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

The antiarrhythmic and antifibrillatory effects of the specific bradycardic agent alinidine were evaluated in a conscious canine model of myocardial infarction and sudden death, and by determination of ventricular fibrillation thresholds (VFT) in anesthetized dogs. Programmed electrical stimulation (PES) was performed in conscious animals, 3-5 days after a 2-h occlusion/reperfusion of the left anterior descending coronary artery (LAD). Dogs in which PES resulted in a reproducible nonsustained or sustained ventricular tachycardia (VT) were randomized to receive either intravenous alinidine (1 mg/kg, n = 11) or intravenous vehicle (n = 10). Programmed electrical stimulation and measurement of electrophysiologic parameters were repeated after 30 min, and the animals were entered into the sudden death protocol by introducing a 150 microA anodal current to the lumen of the left circumflex coronary artery (LCX) via a surgically implanted silver wire electrode. A second alinidine-treated group (n = 3) had heart rates controlled by atrial pacing during this period. Alinidine failed to prevent the programmed electrical induction of VT in 10 of 11 animals, but significantly reduced both sudden (less than 1 h ischemia) and 24-h mortality as compared to the ventricle group. Infarct sizes were similar in the two groups, but the ischemia-related increase in heart rate was attenuated (p less than 0.05) by alinidine and the onset of ischemia tended to be delayed. All of the atrial-paced animals died acutely. Heart rate decreased after alinidine (p less than 0.01), but apart from a single index of refractoriness, the drug was without electrocardiographic or electrophysiologic effects. Neither alinidine nor vehicle demonstrated any effect upon VFT in two groups of five animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Alinidine reduces the incidence of ischemic ventricular fibrillation in a conscious canine model, a protective effect antagonized by overdrive atrial pacing. 247 29

The antiarrhythmic and antifibrillatory effects of the beta-1 adrenoceptor antagonist celiprolol were evaluated in a chronic canine model of myocardial infarction and sudden death. Programmed electrical stimulation (PES) was performed in conscious animals 3 to 5 days after a 2-hr occlusion/reperfusion of the left anterior descending coronary artery. Dogs in which PES resulted in a reproducible nonsustaining or sustained ventricular tachycardia (VT) were randomized to receive i.v. celiprolol (3 mg/kg, n = 10) or vehicle (n = 10). PES and measurement of electrophysiologic (parameters were repeated after 30 min and the animals were entered into the sudden death protocol by introducing a 150-microA anodal current to the lumen of the left circumflex coronary artery via a surgically implanted silver wire electrode. Celiprolol failed to prevent the induction of VT, and the outcome of the sudden death protocol did not differ from vehicle with respect to either sudden (within 1 hr of ischemia) or delayed (greater than 1 hr) mortality. VT cycle length and ventricular refractoriness were prolonged (P less than .05) by celiprolol, but other electrophysiologic parameters were unaffected. Heart rate was not altered after drug, but celiprolol antagonized the ischemia-induced increase in rate seen in the vehicle group. Similar electrophysiologic results and mortality data were apparent in a third group of dogs which received pindolol (0.09 mg/kg, n = 8). The failure of both drugs to protect against ischemic ventricular fibrillation in a model in which beta adrenoceptor antagonism has previously proved beneficial may be due in part to related cardiostimulant properties shared by celiprolol and pindolol.
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PMID:Celiprolol does not protect against ventricular tachycardia or sudden death in the conscious canine: a comparison with pindolol in assessing the role of intrinsic sympathomimetic activity. 257 93

Transient forebrain ischemia produces a spatially and temporally selective pattern of neuronal degeneration in the hippocampal formation of the Mongolian gerbil. Ischemic neuronal death has been suggested to depend on the activation of excitatory hippocampal pathways that project to the vulnerable neurons. This idea was tested by examining the effect of a unilateral entorhinal cortical lesion or a unilateral knife cut lesion of intrahippocampal pathways on the neuropathology produced by 5 min of complete forebrain ischemia. A prior lesion of either the ipsilateral entorhinal cortex or the mossy fiber and Schaffer collateral-commissural pathways partially prevented the destruction of CA1b pyramidal cells in most animals. It did not, however, reduce the extent of ischemic neuronal death in any other hippocampal subfield. Within area CA1b, an entorhinal lesion protected an average of 23% of the pyramidal cells and a transection of both mossy and Schaffer collateral-commissural fibers protected an average of 36.5%. CA1b pyramidal cells saved from ischemia-induced degeneration appeared clearly abnormal when stained with cresyl violet or by silver impregnation. It is suggested that lesions of excitatory pathways attenuate ischemic damage to area CA1b by directly or indirectly reducing the level of synaptic excitation onto the vulnerable neurons. However, only a relatively small percentage of hippocampal neurons can be protected by these lesions in the gerbil ischemia model and there is reason to believe that the neurons protected in this manner may not be electrophysiologically competent. Synaptic excitation therefore appears to play an important, but not an essential, role in this model of ischemic brain damage.
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PMID:Lesions of excitatory pathways reduce hippocampal cell death after transient forebrain ischemia in the gerbil. 276

The thrombolytic and hemodynamic properties of intracoronary streptokinase (SK) application were studied in an in-vivo canine model with left circumflex coronary artery thrombosis, initiated by electrical stimulation (150 microA, DC for 6 h) of the artery's intima via an implanted silver wire. In pentobarbital-anesthetized, open-chest dogs acute myocardial ischemia was determined by a dehydrogenase-dependent staining of the coronary artery perfusion area. Thrombus weight was determined post-mortem. Saline-treated control animals developed coronary thrombosis after 3.1 +/- 0.4 h of stimulation. Thrombus weight was 64 +/- 3.1 mg. Acute infarct volume was 32 +/- 3.1% of total left ventricle, and 53 +/- 6.2% of the coronary artery risk region for infarction. At occlusive thrombosis, blood pressure, ventricular pressure and the LV dP/dtmax fell significantly, whereas heart rate and the end-diastolic filling pressure increased. Severe ST-segment elevation and loss of R wave voltage indicated myocardial ischemia. At 20 min into thrombotic vessel occlusion, 2,000 IU/min SK were infused by way of a Sones-catheter advanced to the thrombus. Coronary thrombosis consistently lysed after 12 +/- 0.7 min of SK infusion, and coronary blood flow as well as hemodynamics were restored. Only minor acute infarction was found indicating viability of ischemic jeopardized myocardium. In another group, the continuous SK-infusion (20 IU/kg/min) concomitant with electrical vessel stimulation prevented coronary thrombosis and acute ischemia, and no significant hemodynamic alterations were noted. These results indicate that intracoronary SK-infusion can lyse acute thrombosis as sequel of electrical stimulation. This prevents development of acute myocardial infarction. Continuous SK-infusion can completely prevent coronary thrombosis in response to intimal injury.
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PMID:Thrombolytic effects of intracoronary streptokinase on canine coronary artery thrombosis. 673 17

Data from numerous experimental infarction studies indicate that rapid myocardial cell depolarization following ischemia causes the flow of injury currents. These currents were measured in the canine myocardium by monitoring voltage gradients across infarct boundaries using silver chloride plunge electrodes, followed by placement of a 100 omega resistor between the electrodes and again measuring the voltage gradients. Current flow was calculated from these measurements with the following results: 1) TQ currents developed within 15 seconds after occlusion and persisted for 120 to 150 minutes, often attaining a magnitude of 1 microA. 2) ST currents also developed within 15 seconds and attained 2 to 3 microA within 15 to 30 minutes, then usually subsided to some degree. 3) T currents were biphasic and attained 2 to 5 microA. Initially, current flowed from normal to ischemic myocardium but usually reversed within 30 minutes after occlusion. 4) The current flow was often disproportionate to the voltage gradient between 120 and 180 minutes after occlusion, possibly indicating electrical uncoupling of the infarcting cells from normal cells. These data indicate that intramyocardial current flow develops early after acute coronary occlusion. These currents may be sufficient to induce reexcitation.
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PMID:Intramyocardial current flow in acute coronary occlusion in the canine heart. 682 55

In anesthetized dogs, a silver wire electrode was inserted into the lumen of the circumflex coronary artery (LCX) and myocardial infarction was produced by a temporary 90-minute occlusion of the left anterior descending coronary artery (LAD) followed by reperfusion. Four days later while in the ambulatory state, a 150 microA current was applied to the intimal surface of the LCX of saline (n = 10) and bretylium (n = 10) treated animals. Intimal injury and coronary thrombosis produced ST segment changes at 138 +/- 39 minutes (chi +/- SEM), followed by premature ventricular beats (at 142 +/- 37 minutes), ventricular tachycardia (at 156 +/- 49 minutes), and ventricular fibrillation (at 163 +/- 51 minutes) in 9 of 10 saline-treated animals. In bretylium-treated animals, ST segment changes appeared at 128 +/- 35 minutes, with six animals surviving for 24 hours (p less than 0.03 vs saline). LAD infarction was present in both saline (14.1 +/- 2.3%) and bretylium (15.1 +/- 2.1% of left ventricle) treated animals with only bretylium-treated animals developing LCX infarcts (16.1 +/- 2.1%). Bretylium prevents ventricular fibrillation (VF) resulting from ischemia at a site distant to prior myocardial infarction in the conscious dog and deserves further attention as a potential antifibrillatory agent for prevention of sudden coronary death in man.
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PMID:Prevention of ventricular fibrillation by bretylium in a conscious canine model of sudden coronary death. 684 13

The purpose of this study was to examine the pharmacokinetics of gentamicin renal uptake in dogs and assess the role of chronic renal ischemia. A stenosing silver clip was place on the left renal artery of four mongrel dogs. Six months later, each dog received an infusion of gentamicin and inulin. Blood and urine samples were collected serially. In each dog, the ischemic left kidney was smaller and had a lower RPF and CCR. The decrease in CCR was highly correlated with the decrease in RPF. Measured gentamicin kidney concentrations were found to be in good agreement with predicted values based on the amount reabsorbed and the kidney weight. Within each animal (control vs. ischemic kidney), there was a significant correlation between the filtered load of gentamicin and both the renal reabsorption and excretion of gentamicin. These relationships exhibited high R2 values, demonstrating that the induced ischemia did not alter the filtration or reabsorbtive mechanisms of gentamicin within the animal, but only decreased the filtered load. Between animals, gentamicin excretion was proportional to filtered load, but gentamicin reabsorption had the lowest r2 value, explaining only 49% of the observed variance. The unexplained variance encountered in gentamicin reabsorption between animals establishes that there are important determinants of renal tissue concentration that are independent of filtration or filtered load. This study suggests that a reduction in glomerular filtration is not an important risk factor for elevated gentamicin renal tissue concentrations, provided that serum concentrations are controlled within the therapeutic range.
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PMID:Renal handling of gentamicin by normal and ischemic canine kidneys. 709 7

Under ether anesthesia a silver clip was placed around the abdominal aorta of pregnant rats, thus reducing the uterine blood flow by 35-45%. This resulted in a toxemia-like syndrome comparable to the one previously produced in other animal species. Consideration is given to the hypothesis that, in a similar way, compression of the abdominal aorta by the pregnant uterus in humans produces uterine ischemia leading to toxemia.
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PMID:Simplified technique to produce toxemia in the rat: considerations on cause of toxemia. 718 66

Distinct morphological changes were demonstrated in the contralateral hemisphere in the brains of Mongolian gerbils that were subjected to transient unilateral cerebral ischemia. The alterations were most obvious in a narrow region of the contralateral dentate gyrus (fascia dentata), where commissural inputs to the dentate gyrus are known to form synapses with the dentate granule cells. Electron microscopic examination revealed that these changes were caused by degenerative processes which took place in presynaptic terminals of the commissural inputs. An interesting fact was that the degenerated terminals were detected by light microscopy without the aid of special silver impregnation methods. After 1 week, these alterations almost disappeared, and after 3 months the dentate gyrus was undistinguishable from normal. These results strongly suggest that the changes were closely related to axonal degeneration and subsequent repair mechanisms of the brain. The present study indicates the importance of such anatomo-pathological study to delineate the effect of focal ischemia upon distant areas of the brain.
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PMID:Changes in the contralateral dentate gyrus in Mongolian gerbils subjected to unilateral cerebral ischemia. 739 66

Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.
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PMID:[An evaluation of the plastic function of the cardiomyocytes by silver staining of the nucleoli in patients operated on for ischemic heart disease]. 752 67


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