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

Recent studies have suggested that topical hypothermia may be unnecessary during coronary bypass operations because of possible pulmonary complications resulting from phrenic nerve damage. This study was undertaken to determine whether topical hypothermia is necessary for optimal myocardial protection when distribution of the cardioplegic solution is heterogeneous because of coronary occlusions. Twenty pigs were subjected to 120 minutes of ischemic arrest with multidose potassium crystalloid cardioplegia (4 degrees C). During arrest, the mid-left anterior descending coronary artery was occluded with a snare that was released on reperfusion. Ten of these pigs received topical hypothermia and 10 others served as controls. Hearts protected with topical hypothermia had lower temperatures in the left anterior descending (7.0 degrees +/- 0.7 degree C versus 18.5 degrees +/- 0.5 degree C; p less than 0.05) and circumflex regions (8.9 degrees +/- 0.5 degree C versus 15.5 degrees +/- 0.5 degree C; p less than 0.05). The pH values were higher in hearts protected with topical hypothermia in both the left anterior descending (7.36 +/- 0.09 versus 6.73 degrees +/- 0.07; p less than 0.05) and circumflex regions (7.40 +/- 0.07 versus 7.05 +/- 0.07; p less than 0.05). Topical hypothermia also resulted in better preservation of postischemic stroke work index (0.64 +/- 0.06 versus 0.40 +/- 0.08 gm-m/kg; p less than 0.05) and wall motion scores (1.0 +/- 0.3 hypothermia versus 1.8 +/- 0.4 no hypothermia; p less than 0.05). We conclude that topical hypothermia affords maximal myocardial protection when coronary occlusions are present and should be used during all coronary operations.
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PMID:Importance of topical hypothermia during heterogeneous distribution of cardioplegic solution. 275 57

Afterload independent, inotropic state sensitive indices of regional function were sought in 31 canine hearts instrumented with piezoelectric crystals to depict trapezoidal areas in the left anterior descending and circumflex arterial beds. Control and postinterventional end-systolic pressure versus regional length and area relationships and regional stroke work versus end-diastolic length and area relationships were inscribed during incremental volume loading on right heart bypass. Hearts were randomized to undergo afterload variation with phenylephrine infusion, contractility augmentation by calcium chloride, or 20 minutes of ischemia in the region of the left anterior descending artery with 30 minutes of reperfusion. All relationships were linear before and after each intervention (mean r = 0.726 to 0.974). The slopes of each correlation were interpreted to quantify intrinsic regional contractility, and all were afterload insensitive (unaffected by phenylephrine). Regional stroke work versus end-diastolic area and length relationships were depressed 55% and 62%, respectively, after ischemia (p less than 0.001 each), whereas neither end-systolic pressure versus regional area nor regional length was significantly altered. Calcium chloride increased regional stroke work versus area 45% in both arterial beds, but significantly increased the other indices only in the left anterior descending and not the left circumflex region. Unlike previous studies of global contractility, correlation of end-systolic events alone did not reliably discriminate perturbations in regional function. The superiority of regional stroke work versus end-diastolic area may be due to incorporating pressure-area changes during the entire cardiac cycle and obviating variability owing to crystal orientation inexactly parallel to fiber shortening.
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PMID:Assessment of the intrinsic contractile state within an area of myocardium. 281 15

In order to validate the measurement of pressure-volume loops and stroke work in humans, simultaneous digital subtraction ventriculography (DSA) and first-pass radionuclide angiocardiography (RNA) coupled with high-fidelity micromanometer left ventricular pressure measurements were undertaken in 34 patients, mean age 75 +/- 9 years, with aortic stenosis. Twenty-nine patients had a repeat study after balloon valvuloplasty, for a total of 63 DSA and RNA pressure-volume loops. All data were analyzed in a systemic fashion in order to minimize intra- and interobserver error. Linear regression analysis was used to calculate the degree of agreement between the two technologies. Left ventricular ejection fraction (RNA: 0.47 +/- 0.17, DSA: 0.49 +/- 0.18) had a correlation coefficient of 0.96; left ventricular end-diastolic volume (RNA: 171 +/- 42 ml, DAS: 168 +/- 52 ml) and end-systolic volume (RNA: 95 +/- 50 ml, DSA: 89 +/- 50 ml) had correlation coefficients of 0.89 and 0.95, respectively. Left ventricular stroke volume (RNA: 75 +/- 26 ml, DSA: 75 +/- 27 ml) had a correlation coefficient of 0.92, while integrated pressure-volume loop or stroke work (RNA: 15.6 +/- 6.6 ergs 10(6), DSA: 15.9 +/- 6.3 ergs 10(6] had a correlation coefficient of 0.89. These data demonstrate that RNA measurements of left ventricular chamber dynamics concur with that obtained with DSA. With semiautomated data analysis, the portable first-pass RNA pressure-volume data are also less labor-intensive. Moreover, multiple measurements of ventricular performance during hemodynamic manipulations in the catheterization laboratory or operating room would allow for a more precise estimation of left ventricular performance.
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PMID:Validation of pressure-volume data obtained in patients by initial transit radionuclide angiocardiography. 281 10

In the present study the hypothesis is tested that hypoxia causes morphological damage to the inner mitochondrial membrane and that this damage can be reversed by modification of the reoxygenated perfusate. Using the working rat heart model, hearts in group I (n = 40) were subjected to a 30 min normothermic, normoxic phase and a 90 min hypoxic phase, followed by 60 min reoxygenation. Hearts in group II (n = 32) were also subjected to a 30 min normoxic and a 90 min hypoxic phase. However, after 30 min of reoxygenation 1.5 mmol/l 2-mercaptopropionylglycine (MPG) was injected in the reoxygenated solution in order to test its ability to improve mitochondrial function. Mitochondrial function was assessed by measuring oxygen uptake (ST3), ST4, respiratory control index (RCI), ADP/O and oxidative phosphorylation rate (OPR). In addition mechanical function (heart rate, aortic and coronary flow, cardiac output, stroke volume) was monitored along with ultrastructural parameters. 90 min of hypoxia caused a deterioration of all parameters with persistent impairment in hemodynamic, morphologic and biochemical functions after 60 min of reoxygenation (group I). The role of the ATP-synthetases in the pathogenesis of oxygen-paradox is discussed. In contrast, the MPG-enriched reoxygenated solution (group II) improved hemodynamics, ultrastructure and mitochondrial function significantly (alpha = 0.05). It is concluded from these data that the ATP-synthetases are damaged during oxygen-deficiency and that MPG may be a useful drug for protecting the inner mitochondrial membranes during reoxygenation.
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PMID:Improvement of myocardial function after global hypoxia by protection of the inner mitochondrial membrane. 295 43

The effects of ethanol and pentobarbital on the function of isolated working hearts from control and ethanol-fed male Long-Evans rats were studied. Hearts from ethanol-fed animals (38% of calories; 10-12 months) exhibited functional tolerance to the cardiodepressive effects of 18-71 mM ethanol in the perfusing medium. Left ventricular systolic pressure, peak relaxation rate, isovolumic pressure indexes, peak aortic flow rate, cardiac output, and stroke work of the control hearts were depressed to a greater extent than were those indexes of the alcoholic rat hearts during exposure to ethanol in vitro. Differences in the functional responses of controls and alcoholics were not the result of differences in energetics; myocardial O2 consumption, O2 supply-to-utilization ratio, and external work efficiency changed similarly in both groups of hearts during perfusion with ethanol. Cross-tolerance of the alcoholic rat hearts to the in vitro cardiodepressive effects of pentobarbital was also apparent. Peak rate of left ventricular pressure development, peak aortic flow rate, isovolumic pressure indexes, and cardiac output of the control rat hearts were significantly lower than those indexes of the alcoholic rat hearts during perfusion with 0.5 mM pentobarbital. In addition, four of the seven control hearts could not be paced during pentobarbital perfusion using 3V electrical pulses; the pacing voltage had to be raised and right ventricular pacing used to maintain stable function of those hearts at a 321 beats/min pacing rate. Myocardial O2 consumption and O2 supply-to-utilization ratios of control and alcoholic rat hearts were similar, but external work efficiency was slightly higher in the alcoholics than in controls during pentobarbital perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tolerance to ethanol and cross-tolerance to pentobarbital by isolated hearts from chronic alcoholic rats. 305 74

Hemodynamic, contractile and energetic functions of isolated working hearts from ethanol-fed and control rats were studied to determine the time course of cardiac dysfunction development during long-term consumption of alcohol. Hearts from fasted, 24 hr withdrawn rats were studied after 2, 4, 7 and 11 months consuming ethanol as 38% of daily calories in a nutritionally-adequate liquid diet. After 2 months, the right ventricle of the alcoholic rat hearts was significantly enlarged; left ventricular weight was not significantly different from control and there was little evidence that left ventricular function was compromised. After 4 months and 7 months, there was biventricular cardiomegaly and evidence of reduced left ventricular function in the alcoholics, although altered sensitivity to the positive inotropic agent, dobutamine, was not evident in those hearts. After 11 months, cardiac output, stroke work, and peak power of the alcoholic rat hearts were significantly depressed, the responsiveness of the left ventricle to dobutamine was diminished, and both ventricles were enlarged compared to controls. Cardiac function during early withdrawal was studied in rats that had consumed alcohol for 14-16 months. Hearts from non-fasted rats at 0 hr of withdrawal exhibited diminished responsiveness to dobutamine compared to controls; at 24 hr and 72 hr of withdrawal no differences between alcoholic and control rat heart dobutamine responsiveness were observed. The data indicated that: (a) cardiomegaly, beginning with right ventricular enlargement, was an early indicator of alcohol's cardiac effects in rats; (b) left ventricular enlargement of the alcoholic rat hearts was associated with basal left ventricular dysfunction; and (c) evidence of cardiac subsensitivity to dobutamine, which is characteristic of this alcoholic rat model, depended on the nutritional status and withdrawal state of the rat at the time that the heart was excised for study.
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PMID:The development of alcohol-induced cardiac dysfunction in the rat. 322 60

The effects of left ventricular venting and distention on myocardial protection during heterogenous distribution of cardioplegic solution remain undefined. This study was undertaken to determine if left ventricular venting enhances and distention impairs myocardial cooling and recovery of global and regional left ventricular function. Twenty-one pigs were placed on cardiopulmonary bypass and subjected to 80 minutes of ischemic arrest with the mid-left anterior descending artery occluded. Hearts were protected with multidose potassium (25 mEq/L) crystalloid cardioplegic solution supplemented with topical (4 degrees C) and systemic (28 degrees C) hypothermia. During arrest, the left ventricle was vented in seven pigs, seven pigs were not vented, and seven others had systemic pump blood infused into the left ventricle to maintain an end-diastolic pressure of 15 mm Hg. Parameters measured included left ventricular temperature, stroke work index, compliance (end-diastolic pressure-end-diastolic volume curves) and wall motion scores (two-dimensional echocardiography). Distended hearts had the lowest mean left ventricular temperature beyond the left anterior descending arterial occlusion (10.1 degrees +/- 1.8 degrees C distended [p less than 0.025 from vented and nonvented groups] versus 14.2 degrees +/- 0.7 degrees C vented versus 15.5 degrees +/- 1.2 degrees C nonvented), the highest postischemic stroke work index (0.78 +/- 0.09 gm-m/kg distended versus 0.62 +/- 0.07 gm-m/kg vented versus 0.66 +/- 0.07 gm-m/kg nonvented at end-diastolic pressure = 10 mm Hg), and the best wall motion scores (0.7 +/- 0.04 distended [p less than 0.025 from vented and nonvented groups] versus 5.5 +/- 1.80 vented versus 4.8 +/- 1.20 nonvented). Postischemic end-diastolic pressure-end-diastolic volume curves were unchanged from preischemic values in each group. We conclude that during heterogenous cardioplegic arrest, left ventricular venting offers no additional myocardial protection and may negate the beneficial effects of moderate (end-diastolic pressure = 15 mm Hg) left ventricular distention.
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PMID:Effects of left ventricular venting and distention during heterogenous distribution of cardioplegic solution. 334 57

The decrease in myocardial contractility during ischemia, hypoxia, and extracellular acidosis has been attributed to intracellular acidosis. Previous studies of the relationship between pH and contractile state have utilized respiratory or metabolic acidosis to alter intracellular pH. We developed a model in the working perfused rat heart to study the effects of intracellular acidosis with normal external pH and optimal O2 delivery. Intracellular pH and high-energy phosphates were monitored by 31P nuclear magnetic resonance spectroscopy. Hearts were perfused to a steady state with a medium containing 10 mM NH4Cl (extracellular pH, 7.4). The subsequent washout of NH3 from the cytosol generated a slight acidosis (from intracellular pH 7.0 to 6.8) which was associated with little change in the determinants of O2 consumption (rate-pressure product) and O2 delivery (coronary flow). Acidosis induced a substantial decrease in aortic flow and stroke volume which was associated with little change in peak systolic pressure. Results were qualitatively similar at different external [Ca2+] (1.75, 2.5, 3.15 mM) and preload (12 or 21 cmH2O) but were most prominent at the lowest external [Ca2+] and left atrial pressure. In contrast to this model of isolated intracellular acidosis, hearts subject to a respiratory (extracellular plus intracellular) acidosis showed a marked reduction in pressure development. It was concluded that 1) for the same intracellular acidosis the influence on tension development was more pronounced with a combined extra- and intracellular acidosis than with an isolated intracellular acidosis, and 2) stroke volume at constant preload was impaired by intracellular acidosis even though changes in developed pressure were minimal. These observations suggest that isolated intracellular acidosis has adverse effects on diastolic compliance and/or relaxation.
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PMID:Influence of intracellular acidosis on contractile function in the working rat heart. 342 50

Effect of a chronic excess or deficit of thyroid hormone on intrinsic myocardial performance in rats was assessed. Animals were thyroidectomized or treated with thyroid hormone or vehicle 6-7 wk before the study. Body weight and heart weight were decreased in the hypothyroid group, and heart weight was elevated in the hyperthyroid group. Hearts were removed from thyroidectomized, euthyroid or thyroid-treated animals and studied as isolated, perfused working heart preparations. Ventricular function curves were generated by increasing left atrial filling pressure, whereas outflow resistance was not varied. Coronary flow, aortic outflow (and thus cardiac output), heart rate, and peak aortic systolic pressure were measured as a function of preload. These studies showed that performance of hearts from hyperthyroid animals was similar to that of euthyroid controls. Hearts from hypothyroid rats had decreased rate, pressure, and cardiac output but normal stroke volume. Since heart weight was 55% lower than control, normalization of volume work to dry heart weight reversed the difference in cardiac output. Comparison of hearts from hypothyroid animals to control rats of similar weight showed minimal differences in pump function. Thus hyperthyroidism did not result in altered in vitro cardiac output or peak systolic pressure as a function of changing preload when compared with age-matched euthyroid controls, hypothyroidism resulted in a decreased in vitro heart rate but greater cardiac output normalized to heart weight when compared with age-matched controls and hyperthyroid animals; external pacing of hypothyroid hearts yielded myocardial work parameters that were comparable to euthyroid control rats of similar body weight; and cardiac efficiency was significantly greater in hypothyroid hearts than in hyperthyroid hearts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of altered thyroid status on in vitro cardiac performance in rats. 356 93

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


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