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

We evaluated the consequences of platelet activation within the coronary circulation and determined the contribution of released thromboxanes, the most potent vasoconstrictors known, to the ensuing cardiac ischemia. Human platelets were isolated by sepharose column chromatography from blood of normal donors and added to the crystalloid perfusate of a Langendorff rabbit heart (platelet counts greater than or equal to 10,000/microliters). Following thrombin-induced (1 U/ml) platelet activation, the coronary flow decreased by 30 +/- 10% (mean +/- SEM, P less than 0.02), the mean concentration of thromboxane B2 in the coronary sinus effluent rose to 62 +/- 25 pmol/ml, and immediate, often irreversible cardiac ischemia as monitored by nicotinamide adenine dehydrogenase autofluorescence photography, ensued. However, with high concentrations of the platelet inhibitor and vasodilator, prostaglandin E1 (1.0 mM), the coronary flow increased by 50 +/-= 15%, and the epicardial fluorescence remained unchanged despite a small (10 +/- 3 pmol/ml) increase in coronary sinus thromboxanes. Platelets isolated from donors who ingested aspirin were incapable of thromboxane synthesis (less than 5 pmol/ml) but remained normally responsive to thrombin-induced activation. When these platelets were challenged by thrombin during cardiac perfusion, however, coronary flow and epicardial fluorescence remained unchanged. We conclude that platelet activation within the coronary circulation can induce irreversible cardiac ischemia, which, however, can be prevented by appropriate pharmacologic inhibition of platelet function. Furthermore, the fact that cardiac perfusion was preserved during a thrombin challenge of platelets from aspirin-treated donors establishes a fundamental role for the products of cyclooxygenase activity (e.g., thromboxanes) in the genesis of this form of myocardial ischemia.
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PMID:Mediation of cardiac ischemia by thromboxanes released from human platelets. 704 97

Although platelets have been associated with angina pectoris, myocardial infarction, and sudden death, the platelet's capacity for induction and propagation of cardiac ischemia remains incompletely defined. We therefore evaluated the effects of platelet activation occurring within the coronary circulation and tested the hypothesis that inhibition of platelet function would prevent platelet-induced cardiac ischemia. Human platelets were isolated from blood obtained from normal donors by Sepharose 2B column chromatography, resuspended in Hepes buffer, and added to the perfusate of a Langendorff rabbit heart (platelet counts greater than 10,000/microliters). Without, and with low dose (10 microM) prostaglandin E1 (PGE1), a reversible inhibitor of platelet function, immediate and irreversible global cardiac ischemia, as monitored by NADH fluorescent photography, ensued (N = 4) following platelet activation with thrombin (0.1 to 1 U/ml). Higher concentrations of PGE1 (0.1 to 1 mM, N = 2) or aspirin ingestion (1000 mg taken approximately 12, 4, and 1 hr prior to experiment, N = 2) completely prevented this platelet-induced myocardial ischemia. Aspirin, unlike PGE1, was effective despite its inability to block thrombin-induced platelet aggregation in our in vitro gel-filtered system. We conclude that activation of platelets within the coronary circulation is sufficient for induction of irreversible cardiac ischemia. The efficacy of aspirin, a cyclooxygenase inhibitor, further suggests that the products of arachidonate metabolism (e.g., thromboxanes) have a fundamental role in the genesis of platelet-mediated myocardial ischemia.
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PMID:Platelet-mediated cardiac ischemia. 713 26

Ischaemia, neuropathies and infections are predisposing factors for the development of ulceration of the diabetic foot. Diabetics have evidently a disposition for affections of the peripheral circulation and impaired regulation of the microcirculation as a result of autonomic neuropathy. The lower the driving pressure (in critical ischaemia), the more important are rheological factors and drugs which can influence them. These preparations include e.g. Trental (pentoxiphilline), Prostavasin (prostaglandin E1), Vessel due F (sulodexide). In advanced stages of ischaemic extremities oedema is a very adverse factor. Non-cardiac oedema can be very effectively handled by manual lymphatic drainage combined with intermittent one-segment pneumatic compression which was successfully used by the authors in ulcerations of the diabetic foot. One of the main general protective measures is adequate care of the foot and protective footwear for diabetics. After 3.5 years' use of protective footwear the authors recorded, consistent with data in the literature, a 50% reduction of relapses of ulcerations (and amputations). By examination on an EMED II apparatus abnormally high local pressures on the sole of risk patients can be detected and at the some time the protective effect of materials used for protective insoles can be tested. Active pharmacological and generally protective care of diabetic foot leads to a reduced number of amputations, in particular supracondylar ones by 50 or more per cent.
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PMID:[New aspects of pharmacologic and general prophylactic care of the diabetic foot]. 748 35

The cytoprotective effect of prostaglandins (PG) was evaluated by in vivo 31P MR spectroscopy. Twenty rabbits were divided into two groups; the control group given physiological saline, and the PG group given prostaglandin E1 (0.5 microgram/kg/min). Each solution was infused for 8 min, after which complete hepatic ischemia was induced for 20 min, followed by reperfusion for 40 min. During ischemia, beta-ATP decreased to 23.6% and 42.3%, phosphomonoester increased to 260% and 200% of their initial values in the control and the PG groups, respectively. Inorganic phosphate also increased. After reperfusion, beta-ATP recovered to 65.2% and 96.5%, phosphomonoester to 130% and 110%, inorganic phosphate to 140% and 120% in the control and PG groups, respectively. The changes during ischemia were significantly smaller and the recoveries during reperfusion were more complete in the PG group. These results may confirm the cytoprotective effect of prostaglandins by in vivo 31P-MR spectroscopy.
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PMID:Evaluation of protective effects of prostaglandin E1 on ischemic liver damage with in vivo 31P-MR spectroscopy. 750 Aug 86

Lower limb critical ischemia is a clinical condition typical of patients with severe chronic obstructive arterial disease (Fontaine's IIIb and IV degree). This condition often leads to amputation of the limb involved. The authors present to the use PGE1 in 50 patients with Fontaine's IIIb-IV degree chronic obstructive arterial disease of lower limbs in which the indication of amputation was done. All the patients, admitted to the emergency ward, complain of rest pain and distal ulcers. The administration of PG5(1) was given as follows: 40 mg/bid/e.v./20 days. A 6 months long follow-up was installed with the instrumental evaluation of: Transcutaneous oxygen pressure; Distal blood perfusion with Doppler; cardiac pulse; blood pressure. Eighteen patients became to a Fontaine's II degree during the next 2 months after therapy, 25 patients came back to a severe claudicatio: of them 18 underwent successfully vascular surgery, 7 underwent amputation of the lower limb. In 7 patients the PGE1 did not influence the natural progression of the disease. Among the side-effects of therapy we can mention: headache (4%), erythema and pain of injected vein (8%), sick (4%). All the side effects were transient and never led to interruption of therapy.
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PMID:[Use of PGE1 in severe ischemia of the lower extremities. Clinical study]. 756 37

The liver has been judged relatively resistant to ischemia, but prolonged inflow occlusion at normothermic conditions can produce evidence of reversible or irreversible hepatocellular damage. Cytoprotective agents have been used both experimentally and clinically to afford extended viability of hepatocytes under reduced perfusion. One agent, prostaglandin E1, has been described clinically as effective in sustaining liver function under ischemic conditions. We have sought to verify this observation in an experimental model using prolonged normothermic inflow occlusion. Twenty miniature pigs were anesthetized and subjected to subtotal normothermic hepatic inflow occlusion (portal vein, hepatic artery, choledochal vessels) to allow for sufficient splanchnic decompression. Half of the animals received pretreatment with prostaglandin E1 (alprostadil) 500 micrograms intravenously. Inflow occlusion was maintained for 2 hours followed by reperfusion and killing 24 hours later. As a measure of functional preservation, the tissue adenine nucleotides adenosine monophosphate, diphosphate, and triphosphate (AMP, ADP, ATP) were measured in ischemic liver by freeze-clamping and high-performance liquid chromatography during occlusion and after reperfusion. Cytosolic enzyme determinations (aspartate transaminase, alanine transaminase, lactate dehydrogenase) were also made before occlusion and after reperfusion. As a possible indicator of cellular injury, blood ionized Ca++ was measured before inflow occlusion and after reperfusion. Although no difference was found in levels of AMP and ADP between prostaglandin E1 and control animals, ATP levels rose significantly higher during recovery in prostaglandin E1 animals at 60 minutes and 24 hours after reperfusion (13.97 +/- 1.29 and 13.60 +/- 0.91 mumoles/gm dry weight prostaglandin E1 vs. 9.25 +/- 0.97 and 9.80 +/- 0.85 mumoles/gm dry weight co control, P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of prostaglandin E1 on liver adenine nucleotides and cytoplasmic enzymes in a porcine model of normothermic hepatic ischemia. 759 Jun 75

Vasospastic reactions are known to be a complication of thromboembolic prophylaxis with Heparin-dihydroergotamine. We describe a rare case after successful replantation of an amputated thumb. On the third day after surgery, Heparin-dihydroergotamine was administered once. Within three hours, the thumb turned pale and cold. At revision, a spasm of the artery proved to be the cause of ischemia. Therapeutic efforts were unsuccessful, even intraarterial injection of Prostaglandin E1 and the interposition of a vein graft. Amputation became necessary. Because of the possible complication with ergotism and the consequence of a failed replantation, we suggest not to use Heparin-dihydroergotamine for thromboembolic prophylaxis in microsurgery.
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PMID:[Loss of the replanted thumb by drug-induced ergotism]. 762 27

To determine the route of prostaglandin E1 (PGE1) administration which would have the greatest protective effect against hepatic warm ischemia, two experiments were performed using dogs. The pharmacokinetics of PGE1 were investigated in a preliminary study, after which, the effects of PGE1 in a 90-min warm ischemic liver model were examined. The dogs were divided into three groups of ten, according to the treatment given: group A was an untreated control group, group B received PGE1 intravenously, and group C received PGE1 intraportally. The PGE1 was infused continuously at a rate of 0.02 microliters/kg/min before and after ischemia. All the dogs in groups A and B died within 24 h of induced ischemia. Whereas, six of the ten dogs in group C survived for over 3 days. The arterial ketone body ratio was not maintained in groups A and B, but it was in group C. Furthermore, in group C the serum lipid peroxide level, which reflects hepatocellular membrane damage, was maintained at a lower level than that in the other groups after ischemia. Electron microscopy revealed sinusoid destruction and changes in both the plasma membrane and parenchymal cell mitochondria in groups A and B, while in group C these structures were well preserved. These findings confirmed that intraportally administered PGE1 improved the hepatic microcirculation and stabilized the hepatocellular membranes. Our results indicate that intraportal administration of PGE1 has a greater protective effect than intravenous administration against warm ischemic liver injury.
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PMID:The effects of intraportal prostaglandin E1 administration on hepatic warm ischemia and reperfusion injury in dogs. 764 Apr 70

Optimal techniques of heart-lung preservation are yet to be defined. The aim of this study was to develop, in a canine model, a method of heart-lung preservation which would permit distant procurement of the organs. The animals were divided into 2 groups. In the experimental group (N = 6) the method of preservation consisted of cold cardioplegic arrest of the heart with St. Thomas' Hospital solution containing superoxide dismutase, catalase and deferoxamine, followed by cold pulmonary artery flush with modified Euro-Collins solution to which prostaglandin E1, superoxide dismutase, catalase, deferoxamine and Dextran 40 were added. Following harvesting, the heart-lung block was stored for 8 hours in cold (4 degrees C) Euro-Collins solution containing superoxide dismutase, catalase, deferoxamine, lactobionic acid, raffinose, mannitol, Dextran 40, magnesium sulfate, insulin and penicillin. In the control group (n = 6), the heart-lung block underwent the same treatment as the experimental group except that lactobionic acid, raffinose and insulin were omitted from the storage solution, and that oxygen radical scavengers were excluded from the cardioplegic, pneumoplegic and storage solutions. Histologic and electron microscopic examinations of heart-lung specimens taken before and after 8 hours cold storage of the organs suggested that our preservation technique may be effective in preventing ischemia-induced injury.
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PMID:Heart-lung protection from ischemic injury during 8 hour hypothermic preservation. 771 31

Effect of LipoPGE1 on liver injury caused by ischemia-reperfusion were compared with that of PGE1-CD, cyclodextrin clathrated PGE1, in rats. LipoPGE1 (10 micrograms/kg) and PGE1-CD (10 micrograms/kg) were gradually injected into the portal vein 5 min both prior to ischemia and prior to reperfusion. In only the group receiving injections of vehicle alone, rats died within 2 days after the episode of 90-min liver ischemia. The survival rate of all rats treated with LipoPGE1 was higher than that of rats who received vehicle alone, which indicates that LipoPGE1 pretherapy improved the survival of rats after liver ischemia-reperfusion. LipoPGE1 markedly suppressed elevations of GOT, GPT, and LDH, lipid peroxide and aromatic amino acid levels in the plasma caused by ischemia-reperfusion of the liver. When animals were given a single dose of LipoPGE1 prior to reperfusion, LipoPGE1 also suppressed elevations of GOT, GPT, LDH and lipid peroxide levels caused by 30-min of liver ischemia followed by 12-hr reperfusion. These suppressive effects with LipoPGE1 were stronger than those of PGE1-CD. These findings suggest that LipoPGE1 may have therapeutic applications in the treatment of hepatic injury.
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PMID:[Protective effects of LipoPGE1, prostaglandin E1 incorporated in lipid microspheres, against liver injury caused by ischemia-reperfusion]. 773 95


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