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)

A patient with conus syndrome following arteriogenic impotence is described. A 62-year-old man became impotent. 7 months after the onset, he was admitted because of a sudden left sensorimotor disturbance (L2 to S5 segments) when he awoke. A marked bilateral reduction of cutaneous sensation in the S2 to S5 dermatome distribution persisted. An MRI of the spinal cord demonstrated no abnormal lesion on T2-weighted and Gadolinium enhanced images. Angiography of the pelvic artery showed severe arteriosclerotic findings. We diagnosed this case as a conus syndrome due to ischemia in the conus medullaris. The impotence in our case was considered to be arteriogenic because there was no detection of the bilateral deep arteries of the penis on angiography after an intracorporeal PGE1 injection. In this case, arteriogenic impotence might be a prodrome of a conus medullaris infarction.
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PMID:[A case of conus syndrome following arteriogenic impotence]. 874 51

To determine the role of thromboxane A2 (TxA2) in ischemic damage of the rat liver, we examined the effects of a TxA2 synthetase inhibitor (OKY 046) and a TxA2 receptor antagonist (ONO 3708). Rats were divided into three groups. In group I, a portion of the liver was subjected to 100 min of warm ischemia and the remaining liver resected. In group II, OKY 046 (30 mg/kg, intravenously) was given 5 min before the same procedure. In group III, ONO 3708 (10 mg/kg, intravenous) was given 5 min before ischemia. We then assessed survival, serum biochemistry, extent of histologic necrosis, and the levels of prostaglandin E2 (PGE2), TxB2, and 6-keto-PGF1-alpha. Pretreatment with OKY 046 and ONO 3708 significantly improved survival, decreased the tissue water content, and lowered the levels of serum transaminases and the extent of histological liver necrosis compared with the control group. OKY 046 markedly suppressed the level of TxB2, but not the levels of PGE2 or 6-keto-PGF1-alpha. ONO 3708 did not change the levels of PGE2, TxB2, or 6-keto-PGE1-alpha. In a liver perfusion model, OKY 046 and ONO 3708 did not suppress the uptake of trypan blue in hepatocytes. Our results demonstrate that either a TxA2 synthetase inhibitor or a TxA2 receptor antagonist can protect the liver from an ischemic insult. The effects of these drugs were due to inhibition of TxA2 synthesis and TxA2 blockade at the receptor, without modulating PGI2 or PGE1. Our results in a perfused rat liver model suggest that these drugs work during reperfusion and prevent postischemic tissue edema.
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PMID:Inhibition of thromboxane A2 activity during warm ischemia of the liver. 876 50

This study is a prospective multicenter cooperative survey of the evaluation and treatment of erectile dysfunction in men with spinal cord injury (SCI). Uniform database questionnaires were completed prospectively by patients seeking therapy for erectile dysfunction. Eighty-five SCI men aged 17-68 years (mean age = 26 +/- 17) were enrolled. Mean duration of traumatic SCI was 3 +/- 3.2 years (Range = 0.3-18 years). The level of injury was cervical in 20 patients, thoracic in 31, lumbar in 29 and sacral in five. Patients were fully evaluated and then counseled as to their therapeutic options. Twenty-eight chose to use a vacuum erection device (VED), 26 preferred pharmacological penile injection and five used both intracorporeal therapy and VED. The remainder were managed with marriage and sexual counseling in 10 patients, three underwent penile prosthesis placement and two used topical pharmacotherapy. Four patients used other forms of treatment and in nine no therapy was recommended. Of the patients that used pharmacologic injection only, 74 percent used papaverine as a single agent, 20 percent used papaverine with phentolamine, five percent used prostaglandin E (PGE1) alone and one percent used a mixture. Patients using injection therapy report sexual intercourse a mean of 3 +/- 3.4 times per month as compared with 5 +/- 3.2 times per month in those using VED. Five intracorporeal injection patients developed priapism while two patients using the VED developed subcutaneous bleeding and one developed penile ischemia. We conclude that although a spectrum of erectile dysfunction treatment is present among SCI centers, VED and pharmacological penile injection are by far the two most popular methods of treatment and papaverine is the most common drug. The incidence of complications is small in the model centers.
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PMID:Epidemiology of current treatment for sexual dysfunction in spinal cord injured men in the USA model spinal cord injury centers. 881 27

The extent of mesenteric infarctions caused by intestinal circulation disorders essentially depends on reactive vasoconstriction and oxygen radical induced lesions of enteric mucosa. Animal experiments indicated protective effects of an intraarterial flushing perfusion of mesenteric arteries with vasodilators and anti-oxidants. We carried out a transaortic perfusion of the superior mesenteric artery with lactated Ringer's-solution and vasodilators (papaverin, tolazolin, PGE1) in acute occlusion of mesenteric arteries in 12 patients (case reports). Three patients were treated successfully without reconstruction by conservative method alone. Only one patient (8.33%) died because of uncontrolled enteric ischemia. Angiological therapy is necessary in modern treatment of acute mesenteric ischemia. Surgical goals are elimination of central vascular occlusions and resection of necrobiotic areas of intestinal organs.
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PMID:[Perioperative intra-arterial irrigation perfusion for adjuvant therapy of acute intestinal circulatory disorders]. 885 43

Effects of Lipo-PGE1, prostaglandin E1 incorporated in lipid microspheres on liver injury caused by ischemia reperfusion were investigated. Lipo-PGE1 (10 micrograms/kg or 3 micrograms/kg) or vehicle was gradually injected twice via portal vein 5 min prior to induction of ischemia and reperfusion. Rats died within 2 d after liver ischemia of 90 min from the group receiving injection of vehicle alone. Lipo-PGE1 had its most profound effect on the survival of animals subjected to liver ischemia followed by reperfusion when given in two doses, one prior to ischemia, and another prior to reperfusion. Lipo-PGE1 markedly suppressed both the increases in plasma PCOOH (phosphatidyl-choline hydroperoxide) levels and the leakage of GOT, GPT, and LDH from the liver during the ischemia reperfusion. These findings suggest that Lipo-PGE1 may have therapeutic applications in treatment of hepatic injury.
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PMID:Lipo-PGE1, prostaglandin E1 incorporated in lipid microspheres, protects injury of the liver caused by warm ischemia reperfusion. 885 46

Microtubules in the hepatocytes have been implicated to serve as lines of cytoplasmic transport of secretory materials, but are highly labile structures sensitive to pathological conditions in the cytosol. We examined the role of ischemia/reperfusion-induced cytoskeletal alterations in postischemic liver dysfunction. Rabbit livers were subjected to 60-min warm ischemia followed by 1 h or 24 h of reperfusion. Liver function was assessed by directly measuring hepatic clearance of indocyanine green (ICG), an organic anion whose cytoplasmic transport is assumed to depend on intact microtubules, using near-infrared spectroscopy. Structural alterations of microtubules were observed immunohistochemically using tissue sections stained with monoclonal anti-beta-tubulin antibody. ICG removal from hepatocytes into bile canaliculi deteriorated 1 h but reversed 24 h after reperfusion. Immunohistochemistry showed fragmentation of microtubules at the end of liver ischemia. This cytoskeletal alteration was evident 1 h but was not observed 24 h after reperfusion. Treatment with prostaglandin E1 exerted its beneficial effect by preserving ICG clearance and microtubular network. These results demonstrate that liver ischemia and subsequent reperfusion both affect the organization of microtubular network and suggest that structural disruption of microtubules may be a cause of postischemic liver dysfunction.
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PMID:Disorganization of microtubular network in postischemic liver dysfunction: its functional and morphological changes. 887 24

The creatine kinase isoenzymes play an important role in maintaining ATP levels in some cell types during times of high energy demand. We have previously shown in primary cell cultures from rat brain that glial cells express much higher levels of brain creatine kinase (CKB) mRNA than neurons. In a separate earlier study we observed that transcription of CKB mRNA in glial cells can be stimulated by a forskolin-mediated increase in cAMP via a pathway involving protein kinase A (PKA). In this report, we show that the level of CKB mRNA in human U87 glioblastoma cells can be increased by either prostaglandin E1 (PGE1), prostaglandin E2 (PGE2), or cholera toxin (an activator of G alpha s proteins). The induction of CKB mRNA occurs rapidly (with maximal induction after 6 h), is at the level of transcription, and is mediated specifically through PKA. In addition, the results indicate that both PGE1 and PGE2 use the same or related signal transduction pathways to increase CKB transcription. These results suggest that in glial cells CKB mRNA can be regulated by extracellular signals acting through G-protein-coupled receptors. This study may contribute to an understanding of the mechanisms underlying the previously-reported, early postnatal increase in CKB enzyme activity in rat brain. The results are also discussed with regard to the potential involvement of the expression of prostaglandins and CKB during hypoxia and ischemia.
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PMID:Prostaglandin E1, E2, and cholera toxin increase transcription of the brain creatine kinase gene in human U87 glioblastoma cells. 892 40

The effects of prostaglandin E1 (PGE1) on transient forebrain ischemia were studied in the gerbil. The animals were randomly divided into six groups of 6 each according to the method of administration as follows: group 1, no administration; group 2, subcutaneous administration with 5 ml.kg-1 of physiological saline, 30 min prior to ischemia; group 3, the same method with 3 mg.kg-1 of PGE1; group 4, 3 mg.kg-1 of PGE1, during 24 hours (12 hours prior to ischemia, and 12 hours following ischemia); group 5, 3 mg.kg-1 of PGE1, during 96 hours (12 hours prior to ischemia and 84 hours following ischemia); and group 6, sham operation. They were anesthetized with isoflurane and transient forebrain ischemia was induced by occluding bilateral common carotid arteries for 5 min. The extracranial electroencephalogram (EEG) was recorded from the electrodes placed at the vertex. During the experimental procedures, temperatures at tympanic membrane and rectum were maintained at 37.0 +/- 0.2 degrees C by means of a heating mat and control of the air temperature in all groups. After 6 days of survival, they were sacrificed, and the brain tissues were fixed for the immunohistochemical and histopathological analyses. The hippocampal CA 1 regions were stained for monoclonal anti microtubule-associated protein 2 (MAP 2), and hematoxylin and eosin. In the 4th group, EEG recovery was recognized earlier than the other groups. Immunoreactivities for MAP 2 and the number of surviving pyramidal cells after ischemia in the CA 1 regions were also well maintained. These results suggest the PGE1, has protective effects against degradation of cytoskeletal proteins and delayed neuronal death in the gerbil, and it might be due to direct protective action of cell membrane in addition to its microcirculatory improvement.
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PMID:[Effects of prostaglandin E1 on transient forebrain ischemia, especially in hippocampal CA 1 regions of the gerbil]. 893 17

Twenty-five patients affected by chronic lower limb obliterating arteriopathy with critical ischemia in one limb were treated with PGE1 for 4 weeks and then followed-up for one year. On day 14 of treatment three groups of patients were selected on the basis of clinical symptoms and instrumental tests; patients were subdivided into Responders, Partial Responders and Non-Responders. The results obtained were satisfactory in view of the fact that the selection into three groups enabled Partial Responders to be reclassified, in some cases by repeating the treatment cycle.
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PMID:[Short- and long-term evaluation of treatment of critical ischemia of the lower lim with PGE1 (alprostadyl alpha-cyclodestrine)]. 896 98

Prostaglandin E1 (PGE1) is commonly used in therapy for obstructive diseases, including ischemic retinopathy, in which pathogenetic reactive oxygen intermediates are responsible. However, the mechanism(s) of PGE1 in reducing tissue damage is still unclear. Adult T-cell leukemia-derived factor/human thioredoxin (ADF) is induced by oxidative stresses and has protective activity against oxidative cellular injury. To evaluate the possible involvement of ADF in the tissue-protective effect of PGE1, we analyzed ADF expression immunohistochemically using a rat transient retinal ischemia model. Rats were treated orally with 300 micrograms/kg/day OP-1206 alpha-cyclodextrin clathrate (OP-1206), a stable PGE1 analogue, for 14 days after photodynamic retinal vascular thrombosis by rose Bengal. Rats without any OP-1206 treatment were used as controls. In the OP-1206-treated rats, minimal retinal atrophy due to ischemia/reperfusion was observed histologically up to 14 days, whereas in the non-treated rats the inner layer of the retina became markedly atrophic. In parallel with the histological change, after 14 days following thrombosis ADF immunoreactivity was preserved on retinal pigment epithelial cells in the OP-1206-treated rats, whereas it was diminished in the non-treated rats. These findings suggest an important role for ADF in the OP-1206-dependent suppression of retinal tissue damage caused by oxidative insult.
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PMID:Analysis of localization of adult T-cell leukemia-derived factor in the transient ischemic rat retina after treatment with OP-1206 alpha-CD, a prostaglandin E1 analogue. 901 Apr 70


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