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

It is important to repair or ameliorate the intestinal ischemia in critically ill patients. Recent study of our suggests the superiority of dobutamine, but not dopamine, in improving the intestinal oxygenation. In this study we examined the effects of pentoxifylline (PF), glucagon (GL) and prostaglandin E1 (PGE1) during reduced blood flow of the superior mesenteric artery (SMA) in 20 anesthetized dogs. As an index of the intestinal oxygenation, tonometrically measured intestinal intramural pH (pHi) was used. A tonometer was inserted into the midjejunum through enterotomy. The SMA blood flow was measured by a transit-time flow meter. A vascular screw clamp for blood flow reduction was placed around the origin of the SMA, proximal to the flow probe. The SMA blood flow was adjusted to 70% of baseline for three hours. After two hours of decreased blood flow, pHi dropped significantly from baseline. Then, either PF (20 mg.kg-1.min-1 over 10 min, followed by 0.1 mg.kg-1.min-1), GL (1 microgram.kg-1.min-1) or PGE1 (0.05 and 0.5 microgram.kg-1.min-1) was infused intravenously for one hour. With infusions of GL and large dose of PGE1, pHi tended to decrease further, although GL increased the cardiac output. Small dose of PGE1 had no significant effect on pHi. PF treatment showed beneficial effects not only on the cardiac output and the SMA blood flow, but also on pHi. We conclude that PF therapy may restore the intestinal microvascular blood flow. Further study of the effects of PF on tissue oxygenation and blood rheology is warranted.
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PMID:[How should we treat intestinal ischemia?--II: Effects of pentoxifylline, glucagon and prostaglandin E1]. 773 95

To determine the most effective route of administering prostaglandin E1 (PGE1) to inhibit warm ischemic liver damage, 90-min warm ischemia was established in a canine model. The dogs were divided into three groups according to the treatment given. Thus, group A (n = 10) was the control group which received no treatment, group B (n = 7) was administered PGE1 intravenously, and group C (n = 7) was administered PGE1 intraportally. PGE1 was continuously administered before and after the ischemia at a rate of 0.02 microgram/kg/min. The branched-chain amino acid to aromatic amino acid ratio in the hepatic vein, and the arterial ketone body ratio of acetoacetic acid to beta-hydroxybutyric acid, were examined to observe the metabolism of each amino acid and the oxidation-reduction ability of hepatocytes. Both ratios were maintained only in the group C dogs, three of which survived for over 3 days, whereas in groups A and B, all the dogs died within 24 h. The results of this study imply that the intraportal administration of PGE1 was more effective against warm ischemic liver damage than the intravenous administration of PGE1.
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PMID:The effect of intraportal PGE1 on warm ischemic liver damage. 777 3

The effect of prostaglandin E1 (PGE1) on ischemia reperfusion injury (IRI) was investigated. The changes of leucocytes in venous blood and infarcted myocardial tissue and the level of lipid peroxide (LPO), superroxide dismutase (SOD) and catalase (CAT) were also studied in these animal models at the same time. The experimental results were as follows: the count and activity of leucocytes and the level of LPO in IRI were obviously increased. The activity of SOD and CAT in the untreated group was much lower than that in the treated group (P < 0.01). The infarcted size (IS) was larger in the untreated group. The count of leucocytes was positively related with the level of LPO and IS, but negatively related with the activity of SOD and CAT. However, the relationship disappeared after the administration of PGE1. These data suggested that leucocyte plays an important role in IRI. PGE1 can inhibit leucocyte activity, decrease peroxidation, reduce LPO production and increase the activity of SOD and CAT. It can decrease the infarct size. PGE1 takes the main role in protecting IRI.
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PMID:[The effect of prostaglandin E1 on myocardial ischemia reperfusion injury]. 779 66

To treat severe painful digital ulcers on progressive systemic sclerosis (PSS) patients, we developed a new combination therapy which included neural blockade, intravenous urokinase, and prostaglandin E1 infusion. All of these are already recognized treatments for circulatory disturbances in PSS. Although each of them alone has a limited effect on the painful ischemic attack in PSS; in stepwise combination, neural blockade for release of vascular spasm and pain, prostaglandin E1 for further vasodilatation, and urokinase for thrombolysis were effective in the treatment of digital ischemia in two PSS patients. This therapy reduced the necrotic areas predicted before therapy and saved fingers from amputation. It also relieved the intolerable digital pain and effected the recovery of digital function.
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PMID:Neural blockade, urokinase and prostaglandin E1 combination therapy for acute digital ischemia of progressive systemic sclerosis. 779 34

Nerve ischemia induces wallerian degeneration and peripheral neuropathy, the nerve constriction injury induces thermal hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal hyperesthesia in the nerve constriction injury model. Prostaglandin E1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal hyperesthesia induced by nerve constriction injury in the rat.
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PMID:OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat. 786 17

We recently encountered a patient with mitral insufficiency, accompanied by PN (polyarteritis nodosa), who developed a cardiac rupture immediately after a mitral valve replacement. The patient was a 60-year-old woman. After she was diagnosed as having mitral stenosis and insufficiency in 1968, the patient developed congestive heart failure and underwent repeated hospital admissions and discharges. In 1989, she was diagnosed as having PN and began to receive a high-dose steroid therapy (prednisolone; total dose 5245 mg). Because of transient brain ischemia and exacerbation of the symptoms of heart failure, the patient underwent mitral valve replacement on December 19, 1991. For anesthesia, oxygen, fentanyl, midazolam and vecuronium were administered. During surgery, catecholamine, nitroglycerin and prostaglandin E1 were continuously infused intravenously. The patient was weaned smoothly from the cardiopulmonary bypass. The operation was completed in about 6 hours. Her postoperative course was satisfactory until she suddenly developed left ventricular rupture and died 6 hours after surgery. The rupture seemed to be attributable to a weakening of the myocardial wall following long-term, high-dose steroid therapy, and to myocardial degeneration caused by PN-associated necrotizing vasculitis of myocardial arterioles.
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PMID:[Anesthetic management of a patient with polyarteritis nodosa who suddenly developed cardiac rupture after valve replacement]. 790 39

In the natural history of patients with peripheral obliterative arterial disease (POAD) the prognosis of the complaint "intermittent claudication" is relatively good and the amputation rate is presently only about 3%. However, POAD patients carry a high risk of cardiovascular events and their cumultative mortality rate within 10 years is as high as 40-50%. Atherothrombotic events in the coronary and, less frequently, cerebral arteries are by far the first cause of death and disability in these patients. The rationale for antithrombotic drugs in the treatment of POAD lies in the pivotal role of platelet activation and thrombin formation in the evolution of the atherothrombotic lesions, but also in the effect of some of these drugs on the regulation of microcirculatory responses. In acute thrombotic arterial occlusion, Heparin is the "first application" drug, especially in support of interventional revascularisation procedures. Regional thrombolysis often coupled with angioplasty (PTA), or systemic thrombolysis, are effective in revascularisation of especially infrainguinal-supra popliteal occlusions. However, controlled clinical trials are needed. In chronic POAD, intermittent claudication can be improved with a rational walking exercise programme, but, besides pentoxyphilline, especially ticlopidine significantly adds to the benefits of exercise. Regarding districtual progression of atherothrombosis and especially cardiovascular events, both aspirin and ticlopidine have been shown effective in single studies or meta-analyses. In a recent observational study of pooled data the cumulative endpoint including myocardial infarction, stroke and vascular death was reduced by 25 +/- 10% in the generality of patients treated with antiplatelet drugs. Finally, in critical limbs ischemia (CLI), some prostanoid compounds as Iloprost and Prostaglandin E1 favourably influence rest pain and ulcer healing, but less evidence is available on their effects on hard events as amputation and death. In conclusion, following the general indication to "be conservative" in the treatment of these patients, it seems clear that antithrombotic drugs have become by far a key medication in all different phases of POAD.
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PMID:Antithrombotic drugs in peripheral obliterative arterial diseases. 795 59

Effects of prostaglandin (PG) E1 on ischemia-reperfusion (I-R) injury to the pancreas was evaluated using isolated in vivo perfused dog pancreas. Pancreatic endocrine and exocrine functions were stimulated with 10(-12) M cholecystokinin octapeptide (CCK-8). This amount of CCK-8 promoted production of insulin, glucagon, PGI2, and thromboxane (Tx) A2 in the pancreas. Sixty minutes of ischemia and subsequent reperfusion induced damage to pancreatic ductular, acinar, and beta cells. Intra-arterial administration of PGE1 at a dose of 0.5 microgram/kg/min throughout the experiment prevented the I-R injury, reducing plasma lipid peroxides, and elevating PGI2 without changing TxA2 in the pancreas. PGE1 thus appears to protect pancreatic function from I-R injury both by depressing the effect of free-radicals and by decreasing TxA2/PGI2 which predicts cell injury.
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PMID:Prostaglandin E1 protects dog pancreas from ischemia-reperfusion injury. 802 58

Studies were carried out to investigate the effects of prostaglandin E1 (PGE1) pretreatment on normothermic liver ischemia. Mixed-breed dogs were divided into three groups: a control group, a group with induced liver ischemia, and a group pretreated with PGE1 followed by induced liver ischemia. Liver ischemia was induced by the Pringle procedure for 60 min. PGE1 was administered intravenously to some dogs at a dose of 0.5 microgram/kg/min for 30 min prior to the Pringle procedure. Sham operations were performed without induction of liver ischemia in control animals. Insulin, glucagon, and glucose metabolic clearance rates were examined before and after the Pringle procedure in the control and experimental groups. Insulin and glucose metabolic clearance rates decreased 5 min after declamping in the ischemic group, while the glucagon metabolism was not affected, and lipid peroxide production increased. In contrast, hepatic insulin metabolism improved, and lipid peroxide production normalized in the ischemic group which was pretreated with PGE1. This study suggests that PGE1 prevents hepatic metabolic disturbances due to warm ischemia and subsequent reperfusion.
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PMID:Prostaglandin E1 protects liver from ischemic damage. 807 86

Prostanoids are derivative of arachidonic acid and arising from a common endoperoxide and they possess multiple and even opposing effects. Their main function is to control haemostasis and to maintain vascular homeostasis. Among these compounds thromboxane, generated by platelets, is a powerful vasoconstrictor and an inducer of platelet aggregation; prostaglandin E1 (PGE1) and prostacyclin (PGI2) are potent vasodilator and inhibitor of platelet aggregation. For these properties PGE1 and PGE2 are object of interest for the potential therapeutical use in treatment of atherosclerotic diseases, where mechanisms of vascular defense are altered and amplified. Pharmacokinetic and pharmacodynamic characteristics of these compound have been per se a good rationale for plenty of experimental studies which generated enthusiasm and hope of new therapeutic means in patients with surgically unreconstructible peripheral arterial disease. Nevertheless clinical trials have to face many difficulties deriving from their properties themselves. PGE1 and PGI2 are unstable hormones with local action and it is difficult to employ them in clinical practice. Moreover their protean action is often implicated in not unusual adverse effects. The development of compounds with a prostacyclin-type of action, but long lasting and therefore easier to handle, undoubtedly facilitated clinical research. But we still lack firm indications for a correct therapeutic use. Limb ischemia is the condition in which prostanoids were mostly studied. Although anecdotal reports or uncontrolled studies provided encouraging results, several controlled trials failed to demonstrate a consistent efficacy of either PGE1 or PGI2, whilst metanalytic review of controlled trials on iloprost demonstrated an efficacy on critical and less severe limb ischemia, thromboangiitis obliterans and Raynaud's phenomenon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The pharmacology and clinical aspects of the prostanoids]. 811 24


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