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

The influence of ischemic zone size and hemodynamics on the reperfusion-induced arrhythmia in the anesthetized rat heart was examined. The heart was subjected to regional ischemia for 4 min by the occlusion of LAD followed by reperfusion for 7 min. After the reperfusion, 64% of the rats died due to irreversible VF. The size of the ischemic zone, the increase in heart rate during ischemia and the incidence of ischemic arrhythmia (VPBs and/or VT) of the animals that died after the reperfusion were significantly greater or higher than those of the surviving animals. There were positive correlations between the size of the ischemic zone and the increase of heart rate during ischemia and the incidence of ischemic arrhythmia. These results indicate that the size of the ischemic zone is a main factor that determines the degree of reperfusion-induced arrhythmia and also contributes to the increase in heart rate and the occurrence of arrhythmia during ischemia. Therefore, in addition to monitoring the blood pressure, heart rate and electrocardiogram, measurement of the size of the ischemic zone is essential for the evaluation of drug effects on reperfusion-induced arrhythmia using this animal model.
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PMID:[Analysis of factors influencing reperfusion-induced arrhythmia in the anesthetized rat heart: the influence of ischemic zone size and hemodynamics]. 164 73

Local inhibition of angiotensin-converting enzyme (ACE, kininase II) produces both attenuation of angiotensin (Ang) II generation and bradykinin (BK) degradation. To delineate the participation of BK in the cardioprotective actions of ACE inhibitors, experiments were performed in rats and dogs with cardiac ischemia-reperfusion injuries. (I) In rat isolated perfused working hearts with regional myocardial ischemia, BK in concentrations as low as 1 X 10(-9) M increased coronary flow (CF) and reduced the incidence and duration of reperfusion ventricular fibrillation (VF). In addition, enzyme activities of lactate dehydrogenase (LDH) and creatine kinase as well as lactate output were decreased in the venous effluent of BK-perfused hearts, which also showed improved cardiodynamic and metabolic parameters. Even concentrations of BK lower than 1 X 10(-10) M, which were without influence on coronary flow, exerted comparable beneficial metabolic effects connected with reduced incidence and duration of VF. Combined perfusions with threshold concentrations of BK (1 X 10(-12) M) and the ACE inhibitor ramiprilat (2.58 X 10(-9) M), which were ineffective given alone, resulted in a marked cardioprotective effect. Perfusion with Ang II (1 X 10(-9) M) aggravated reperfusion arrhythmias and worsened myocardial metabolism. BK perfusion prevented this deterioration in a concentration-dependent manner, whereas the Ang II receptor antagonist saralasin was only marginally effective. The BK antagonist D-Arg-[Hyp2, Thi5,8, D-Phe7]-BK (1 X 10(-5) M) completely abolished the cardioprotective effects of BK or the ACE inhibitor. However, higher concentrations of BK (1 X 10(-7) M) or ramiprilat (2.58 X 10(-5) M) competitively reversed these properties of the BK antagonist. (II) In anesthetized dogs, BK was infused into the coronary artery in a dose of 1 ng/kg/min during occlusion (90 min) and reperfusion (30 min) of the left descending coronary artery (LAD)--a dose without effects on cardiovascular parameters. In line with the findings in isolated ischemic rat hearts, BK infusion reduced LDH activities and lactate concentrations in the coronary sinus blood, whereas myocardial tissue levels of glycogen and energy-rich phosphates were increased in the infarcted area. The cardioprotective effects produced by perfusion with BK or by reduction of BK degradation through local interference with ACE favor a role for BK in ischemia-reperfusion injuries in rats and dogs.
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PMID:Local inhibition of bradykinin degradation in ischemic hearts. 169 70

Prostacyclin (PGI2) improves regional contractility of postischemically dysfunctional ("stunned") myocardium. We determined whether defibrotide, a fraction of mammalian DNA known to stimulate endogenous formation of PGI2, also improves contractile recovery of stunned myocardium. Anesthetized, open-chest minipigs were subjected to coronary occlusion of 5 min (left anterior descending branch, LAD) followed by 120 min of reperfusion. The animals were treated with defibrotide (32 mg x kg-1 x h-1, intravenously, i.v.) or vehicle throughout the experimental period. Defibrotide improved regional contractility in the ischemic reperfused area from 30 (vehicle) to 78% of the preischemic control without altering the contractility of nonischemic myocardium. Transcardiac PGI2 formation, determined from the difference between coronary venous and arterial plasma concentrations, was elevated from 437 (preischemic control) to 869 pmol x l-1 in defibrotide-treated animals, but was unchanged in the vehicle-treated and a sham-operated group. Thromboxane A2 (TXA2) release was not modified. Defibrotide reduced ischemia-induced formation of platelet aggregates but did not affect the activity of polymorphonuclear neutrophil granulocytes. The data demonstrate an improvement of contractile recovery from stunning by defibrotide that may be related to an inhibition of ischemia-induced platelet activation and (or) membrane protection owing to enhanced transcardiac formation of PGI2.
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PMID:Stimulation of prostacyclin synthesis by defibrotide: improved contractile recovery from myocardial "stunning". 170 43

The effects of the Hemopump (HP) on left ventricular (LV) and coronary hemodynamics, with and without myocardial ischemia, were studied in an acute, anesthetized, open-chest dog preparation (n = 6). Coronary blood flow velocity in the left circumflex was assessed with an intracoronary Doppler catheter. Measurements were made at two pump speeds (minimal = HP1 and maximal = HP7) before coronary ligation (control), after ligation of the LAD (ischemia), and after induction of cardiac failure by multiple ligations of the diagonal branches (failure). Changing from HP1 to HP7 resulted in 1) Increased total cardiac output in ischemia and failure; 2) Increased mean aortic pressure and systemic vascular resistance in control, ischemia, and failure; 3) Decreased LV external work (LV systolic pressure X stroke volume) in control, ischemia, and failure; 4) Decreased LV end diastolic pressure in ischemia; 5) Decreased LV systolic pressure and pressure-rate product in failure; and 6) Increased coronary blood flow/O2 demand ratio in failure. Hemopump support reduced O2 demand by LV decompression, and improved blood flow/O2 demand ratio in the nonoccluded coronaries of ischemic, failing hearts.
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PMID:Effects of Hemopump support on left ventricular unloading and coronary blood flow. 175 Nov 87

Tl-201 myocardial scintigrams in patients with left bundle-branch block (LBBB) are frequently non-diagnostic with respect to presence or absence of coronary artery disease (CAD). The new myocardial perfusion tracer Tc-99m-MIBI requires a different protocol due to its insignificant redistribution. Therefore, scintigraphic patterns in LBBB cannot be deduced from experiences with Tl-201. In a total of 132 patients with LBBB, 81 studies were carried out with Tl-201, another 81 studies with Tc-99m-MIBI. In 30 patients both radiopharmaceuticals were employed. 72% of the Tl-201 scintigraphies in constant LBBB resulted in a reversible septal deficit and 9% in a constant septal deficit. In contrast, 70% of the Tc-99m-MIBI scintigraphies resulted in a constant septal deficit and only 19% in a reversible septal deficit. Similar "discrepancies" were found in LBBB patients in whom CAD has been angiographically excluded (N = 17). All patients, however, with LAD or RCA stenoses and constant LBBB showed reversible septal deficits with either tracer, Tl-201 (N = 12) or Tc-99m-MIBI (N = 10). It is concluded: 1) that the majority of patients with LBBB has reduced septal perfusion, 2) that this reduction is typically stress-independent in absence of CAD, and 3) that this stress-independent perfusion deficit is, in general, only differentiated from stress-induced ischemia (in case of CAD) with using the Tc-99m-MIBI protocol.
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PMID:[Results of myocardial scintigraphy in patients with left bundle-branch block using Tl-201 and Tc-99m-MIBI]. 177 26

A study was designed to quantify the influence of the Hemopump on myocardial metabolism in regional myocardial ischemias induced by repetitive balloon-occlusions (3.5 minutes) of the LAD in 12 sheep (b.w. 49-61 kg). In order to make immediate comparisons and obtain paired-couples, ischemias were carried out with and without the Hemopump in operation. An energetic unloading of the left ventricle was achieved by the Hemopump already under preocclusion conditions, reducing myocardial O2-consumption from 7.52 to 5.98 ml/min/100 g LV (= 20%) as well as lowering the LVEDP from 13.3 to 9.8 mmHg (p less than or equal to 0.01). During ischemia a clear increase of LVEDP (13.3 to 21.0 mmHg) occurs, which was prevented in the group with Hemopump-assist (9.8 to 12.1 mmHg). Combined with a sustained higher diastolic aortic pressure, a better myocardial perfusion pressure resulted. Energetic unloading and improvement of perfusion conditions might be the cause of the significantly lowered release of lactate and potassium. Due to theses fibrillation (n = 3) only occurred during occlusions without Hemopump-support. In summary, a significant reduction of the ischemic burden on the myocardium was found. Thus the Hemopump could be of benefit to patients who fail to be weaned from CPB or who are suffering from instable cardiovascular performance.
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PMID:Myocardial support and protection during regional myocardial ischemia using the Hemopump assist device. 178 11

Directional coronary atherectomy (DCA) was used in 74 patients with an average age of 56 years. They were categorized into three different groups depending on the indications for atherectomy. Group I included all patients who had atherectomy as their primary intervention (n = 26), because they were assumed to be unsuitable for PTCA. Group II consisted of patients in whom DCA was used after failed balloon dilatation with unsuccessful but uneventful treatment (n = 20). Group III (n = 28) included cases where DCA was performed as a "rescue" or "bail-out" procedure after failed PTCA resulted in critical ischemia (ECG changes, chest pain, hypotension, and shock). The target lesions were located in LM 2, LAD 52, RCA 16, ACVB 4. The mean length of lesion was 8 mm (2-25 mm). The overall success rate was 94%. The mean stenosis was reduced from 90.6 +/- 10% to 17.2 +/- 14.8% in cases with primary success. The presently available follow-up angiography (n = 31) showed six restenoses. Major complications occurred in seven cases (death: 0, myocardial infarction: 2, CABG within 24 h: 5). Histological analysis revealed highly cellular areal as a major characteristics of a coronary lesion and also of restenotic tissue. Tissue of the lamina elastica was present in 44% and of media in 14%. Thrombus was found only rarely. Ultrastructure showed a significant amount of extracellular matrix in the primary coronary lesions and isolated smooth muscle cells without gap-junctions. RER, mitochondria were typical for the synthesizing type of smooth muscle cell. In restenotic tissue a focal high density of smooth muscle cells with increased synthesizing activity and gap-junctions was present. Endothelial cells (and macrophages) were found only rarely. Furthermore, altered smooth muscle cells from restenotic tissue showed a significantly increased migration and proliferation. Our results show that DCA is a safe and effective technique that can extend the use of percutaneous procedures and provide a promising, nonsurgical option in cases of failed PTCA. Histological analysis revealed a proliferative process as a characteristics of restenosis development.
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PMID:[Current status of directional coronary atherectomy in interventional cardiology]. 179 47

The effect of thoracic epidural anesthesia (TEA) on the ischemic myocardium was examined in open-chest dogs anesthetized intravenously. Ischemia induced by brief coronary artery occlusion caused an elevation of the ST segment in epicardial ECG and a reduction in myocardial pH and contractile force. TEA with 0.15 ml/kg of 0.4% bupivacaine solution attenuated an ischemia-induced decrease in myocardial pH and an increase of the ST segment in epicardial ECG. This attenuation was maintained even after the restoration of blood pressure and heart rate, which had been decreased significantly after TEA, to pre-TEA levels, suggesting that a beneficial effect of TEA should not be confined to its hemodynamic changes such as decreased blood pressure and heart rate. In contrast, the subendocardial contents of ATP, creatine phosphate (CP) and lactate were not affected by TEA, either in the presence or the absence of 5 min LAD occlusion. These results suggest that neither hemodynamic nor metabolic changes are responsible for the reduced myocardial ischemic acidosis induced by TEA after brief coronary artery occlusion. The acidosis-saving property of TEA is favorable for the ischemic heart.
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PMID:Effects of thoracic epidural anesthesia on myocardial pH and metabolism during ischemia. 189 46

We used directional coronary atherectomy (DCA) as a therapeutic option for coronary lesions unsuitable for PTCA (eccentric, ostial, branching or restenotic) and as "rescue device" for failed PTCA. Forty-two patients were treated by DCA using the Simpson coronary atherectomy device, including four female and 38 male patients with an average age of 55.7 years. Atherectomy as primary intervention was performed in 16 patients (Group I), because morphology of their lesions was assumed to be unsuitable for PTCA. DCA was also used after failed balloon dilatation in eight patients with unsuccessful, but uneventful treatment (Group II). In 18 cases (Group III) DCA was performed as "rescue procedure" after failed PTCA and resulting critical ischemia (local dissection, signs and symptoms of ongoing ischemia, occlusion after PTCA). Target lesions were located in LM 1, LAD 33, RCA 9, CABG 3. Mean length of lesion was 8.1 mm (2-25 mm). The overall success rate for 46 lesions was 93%. Mean stenosis was reduced from 92% to 17% in cases with primary success. Presently, available follow-up angiography (24) showed six restenoses (defined as greater than 50% stenoses). Major complications occurred in seven cases (death: 0, MI: 2, CABG within 24 h: 5; 3 in Group III). "Rescue indication" (Group III) after failed balloon dilatation procedure showed a favorable primary result with a success rate of 78%; only three cases of this group needed CABG. Our results show that DCA is a safe and effective technique which can extend the indication for percutaneous procedures and gives a successful nonoperative option in cases of failed PTCA.
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PMID:[Directional coronary atherectomy: acute results and angiography follow-up in 42 treated patients]. 195 70

The exact time of onset of functional expansion after acute myocardial infarction/ischemia remains unclear in spite of its potential link to chronic pathologic infarct expansion and its potential implications for therapy. To examine this early change in ventricular morphology, 14 open-chest dogs were studied with two-dimensional echocardiography before and after occlusion (10 minutes) of the left anterior descending coronary artery (LAD, n = 7) or circumflex artery (CIRC, n = 7). The endocardial surface area (ESA) and the area of abnormal wall motion (AWM) were reconstructed from the echocardiographic data using a previously reported technique for quantitatively mapping the ESA and extent of AWM. For the total group (N = 14), the mean ESA before occlusion was 48.9 +/- 9.8 cm2, increasing to 65.7 +/- 18.9 cm2 at 10 minutes occlusion (p less than 0.001). For the LAD subgroup, the mean ESA before occlusion was 50.7 +/- 9.3 cm2, increasing to 79.1 +/- 14.1 cm2 at 10 minutes following occlusion (p less than 0.001). For the CIRC subgroup, the mean ESA before occlusion was 47.1 +/- 10.8 cm2, increasing to 52.3 +/- 12.6 cm2 at 10 minutes after occlusion (p less than 0.001). The ESA increase for the LAD subgroup was significantly larger than that of the CIRC subgroup (LAD range 14.5 to 49.9 cm2 versus CIRC range 1.5 to 9 cm2, p less than 0.0001). Coronary occlusion resulted in similarly sized regions of AWM for both subgroups (LAD, 31.3 +/- 12.2 cm2 versus CIRC, 25.9 +/- 10.3 cm2, p = n.s.). For the LAD group, the largest increase in endocardial circumference occurred within the zone of AWM at the apex (39.9 +/- 12%). The endocardial surface area therefore expands immediately after coronary occlusion and the magnitude of this process is primarily related to the site (anteroapical) rather than to the extent of AWM.
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PMID:Immediate regional endocardial surface expansion following coronary occlusion in the canine left ventricle: disproportionate effects of anterior versus inferior ischemia. 200 Jul 41


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