow and preventing nerve tissue ischemia.
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PMID:Hemodynamic effects of cilostazol on peripheral artery in patients with diabetic neuropathy. 164 79

The effect of lower-limb ischemia on the severity of neuropathy was examined in 48 diabetic patients with peripheral vascular disease. The severity of the vascular disease, as determined by medical history, physical findings, and laboratory data, was scored for each leg. Neuropathy was rated clinically and based on the results of nerve conduction studies of the common peroneal, posterior tibial, and sural nerves. A significant correlation was found between the vascular scores and neurologic variables of the two legs, most strikingly so in electrophysiologic data, with coefficients of .6 to .7. Nondiabetic control patients showed no evidence of neuropathy, regardless of the severity of ischemia, whereas diabetic controls without limb ischemia showed symmetrical neuropathy. These findings support the hypoxic theory in the pathogenesis of diabetic neuropathy.
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PMID:Vascular insufficiency quantitatively aggravates diabetic neuropathy. 184 25

Painful diabetic distal sensory neuropathy is a disabling and common complication of diabetes mellitus. There is evidence that microvascular changes resulting in ischemia to the vasa nervorum may contribute to this problem. Pentoxifylline has been shown to improve circulation through partially occluded peripheral vessels and has been postulated to be of potential benefit. Forty adult type II diabetics were enrolled in a double-blind, placebo-controlled study utilizing pentoxifylline for six months. Visual analog scores, nerve conduction studies, and physical examinations were used to evaluate response to treatment. At the end of the six-month trial, there was no significant difference in the patients' pain between the pentoxifylline- and placebo-treated groups. The authors conclude that pentoxifylline is not useful in the treatment of painful distal diabetic neuropathy.
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PMID:Pentoxifylline in the treatment of distal diabetic neuropathy. 192 15

The amplitudes of photo-electric-plethysmography (PPG) tracings were significantly increased by subcutaneous injections of methacholine (MC) and diminished by injections of atropine (AT) as compared with placebo injections of multi-electrolyte solution (MES) both in 8 normal subjects and 11 patients with diabetic peripheral neuropathy. AT-containing lotion delayed healing compared with placebo in the forearms of 6 normal subjects. MC-containing lotion sped healing compared with placebo in the forearms of 6 subjects with diabetic neuropathy. Thigh incisions in 6 neuropathic patients were shown to heal faster if soaked in MES rather than saline. Healing with the MES solution was shown to be further increased by the addition of MC to the solution and to be decreased by the addition of AT. The addition of MC produced erythema and an increase in the amplitude of PPG tracings. AT solutions produced blanching and a decrease in the PPG amplitude. It was concluded that (1) the slow healing characteristic of neuropathic ulcers is associated with a loss of cholinergic nerve function; (2) cholinergic stimulation will increase capillary blood flow and promote healing while cholinergic blockade has opposite effects; (3) secondary ischemia makes the ulcers susceptible to the deleterious effects of therapeutic agents such as saline; (4) the ischemic tissue will heal faster with a balanced MES than with saline; and (5) the benefits of MES on healing are augmented in patients with diabetic neuropathy by the addition of cholinergic agents to the solution.
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PMID:Role of cholinergic nervous system in healing neuropathic lesions: preliminary studies and prospective, double-blinded, placebo-controlled studies. 195 66

31 patients with coronary artery disease (11 patients with diabetes mellitus and autonomic neuropathy. 10 patients with diabetes without neuropathy, and 10 patients with asymptomatic myocardial ischemia) participated in a study designed to investigate whether there is a difference in forearm skeletal muscle ischemia and pain threshold. The degree of ischemia was determined by plethysmographically measured reactive hyperemia. There was no difference in maximum reactive hyperemia after passive forearm ischemia of 5-min duration in the three groups. After symptom-limited ischemic work, there was significantly more reactive hyperemia in patients with silent myocardial ischemia as compared to diabetic patients. Exercise time was longer in patients with silent myocardial ischemia (153 +/- 51 s) than in patients with diabetic neuropathy (139 +/- 45 s) and diabetics without neuropathy (120 +/- 45 s). Pain as a cause of termination of symptom-limited ischemic forearm exercise occurred less frequently in patients with diabetic neuropathy (2/11) and patients with silent myocardial ischemia (3/10) as compared to patients with diabetes without neuropathy. Patients with silent myocardial ischemia had a higher ischemic tolerance in the ischemic working forearm than did diabetic patients with and without neuropathy. In patients with neuropathy, however, ischemic pain occurred less frequently at the same ischemic work level compared to diabetics without neuropathy. Therefore, diabetic neuropathy appears to facilitate the occurrence of silent myocardial ischemia. The data presented here suggest that there is a qualitative difference in ischemic tolerance between patients with silent myocardial ischemia and patients with diabetic neuropathy.
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PMID:[Comparison of ischemic pain threshold and reactive hyperemia in autonomic diabetic neuropathy and silent myocardial ischemia]. 205 51

We previously reported the presence of endoneurial hypoxia, ischemia, impairment of the blood-nerve barrier, and reduction of norepinephrine and 6-ketoprostaglandin F1 alpha in chronic streptozocin-induced diabetic neuropathy (SDN) and interpreted these findings as suggesting the involvement of oxygen free radicals (OFRs) but did not directly measure indices of OFR activity. In this study, we report on sciatic nerve conjugated dienes, hydroperoxides, norepinephrine, and malondialdehyde in SDN at 1, 4, and 12 mo in male Sprague-Dawley rats. Severe hyperglycemia was present throughout in diabetic rats. Conjugated dienes were consistently increased at all time points, hydroperoxides were consistently reduced, and malondialdehyde was not significantly different in diabetes compared with controls. These findings are consistent with increased OFR activity in experimental diabetes. It is necessary to monitor several indices of OFR activity in a metabolically active tissue such as the peripheral nerve.
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PMID:Oxygen free radical effects in sciatic nerve in experimental diabetes. 206 Jul 23

Since advanced glycosylation end products have been suggested to mediate hyperglycemia-induced microvascular atherogenesis and because aminoguanidine (AG) prevents their generation, we examined whether AG could prevent or ameliorate the physiologic and biochemical indices of streptozotocin (STZ)-induced experimental diabetic neuropathy. Four groups of adult Sprague-Dawley rats were studied: group I received STZ plus AG (25 mg.kg-1.day-1), group II received STZ plus AG (50 mg.kg-1.day-1), group III received STZ alone, and group IV was a control. We monitored conduction and action potential amplitudes serially in sciatic-tibial and caudal nerves, nerve blood flow, oxygen free radical activity (conjugated dienes and hydroperoxides), and the product of the permeability coefficient and surface area to 125I-labeled albumin. STZ-induced diabetes (group III) caused a 57% reduction in nerve blood flow and in abnormal nerve conduction and amplitudes and a 60% increase in conjugated dienes. Nerve blood flow was normalized by 8 weeks with AG (groups I and II) and conduction was significantly improved, in a dose-dependent manner, by 16 and 24 weeks in sciatic-tibial and caudal nerves, respectively. The permeability coefficient was not impaired, suggesting a normal blood-nerve barrier function for albumin, and the oxygen free-radical indices were not ameliorated by AG. We suggest that AG reverses nerve ischemia and more gradually improves their electrophysiology by an action on nerve microvessels. AG may have potential in the treatment of diabetic neuropathy.
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PMID:Aminoguanidine effects on nerve blood flow, vascular permeability, electrophysiology, and oxygen free radicals. 206 89

Structural alterations of endoneurial microvessels occur in diabetic neuropathy and are statistically associated with severity of nerve fiber loss and teased fiber abnormality. It is therefore hypothesized that the microvessel alterations may cause or contribute to pathologic alterations of nerve fibers in diabetic neuropathy, possibly through hypoxic injury. The mechanism of the microvessel change in diabetic neuropathy is unknown. The role of microvessels and details of microvessel structure in other possible ischemic neuropathies has not been studied completely. Already there is evidence that hypoxia induces endothelial swelling but this has not been characterized or quantitated in nerve. To determine the acute morphologic effect of ischemia on ultrastructural features of transverse profiles of endoneurial microvessels major pelvic arteries were ligated in rats. At 36 h mean lumen and mural areas were greater in ischemic than in control nerves. All components (endothelium, pericytes and basement membrane) were on average greater in ischemic than controls. The greatest increase was in endothelial cells. In these cells swollen mitochondria were abundant. This study demonstrates that acute ischemia induces swelling of the cells and organelles of endoneurial microvessels.
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PMID:Acute endothelial swelling is induced in endoneurial microvessels by ischemia. 225 Jan 70

The effect of a newly developed oral agent, prostaglandin E1 (PGE1) analogue TFC 612, on diabetic neuropathy was studied by giving it for 6 wk to streptozocin-induced diabetic rats that had been diabetic for 3 mo and was compared with the effects of aldose reductase inhibitor ONO 2235. Although both compounds improved decreased motor nerve conduction velocity, the effect of TFC 612 continued during the 6 wk of treatment, whereas that of ONO 2235 became weaker from wk 4. The abnormality in sciatic nerve sorbitol and myo-inositol levels was reversed with ONO 2235, whereas it was unchanged with TFC 612. With the laser Doppler flowmetry technique, a decrease in the sciatic nerve blood flow in diabetic rats was shown to improve with both compounds, but TFC 612 had a greater effect than ONO 2235, and the increased lactate level of the diabetic nerve was corrected with both compounds, suggesting that both may be associated with the amelioration of ischemia in the diabetic endoneurium. Both TFC 612 and ONO 2235 partially but significantly normalized decreased fiber size in diabetic rats. On the other hand, TFC 612 completely normalized the dilated lumen area in diabetic rats, whereas ONO 2235 did not. These results suggest that the PGE1 analogue TFC 612 has a significant effect on diabetic neuropathy, possibly via vasotropic action, and may be a potent compound for the treatment of diabetic neuropathy.
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PMID:Effect of prostaglandin E1 analogue TFC 612 on diabetic neuropathy in streptozocin-induced diabetic rats. Comparison with aldose reductase inhibitor ONO 2235. 252 92


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