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)

Ergometric tests (ET) were used to study 900 patients undergoing surgical myocardial revascularisation during the period between January 1983 and December 1989. ET was carried out without medical therapy between the 30th and 35th day post surgery. The test was positive in 193 subjects (21%); in 42 of the latter (5% of the total and 229 of positive subjects) symptoms of effort angina were found to persist. ET was negative in 557 patients (62%); 150 subjects (17%), although not positive, did not attain a sufficient heart rate to enable a 100% negative diagnosis to be made. No major complication was observed. Maximal short-term ET is a reliable and safe test for checking the efficacy of myocardial revascularisation and to assess functional recovery. In view of the relatively high percentage of positive tests due to ischemia but with the complete absence of symptoms, the authors affirm that the mere onset of anginous symptoms alone cannot be considered indicative of the success of cardiosurgery.
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PMID:[The early ergometric test after myocardial revascularization]. 178 92

Myocardial protection by the water-soluble vitamin E analogue, Trolox, was investigated in 18 regionally ischemic, reperfused porcine hearts. The left anterior descending coronary artery was distally ligated for 45 min and was reperfused for three days. Five grams of Trolox (n = 9) were infused intravenously before coronary occlusion. Treatment was continued with an intravenous dose of 5 grams Trolox/24 hours until the end of the experiment. Infarct size was determined as the ratio of infarcted (tetrazolium stain) to ischemic myocardium (dye technique). Regional systolic shortening was assessed by sonomicrometry. Generation of free radicals by stimulated neutrophils was evaluated by luminol-enhanced chemiluminescence. Plasma concentrations of Trolox were measured by high-performance liquid chromatography. Aside from heart rate before ischemia, global hemodynamic values including calculated left ventricular oxygen consumption did not differ significantly between the two groups. Plasma concentrations of Trolox measured 1.8 +/- 0.3 mmol/l (before ischemia), 0.96 +/- 0.13 mmol/l (before reperfusion), 0.77 +/- 0.1 mmol/l (40 min of reperfusion), and 0.08 mmol/l (end of the experiment). Generation of free radicals by stimulated neutrophils was reduced by about 30% in the treatment group before ischemia and immediately before reperfusion, but was not reduced at the end of the experiment. Risk regions (control group 19.4 +/- 6 g, treatment group 19.3 +/- 7 g) and infarct sizes (control group 69.3 +/- 8%, treatment group 69.3 +/- 12%) were almost identical. Regional systolic shortening of a control segment and of the risk region were similar in both groups before ischemia, before reperfusion, and after 45 min of reperfusion. After 3 days of reperfusion, regional systolic shortening of the reperfused myocardium of the treated group had recovered to a significantly greater extent (P = 0.027). This parameter amounted to 9 +/- 6% in the treated group and to 3 +/- 3% in the control group. Improved functional recovery was not accompanied by higher tissue concentrations of adenosine triphosphate. It is concluded that the chosen treatment with Trolox does not reduce infarct size but accelerates functional recovery. This finding suggests that the mechanisms resulting in myocardial necrosis during ischemia/reperfusion and in post-ischemic myocardial dysfunction may differ.
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PMID:The effects of Trolox, a water-soluble vitamin E analogue, in regionally ischemic, reperfused porcine hearts. 179 Oct 83

Twelve rabbits were submitted to 20-min global cerebral ischemia. Half of them were treated continuously with prostacyclin (PGI2) for 3 min before and during ischemia, and for 15 min after it. Untreated animals were not given PGI2 medication. The cases treated with PGI2 were found to have recovered bioelectric activity of the brain in half the time that its return took in the untreated cases. In the group that received PGI2, the ischemic ultrastructural changes in the cytoplasm of neuroglial cells were abolished, however, PGI2 did numerous vesicular structures, nuclear inclusions and chromatin clumping and margination. The vesicular structures were enclosed in a single smooth membrane without contact with the nuclear envelope. It is suggested that the vesicular structures may form as the result of disturbances in the water-electrolyte exchange between the cytoplasm and karyoplasm of neuroglial cells. The inclusions consisted of filaments and/or membranes. The amassing in the karyoplasm of vesicular structures and intranuclear inclusions with chromatin clumping and margination probably leads later to the death of the neuroglial cells after total cerebral ischemia. Hence, the described data indicate that the curative effects of PGI2 are directed only to early changes in the neuroglial cells cytoplasm and reflect a transient facilitation of functional recovery and/or metabolism rather then permanent brain protection after complete cerebral ischemia.
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PMID:The effects of prostacyclin on early ultrastructural changes in the cytoplasm and nuclei of neuroglial cells following complete cerebral ischemia. 179 Dec 98

Previously in our laboratory, nimodipine was effective in reversing posttraumatic ischemia and promoting electrophysiologic recovery in a rat spinal cord injury (SCI) model. However, these beneficial effects were achieved when nimodipine was combined with adjuvant therapy to reverse posttraumatic hypotension, by either volume expansion or vasopressor therapy. The present experiments determined if nimodipine alone can increase spinal cord blood flow (SCBF) and improve function after SCI. The hydrogen clearance technique was used to measure SCBF, and motor and somatosensory evoked potentials (MEP and SSEP) were used to quantitate electrophysiologic function. SCBF, MEP, and SSEP were recorded before and after a 52 g clip compression injury at the T1 segment and then repeated after a 35 minute infusion of nimodipine. Twenty-five rats were allocated randomly to five equal groups, each of which received 35 minute infusions of one of the following doses of nimodipine: (1) 0 mg/kg, (2) 0.005 mg/kg, (3) 0.01 mg/kg, (4) 0.025 mg/kg, or (5) 0.05 mg/kg. SCBF decreased after injury in all groups, and there was no increase in SCBF after nimodipine infusion in any group. MEP and SSEP were abolished by the injury in all rats, and there was no recovery of the evoked potentials in any group. It is concluded that adjuvant therapy for posttraumatic hypotension may be necessary for nimodipine to improve SCBF and promote recovery of function in the injured spinal cord.
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PMID:Further studies of nimodipine in experimental spinal cord injury in the rat. 180 31

High buffer cardioplegia may provide protection against ischemic damage by reducing the extent of intracellular acidosis. Secondary cardioplegia may improve postischemic recovery by restoration of high energy phosphates, ionic gradients, and intracellular pH. To test these hypotheses, pig hearts were arrested with high buffer (150 mM MOPS) cardioplegia or modified St. Thomas' solution II and then kept ischemic at 12 degrees C for 8 h. High energy phosphates and intracellular pH were followed during the period of ischemia, using 31P nuclear magnetic resonance spectroscopy, and functional recovery was followed during reperfusion. The hearts arrested by high buffer cardioplegia showed significantly higher intracellular pH than hearts preserved with St. Thomas' solution, but there were no significant differences in high energy phosphates. There were no significant differences in functional recovery. We found, however, that secondary cardioplegia abolished ventricular fibrillation, and resulted in improved functional recovery after 8 h of ischemic preservation compared with the hearts reperfused with Krebs-Henseleit solution alone. Our results suggest that despite attenuating the decreases in intracellular pH, high buffer cardioplegia does not improve recovery following 8 h of preservation at 12 degrees C. Secondary cardioplegia reduces the incidence of ventricular fibrillation and improves postischemic functional recovery of the myocardium.
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PMID:The effect of high buffer cardioplegia and secondary cardioplegia on cardiac preservation and postischemic functional recovery: a 31P NMR and functional study in Langendorff perfused pig hearts. 180 20

The present study was designed to evaluate the effects of POCA, a carnitine palmitoyltransferase I (CPT I) inhibitor, and pyruvate, a substrate inhibiting fatty acid (FA) oxidation, on post-ischemic cardiac FA accumulation on the one hand, and hemodynamic recovery and loss of cellular integrity on the other. To this end isolated, working rat hearts, receiving glucose (11 mM) as substrate, were subjected to 45 min of no-flow ischemia and 30 min of reperfusion. Hearts were perfused with or without POCA (10 microM) and/or pyruvate (5 mM). In the control group the FA content increased significantly during ischemia and remained elevated during reperfusion. Administration of POCA did not affect functional recovery and LDH release significantly, but resulted in about two-fold increased FA levels upon reperfusion as compared to glucose-perfused hearts. Pyruvate markedly improved functional recovery. Addition of this substrate did not affect lactate dehydrogenase (LDH) release, but enhanced FA accumulation during reperfusion. The combined administration of pyruvate and POCA nullified the positive effect of pyruvate on hemodynamic recovery, aggravated LDH release, and further enhanced the accumulation of FAs. The adenine nucleotide content of reperfused hearts was comparable for all groups investigated. In conclusion, during transient ischemia POCA and pyruvate markedly increased cardiac FA accumulation through inhibition of the oxidation of FAs released from endogenous lipid pools. No clear relation was found between the FA content of reperfused hearts and post-ischemic functional recovery.
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PMID:Fatty acid accumulation during ischemia and reperfusion: effects of pyruvate and POCA, a carnitine palmitoyltransferase I inhibitor. 181 Oct 59

Cardiac reperfusion injury after heart transplantation or cardiopulmonary bypass has been difficult to control due to the variable degree of myocardial damage with respect to the length of ischemia and the complexity of the surgical procedure. Here, we evaluated the myocardial metabolic and functional recovery of hearts infused with a nicorandil vasodilator-magnesium (Mg) solution just prior to reperfusion (terminal cardioplegia). Donor hearts (20 dogs) were removed and immersed in a 4 degrees C water bath containing 20 mEq/l KCL-5% glucose for 6 hours, and then were transplanted to recipient dogs. Orthotopically transplanted dog hearts were either reperfused without any further treatment or received a terminal cardioplegic solution containing 8 mg/l nicorandil, 30 mEq/l Mg, and 50 g/l glucose, which was infused at a pressure of 75 cm H2O for 2 minutes. During the reperfusion period, myocardial tissue PCO2 (t-PCO2) and calcium ion (t-Ca) were continuously monitored by an ISFET (ion-sensitive field effect transistor) sensor. Myocardial oxygen consumption and lactate flux were calculated/monitored at 5, 10, 20 and 40 minutes of reperfusion. Thereafter, myocardial function was evaluated at 45 minutes of reperfusion using LVSWI. Just after reperfusion, the treatment group (group B, n = 10) had a significantly greater coronary flow than the control group (Group A, n = 10, 35.0 +/- 10.1; group B, 47.4 +/- 8.5 ml/100 g/min, p less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Accelerated myocardial metabolic and functional recovery with terminal nicorandil-Mg cardioplegia in heart transplantation. 183 90

In this study, we evaluated the postischemic myocardial tissue blood flow, specific enzymes, and functional recovery infused with a Nicorandil vasodilator-magnesium solution (Nico.: 8 mg/L, Mg: 20 mEq/L) given just prior to reperfusion (Terminal Cardioplegia, TCP). 27 patients undergoing valve replacement were divided into two groups; the hearts of group non-TCP (nTCP) (n = 15) were reperfused after ischemia without TCP, and in the other hearts of group TCP (n = 12), TCP was given for 2 min prior to reperfusion. During the reperfusion period, myocardial tissue blood flow (TBF) on the anterior wall of left ventricle were monitored by a laser blood flow-meter. Thereafter, serum CK-MB levels, MM3/MM1 values by CK-MM subbands (MM1, MM2, MM3) levels and LVSWI were measured until 24 hours after surgery. At 5 and 10 min of reperfusion, Group TCP had a significantly greater TBF than Group nTCP (5 min; G-TCP: 69.9 +/- 19.0 ml/100 g.min, G-nTCP: 47.5 +/- 20.9, p less than 0.05, 10 min; G-TCP: 74.9 +/- 22.8, G-nTCP: 56.1 +/- 23.4, p less than 0.05). At 3 hrs after surgery, an increase of MM3/MM1 values was significantly suppressed in Group TCP compared to Group nTCP (G-TCP: 2.6 +/- 0.6, G-nTCP: 3.4 +/- 1.0, p less than 0.05). Also, Group TCP had better recovery of LVSWI. These results indicate that the TCP might reduce the postischemic reperfusion injury by the improvement of myocardial TBF and metabolism.
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PMID:[Preventive effect of post-ischemic reperfusion injury by terminal Nicorandil-Mg cardioplegia]. 183

Motor evoked potential monitoring was tested as an alternative to somatosensory evoked potential monitoring in evaluating spinal cord function during thoracic aortic occlusion in dogs. Twenty-seven animals underwent 60 minutes of cross-clamping of the proximal descending thoracic aorta with (n = 18) or without (n = 9) cerebrospinal fluid drainage. Spinal cord blood flow was measured with microspheres, and neurologic outcome was evaluated at 24 hours with Tarlov's scoring system. Cerebrospinal fluid drainage improved neurologic outcome (p less than 0.05). Motor evoked potentials recorded over the lumbar spinal cord were lost in 9 of 20 dogs with ischemic cord injury and were not lost in any of the 7 dogs that were neurologically normal. Somatosensory evoked potential were lost in 19 of 20 paraplegic/paraparetic dogs and lost in 3 of 7 normal dogs (p less than 0.01). After reperfusion, motor evoked potentials returned in all nine neurologically injured dogs that lost the potentials and were still present at 24 hours. Changes in amplitude, latency, or time until loss or return of motor evoked potentials or somatosensory evoked potentials did not predict neurologic injury. Loss of somatosensory evoked potentials had a high sensitivity (95%) but had low specificity (67%) because of peripheral nerve ischemia. Loss of motor evoked potentials recorded from the spinal cord had high specificity (100%) but a low sensitivity (46%) and was therefore not a reliable predictor of neurologic injury. Return of motor evoked potentials during reperfusion did not correlate with functional recovery. Motor evoked potentials stimulated in the cortex and recorded from the spinal cord had low overall accuracy (59%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Failure of motor evoked potentials to predict neurologic outcome in experimental thoracic aortic occlusion. 186 23

Human heart preservation for transplantation commonly involves infusion of cold cardioplegic solutions and subsequent immersion in the same solution. The objectives of the present study were (1) to establish the temporal relationship between storage time (at 10 degrees C) and the postischemic recovery of function in the isolated rat heart, (2) to assess, by metabolic and functional measurements, whether storing the heart in fluid as opposed to moist air had any effect on the viability of the preparation, and (3) to ascertain the optimal storage temperature. Isolated rat hearts (at least 6 in each group) were infused for 3 minutes with St. Thomas' Hospital cardioplegic solution No. 2 at 10 degrees C, stored at 10 degrees C for 6, 12, 18, or 24 hours, and then reperfused at 37 degrees C. Mechanical function, assessed by construction of pressure-volume curves (balloon volumes: 20, 40, 60, 80, 100, and 120 microliters), was measured before ischemia and storage and after 60 minutes of reperfusion. Function deteriorated in a time-dependent manner; thus at a balloon volume of 60 microliters the recovery of left ventricular developed pressure was 84.2% +/- 5.3% after 6 hours (p = not significant when compared with preischemic control); 69.1 +/- 3.3% after 12 hours (p less than 0.05); 55.6% +/- 4.4% after 18 hours (p less than 0.05), and 53.0% +/- 6.8% (p less than 0.05) after 24 hours of storage. Other indices of cardiac function, together with creatine kinase leakage and high-energy phosphate content, supported these observations. Since the recovery of the left ventricular developed pressure balloon volume curves were essentially flat after 18 and 24 hours of storage, either 6 or 12 hours of storage were therefore used in subsequent studies. Comparison of storage environment (hearts either immersed in St. Thomas Hospital cardioplegic solution No. 2 or suspended in moist air at 10 degrees C for 6 or 12 hours) revealed no significant differences in functional recovery between the groups. Thus hearts recovered 94.9% +/- 3.5% and 113.7% +/- 12.4%, respectively, after 6 hours of storage and 71.6% +/- 2.4% and 54.2% +/- 7.9%, respectively, after 12 hours of storage. Enzyme leakage and tissue water gain were also similar in both groups of hearts. Finally, hearts (n = 6 per group) were subjected to 12 hours' storage at 1.0 degree, 5.0 degrees, 7.5 degrees, 10.0 degrees, 12.5 degrees, 15.0 degrees, and 20.0 degrees C.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Long-term preservation of the mammalian myocardium. Effect of storage medium and temperature on the vulnerability to tissue injury. 186 98


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