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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Quantification of myocardial performance after regional ischemic injury is difficult because available performance indexes are markedly dependent on concurrent load changes. To develop a more load-insensitive index of myocardial function during ischemia, eight conscious dogs were instrumented to measure left ventricular pressure with micromanometers and myocardial segment length with ultrasonic dimension transducers. Preload was varied by transient vena caval occlusion during control conditions, after 15 min of coronary occlusion, and at intervals during 24 h of reperfusion. Acute ischemia shifted the linear relationship between segmental stroke work (SW) and end-diastolic segment length (EDL) rightward, diminishing the slope and increasing the chi-intercept. Preload recruitable work area (PRWA), defined as the area under the SW-EDL curve, reflected changes in both slope and intercept. During acute ischemia, conventional performance indexes and PRWA decreased significantly and required up to 24 h of reperfusion to return to control values. Of all parameters examined, PRWA was most responsive to prolonged ischemic dysfunction after reperfusion and was insensitive to concurrent load changes. Thus PRWA provides improved precision in quantifying of myocardial dysfunction after regional ischemic injury. This parameter should be especially useful in assessing the subtle effects of acute interventions designed to modify functional recovery.
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PMID:Quantification of regional myocardial dysfunction after acute ischemic injury. 339 29

The mechanical function and perfusion in ischaemic and non-ischaemic myocardium after coronary occlusion was studied in 10 cats using pressure-length loop analysis and radiolabelled microspheres. Measurements in three regions--ischaemic, adjacent normal and remote normal myocardium--all showed different responses to coronary occlusion. In the ischaemic region loop area, segment shortening and tissue flow were markedly reduced. In the adjacent normal region, both loop area and segment shortening as well as flow increased. In the remote normal region, neither loop area, segment shortening nor flow showed consistent changes. End-diastolic segment length increased in all regions, most in the ischaemic region and least in the remote region. The increased end-diastolic segment length in all regions after coronary occlusion indicates activation of the Frank-Starling mechanism as an attempt to maintain stroke volume. However, the end-diastolic segment length did not increase uniformly for all normal myocardium: it depended on the proximity to the ischaemic region. Increased contractile function in the adjacent normal myocardium due to non-uniform distribution of the Frank-Starling effect is the most likely mechanism behind the left ventricle's ability to partially compensate for loss of contractile mass during acute regional ischaemia in anaesthetized cats.
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PMID:Local myocardial function following coronary occlusion in cats. Effect on non-ischaemic regions. 342 84

Peak aortic blood velocity (Vel), peak acceleration (Acc), stroke volume (SV), and left ventricular (LV) ejection fraction (EF) have been used as noninvasive indicators of global LV performance. The purpose of this study was to determine which of these indices of LV performance relates best to the extent of LV ischemic mass at risk. Studies were performed in 24 open-chest anesthetized dogs. Acute ischemia was produced by occlusion of various levels of the left anterior descending and circumflex coronary arteries. LV ischemic mass, measured as a percent of total LV mass, was delineated by injection of Evans blue dye into the nonischemic zone. Acc and Vel were measured with continuous-wave Doppler ultrasound. EF was measured angiographically. All parameters were measured during a control period and within 6 minutes of coronary occlusion. The percent change during ischemia of each parameter relative to control (% delta) was calculated. The correlation coefficient between the percent ischemic mass at risk and % delta Acc was 0.88. It was 0.84 for % delta EF, 0.77 for % delta Vel, and 0.17 for % delta SV. These results indicate that among the various global indices of LV performance that have been used noninvasively, Acc correlates most closely with the extent of LV ischemic mass at risk.
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PMID:Peak aortic blood acceleration reflects the extent of left ventricular ischemic mass at risk. 355 72

We evaluated left ventricular (LV) regional work from a wall tension-regional area (T-A) loop using sonomicrometers in the excised cross-circulated canine left ventricle connected to a volume servo pump. Regional work assessed from a T-A loop closely agreed with the predicted value calculated from LV stroke work and percent regional area under conditions of the control state, dobutamine infusion, and global ischemia. In addition, globally integrated regional work over the entire ischemic and non-ischemic zones agreed closely with LV stroke work either before or after coronary occlusion. These results indicate that LV regional work can be assessed reliably from the T-A loop in both normal and regionally ischemic hearts. Regional work correlated linearly with end-diastolic regional area, indicating a regional Frank-Starling relation, and the slope of this relationship increased with dobutamine infusion and decreased with global ischemia. The correlation between regional work and LV stroke work was also linear and the regression line was the same during the control state and global ischemia, indicating a constant relationship between the work of a specific wall region and LV stroke work regardless of global changes in contractile state. However, after regional ischemia, this regression line apparently shifted downward because T-A loops in the ischemic region were extremely deformed and regional work markedly decreased. From these results, we conclude that T-A loops are a reliable and useful means of assessing regional contractile performance of the LV.
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PMID:Quantitative evaluation of left ventricular regional work from wall tension-regional area loop in canine heart. 358 3

Although prolonged functional abnormalities after transient myocardial ischemia have been well described, the interrelationship between postischemic systolic and diastolic alterations remains controversial. Therefore, 24 chronically instrumented conscious dogs were studied with left ventricular and pleural micromanometers, ultrasonic dimension transducers in the left anterior descending (LAD) coronary distribution, and vena caval and coronary artery occluders. The LAD was occluded for 15 minutes and reperfused for 24 hours while vena caval occlusions were performed at intervals to measure myocardial segment length at 0 mm Hg transmural diastolic left ventricular pressure (L0). Coronary occlusion produced an immediate fall in systolic function as assessed by ejection shortening and stroke work and also induced a 16 +/- 4% increase in L0, which was termed diastolic creep. Throughout reperfusion, reversal of diastolic abnormalities correlated strongly with recovery of segmental shortening and stroke work (p less than 0.001). Correlation between systolic dysfunction and diastolic creep was also observed during alteration of inotropic state by dopamine, during initial reperfusion hyperfunction, and during pharmacologic manipulation of afterload. In 5 additional dog hearts fixed in diastole by rapid glutaraldehyde infusion after coronary occlusion, myocardial creep measured by the segment length transducers paralleled sarcomere elongation measured by electron microscopy. Thus, the direct correlation between diastolic creep and systolic dysfunction throughout reperfusion and during hemodynamic alterations suggests that diastolic properties of postischemic myocardium may not be entirely passive and that systolic and diastolic dysfunction induced by ischemia may have a common basis at the cellular level.
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PMID:Relation between reversal of diastolic creep and recovery of systolic function after ischemic myocardial injury in conscious dogs. 359 57

The ability to reverse acute coronary occlusion with fibrinolytic agents and percutaneous transluminal angioplasty has increased interest in the revascularization of ischemic myocardium. This study defines changes in global ventricular function, mass, and compliance during acute coronary occlusion and following reperfusion with blood in the beating and arrested heart. In 17 dogs on cardiopulmonary bypass, the proximal left anterior descending coronary artery was occluded for 45 minutes. In 12 dogs, flow was reestablished by releasing the coronary snare in the beating heart. In the other 5 dogs, the snare was released during a continuous 10-minute infusion of blood potassium cardioplegia in the arrested heart. Coronary occlusion resulted in significant decreases in stroke work index and left ventricular (LV) mass, but compliance was unchanged. Reperfusion in the beating heart increased LV mass compared with the values measured before ischemia (104 +/- 5 versus 95 +/- 5 gm; p less than 0.05) and decreased LV compliance (39 +/- 4 versus 53 +/- 4 ml at LV end-diastolic pressure of 8 mm Hg; p less than 0.05). In contrast, with blood cardioplegia-based reperfusion in the arrested heart, LV mass and LV compliance remained unchanged from control values. We conclude that revascularization of acutely ischemic myocardium in the beating heart further impairs LV function by increasing LV mass and decreasing compliance. This damage can be avoided by reperfusion with blood cardioplegia in the arrested heart.
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PMID:Controlled reperfusion following regional ischemia. 366 81

Left ventricular function and systemic regional blood flow (radioactive microspheres, 15 +/- 5 mu) were studied 1, 3, 10 or 42 days after left coronary occlusion in conscious rats. One day after coronary occlusion, vascular resistance in the skeletal muscle and cutaneous beds increased while stroke work and left ventricular systolic pressure were depressed. Regional blood flow and hemodynamic data were similar for sham and infarction groups at 3 and 10 days after surgery, except for left ventricular end-diastolic pressure, which was significantly increased in rats with infarction (sham versus infarct: 11.5 +/- 1.0 versus 18.4 +/- 3.2 at day 3 and 12.2 +/- 1.4 versus 19.9 +/- 3.2 at day 10) (p less than 0.05). At 42 days after myocardial infarction, manifest heart failure occurred as documented by decreased cardiac output and left ventricular systolic pressure and elevated left ventricular end-diastolic pressure and vascular resistance in the cutaneous, skeletal muscle and renal beds. In a separate group of animals with moderate (33.2 +/- 2% of left ventricle) and large infarctions (45 +/- 1.3% of left ventricle), regional blood flow was compared with the sham group. Rats with a large infarct demonstrated significant (p less than 0.05) reduction in flow to kidney, gut and liver. In rats with a medium sized infarct, only renal blood flow was significantly reduced. It is concluded that in this model of myocardial infarction, early cardiocirculatory depression is followed by a partially compensated state with increased left ventricular end-diastolic pressure and subsequent systemic and regional vasoconstriction which, in turn, may contribute to late deterioration of heart failure.
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PMID:Regional vascular adjustments during recovery from myocardial infarction in rats. 371 8

This study tests the hypotheses that postischemic adenosine triphosphate levels are unreliable predictors of functional recovery, myocardial adenosine triphosphate concentration of less than 2 mumol/gm does not indicate irreversible damage, mitochondrial adenosine triphosphate generating capacity can be nearly normal despite low levels of tissue adenosine triphosphate and the failure to replenish adenosine triphosphate after ischemia is due to depletion of the adenosine nucleotide pool, which can be replenished partially by exogenous precursors (e.g., 5-amino-4-imidazolecarboxamide ribotide [AICAR]). Myocardial adenosine triphosphate was depleted to less than 2 mumol/gm by either global ischemia (37 degrees C aortic clamping) or regional ischemia (acute coronary occlusion). Reperfusion was either with normal blood or with substrate-enriched blood cardioplegic solution during total vented bypass. Tissue adenosine triphosphate content and mitochondrial adenosine triphosphate generating capacity were measured, and functional recovery was determined by right heart bypass function curves or regional segmental shortening (ultrasonic crystals). Hearts undergoing 15 minutes of global ischemia and normal blood reperfusion had impaired functional recovery (stroke work index = 58 +/- 5%; p less than 0.05 of control) despite adenosine triphosphate concentration greater than 2 mumol/gm. Transmural mitochondrial State 3 respiration averaged 83% of control values despite adenosine triphosphate levels of 1 mumol/gm in hearts undergoing 45 minutes of 37 degrees C global ischemia and 2 additional hours of aortic clamping with multidose glutamate-enriched blood cardioplegia. AICAR increased adenosine triphosphate to 2 mumol/gm (p less than 0.05), but functional recovery was nearly complete (stroke work index = 94 +/- 2% of control) and was comparable with and without AICAR. Hearts undergoing 4 hours of regional ischemia recovered 31 +/- 5% systolic shortening after controlled reperfusion despite tissue adenosine triphosphate less than 0.5 mmol/gm (15% of control), and they retained 63% adenosine triphosphate generating capacity. Postischemic adenosine triphosphate levels correlate poorly with functional recovery, and adenosine triphosphate levels less than 2 mumol/gm do not indicate irreversible ischemic injury. Low postischemic levels may be repleted partially by adenine nucleotide precursor supplementation (AICAR).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Biochemical studies: failure of tissue adenosine triphosphate levels to predict recovery of contractile function after controlled reperfusion. 374 77

The antiarrhythmic and haemodynamic effects of tiapamil, a new calcium antagonist, were studied in 28 anaesthetised open chest dogs. Tiapamil (2 mg X kg-1 intravenously over 5 min) was infused 15 min before a 20 min ligature of the left anterior descending coronary artery in 11 dogs. In 17 dogs physiological solution was given instead of tiapamil. In this control group, ventricular fibrillation developed during coronary occlusion in 14 (82%) dogs and after coronary reperfusion in seven of 9 (77%) dogs, which reached this stage. In contrast, in the dogs pretreated with tiapamil, ventricular fibrillation did not develop during coronary occlusion in any of the 11 dogs and did develop after coronary reperfusion in only one (9%). In addition, tiapamil appreciably decreased heart rate and blood pressure and increased cardiac output and stroke volume. These antiarrhythmic and haemodynamic effects of tiapamil suggest that this drug would be useful in the management of patients with coronary artery disease.
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PMID:Antiarrhythmic and haemodynamic effects of tiapamil, a new calcium antagonist, during coronary artery occlusion and reperfusion in dogs. 379 54

The effects of nafazatrom (10 mg/kg, b.i.d., orally for 2 days preoperatively; 10 mg/kg, intraduodenally, 30 min before coronary occlusion) on hemodynamics and arrhythmias were assessed in a group of drug-treated anesthetized pigs and compared with the effects in animals that received the drug vehicle and were treated identically. Infarct size (triphenyl-tetrazolium method) of the left anterior descending coronary artery was 24.4 +/- 2.4% of the left ventricle in nafazatrom-treated hearts after 2 h of occlusion and 26.2 +/- 3.2% in control hearts. Blood pressure, heart rate, left ventricular systolic and end-diastolic pressure, cardiac output and stroke volume were not different between the groups during cardiac insult. There were no differences in the number of premature ventricular contractions, arrhythmia and tachycardia, and ventricular fibrillation. It is concluded that short-term administration of the 5-lipoxygenase inhibitor nafazatrom had no effect on infarction, hemodynamics or arrhythmias in the acutely ischemic porcine myocardium.
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PMID:Failure of nafazatrom to reduce infarct size and arrhythmias in a porcine model of acute coronary occlusion. 393 Feb 68


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