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Biomedical subjects

D R Abendschein

Publications and source records attributed to D R Abendschein.

At least 73 records · Page 4Linked to original sources
PubMed1988

Compromise of beneficial effects of reperfusion on myocardium supplied by vessels with critical residual stenosis.

Coronary thrombolysis in patients frequently unmasks high grade residual stenosis. To determine whether beneficial effects of reperfusion are compromised by critical residual coronary stenosis, 14 dogs were instrumented with an external left anterior descending coronary artery balloon occluder, Doppler flow probe and adjustable screw clamp. In eight of the dogs, critical stenosis (abolition of reactive hyperemia after a 20 s occlusion; 95.7 +/- 1.0% cross-sectional area reduction) was induced before occlusion and maintained. In the control group (n = 6), no stenosis was induced. Each dog was subjected to 2 h of myocardial ischemia followed by balloon deflation and 24 h of reperfusion. Myocardial blood flow assessed with microspheres was similar during balloon inflation in both groups and indicative of profound ischemia. Transmural blood flow to the reperfused zone assessed 1 min after balloon deflation was significantly greater in control dogs without residual stenosis (383% of normal compared with 120% of normal in dogs with stenosis) (p less than 0.01). Compromise of transmural flow persisted in dogs with stenosis (85% compared with 121% of normal in control dogs after 1 h, p less than 0.05; and 49% compared with 68% after 24 h of reperfusion, p less than 0.05). Diminution of subendocardial blood flow after reperfusion was particularly marked. The extent of infarction was greater in the heart of dogs with residual stenosis. Thus, residual critical coronary stenosis compromises nutritional perfusion and salvage of reperfused myocardium after recanalization. These observations underscore the need for prompt identification of patients with high grade residual stenosis early after coronary thrombolysis and the potential value of angioplasty or coronary surgery in selected patients soon after initial recanalization.

Angioplasty, Balloon↗
PubMed1988

Quantitative analysis for isoforms of creatine kinase MM in plasma by chromatofocusing, with on-line monitoring of enzyme activity.

Changes in the proportions of individual isoforms of the MM isoenzyme of creatine kinase (CK; EC 2.7.3.2) in plasma promptly reflect both myocardial infarction and coronary recanalization. However, quantitative methods developed thus far are too slow or cumbersome for routine use in making clinical decisions. We report a convenient, quantitative chromatofocusing assay with on-line fluorometric detection of isoform activity in the column eluent that provides results within 40 min from the time of sample application. Sample eluted from a microbore chromatofocusing column (1.8-mL bed volume) is split between a reaction stream, into which CK reagents are added, and a reference stream. After incubation at 37 degrees C, NADPH formed by reaction of isoforms with CK reagent is detected at 340 nm. The system can detect activity of individual isoforms in plasma samples having total CK activity greater than or equal to 21 U/L (30 degrees C). Results correlated closely with those obtained by previously validated, but slow, chromatofocusing (r = 0.98, n = 30) and protein immunoblotting (r = 0.90, n = 20) procedures.

Animals↗
PubMed1987

Metabolism of beta-methyl[1-11C]heptadecanoic acid in canine myocardium.

To assess the contributions of metabolism to CO2 and back-diffusion of nonmetabolized tracer to total clearance of beta-methyl[1-11C]heptadecanoic acid ([1-11C]BMHDA) from myocardium and its distribution into lipid pools, 10-15 mCi of [1-11C]BMHDA were rapidly infused into the circumflex coronary artery of seven open-chest dogs. Externally detected clearance of myocardial 11C-activity was protracted (t1/2 = 41 +/- 18 min) with over 50% of extracted tracer retained in tissue after 20 min. Efflux of extracted [1-11C]BMHDA between 5 and 20 min was comprised of both 11CO2 (16.5 +/- 15.2%) and nonmetabolized [11C]BMHDA (24.6 +/- 11.5%). At 20 min, 11C-activity in lipid was distributed primarily between triglyceride (47 +/- 16% of total) and phospholipid (39 +/- 17%) pools. Partial oxidation to 11CO2 and partitioning into more than one lipid pool are likely to hinder evaluation of fatty acid metabolism based on residue detection of [1-11C]BMHDA with tomography.

Animals↗
PubMed1987

Metabolic fate of radiolabeled palmitate in ischemic canine myocardium: implications for positron emission tomography.

Interpretation of dynamic and integrated myocardial tomograms requires elucidation of the biochemical fate of the tracer and characterization of its tissue distribution and rate of efflux. The fate of [1-11C] and [1-14C]palmitate was studied in 13 open-chest dogs during control or ischemic extracorporeal perfusion of the left circumflex coronary artery. Residue detection of myocardial radioactivity, and radio-biochemical analyses of sequential transmural biopsies and arterial and coronary venous effluent were performed for 30 min after intracoronary bolus administration of tracer. In control hearts, 10.3% of initially extracted tracer was retained in tissue (2.9% in triglyceride, 3.5% in phospholipid, and 3.9% in other lipid and aqueous fractions), 73.7% was oxidized, and 16.1% back-diffused unaltered. With ischemia (pump flow 10% of normal), 28.1% was retained (18% in triglyceride, 6.0% in phospholipid, and 4.1% in other lipid and aqueous fractions), 27.2% was oxidized, and 44.4% back diffused (p less than 0.05 compared to control). Throughout the 30-min study interval, triglyceride, diglyceride, and nonesterified fatty acid comprised a significantly greater fraction of initially extracted radioactivity in ischemic than in control hearts. Thus, during ischemia externally detected clearance rates cannot be used as a direct measure of fatty acid metabolism because of marked influences on efflux of nonmetabolized radiolabeled palmitate and the distribution of tracer retained in tissue. Quantitative measurements of specific metabolic processes by tomography will require development and validation of tracers confined to individual metabolic pathways or pools.

Animals↗
PubMed1987

Assessment of coronary thrombolysis.

The efficacy of coronary thrombolysis may be assessed by several invasive and noninvasive means, including coronary angiography, contrast and radionuclide angiography, thallium 201 or 99mTc-pyrophosphate scintigraphy, positron emission tomography, cardiac ultrasonography, electrocardiography, and analysis of plasma creatine kinase activity. Each technique has its own strengths and limitations, but when used in concert these methods may provide insight into the physiology of coronary reperfusion and the efficacy of reperfusion in individual patients and populations.

Angiocardiography↗
PubMed1987

Conversion of MM creatine kinase isoforms in human plasma by carboxypeptidase N.

This study was undertaken to identify the carboxypeptidase(s) (CPase) in plasma mediating sequential conversion of the tissue isoform of the MM isoenzyme of creatine kinase (MM3 CK) to MM2 and MM1 isoforms and to elucidate relationships between CPase activity measured in plasma and observed rates of isoform conversion in vitro. Purified MM3 was incubated at 37 degrees C in plasma from normal subjects and patients with acute myocardial infarction. Isoforms were quantified by chromatofocusing. Preincubation with antiserum to CPase N prevented conversion of added MM3 to MM2 and MM1. Isoform conversion rates in the absence of antibody were proportional to plasma CPase N activity assayed spectrophotometrically by hydrolysis of furylacryloyl-L-alanyl-L-lysine substrate (r = 0.89, n = 8). Plasma CPase N activity varied by nearly 300% among individuals, but average activity was similar in samples from normal subjects (267 +/- 45 [SD] U/L, n = 18), those from outpatients with angina (289 +/- 43 U/L, n = 9), and those obtained at hospital admission from patients with acute infarction (Q wave: 279 +/- 70 U/L, n = 16; non-Q wave: 272 +/- 61 U/L, n = 14) or unstable angina (280 +/- 71 U/L, n = 11). In patients with Q wave infarction, CPase N activity increased by 43% +/- 25% between 48 hours and 72 hours (P less than 0.005 compared with admission) with a concomitant change in the rate of conversion of isoforms. Thus, the rate of conversion of isoforms in individual subjects can be estimated by assay of CPase N activity in plasma.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Mercaptopropionic Acid↗
PubMed1986

Early detection of myocardial reperfusion by assay of plasma MM-creatine kinase isoforms in dogs.

To determine whether myocardial reperfusion can be detected promptly by changes in profiles of isoforms of MM-creatine kinase (CK) in plasma, coronary occlusion was induced in 30 conscious dogs and reperfusion was initiated after 1, 2, 3, or 4 hr in 21. The myocardial isoform of MM-CK, MMA, was quantified in serial plasma samples by chromatofocusing. Before coronary occlusion, MMA comprised 13 +/- 7% (SD) of the total CK activity in plasma. The percentage of MMA (MMA%) was elevated before reperfusion, but increased markedly and consistently to a peak of 52 +/- 13% (n = 21) between 30 min and 1 hr after the time of onset of reperfusion. The rate of increase in MMA% was significantly faster with reperfusion at 1 hr (1.44 +/- 0.42% min-1), 2 hr (1.28 +/- 0.45% min-1), or 3 hr (1.02 +/- 0.27% min-1) (p less than .001), but not with reperfusion at 4 hr (0.48 +/- 0.34% min-1) compared with the rate in nonreperfused control dogs (0.29 +/- 0.09% min-1). Furthermore, the rate of increase in MMA% was neither influenced by peak total CK activity (r = -.1) nor dependent on infarct size measured histochemically 24 hr after coronary occlusion (r = -.003). The time from coronary occlusion to the peak of MMA% was reduced by reperfusion at 1 to 3 hr compared with control, but this index was not identified as rapidly as the rate of increase in MMA%. Accordingly, characterization of the rate of increase in MMA% in plasma when reperfusion occurs early after the onset of myocardial infarction permits prompt, reliable, and noninvasive detection of myocardial reperfusion.

Animals↗
PubMed1985

Early detection of myocardial infarction in conscious dogs by analysis of plasma MM creatine kinase isoforms.

To determine whether myocardial infarction could be detected early after onset by analysis of subforms of the MM isoenzyme (isoforms) of creatine kinase (MM CK) in plasma, we subjected eight conscious dogs to coronary occlusion and quantified isoforms in serial plasma samples by chromatofocusing. The fractions of MMA (isoelectric point [pI] = 7.91), MMB (pI = 7.74), and MMC (pI = 7.51) in plasma samples before coronary occlusion averaged 11.4 +/- 4.8% (SD), 22.3 +/- 5.5%, and 66.3 +/- 9.6% of total MM CK activity. The fraction of MMA, the isoform of MM CK found in myocardium, increased significantly in plasma 1 hr after coronary occlusion, reached a maximum of 49.7 +/- 8.0% in 4.1 +/- 1.3 hr, and returned to baseline in 12.0 +/- 2.3 hr. The fraction of plasma MM CK activity attributable to MMC, an isoform formed slowly in plasma from MMA via MMB as an intermediate, decreased significantly within 1 hr, reached a minimum of 14.0 +/- 4.1% in 4.8 +/- 1.1 hr, and returned to baseline in 13.0 +/- 2.9 hr after coronary occlusion. Total CK activity did not increase significantly until later, i.e., 5 hr after occlusion, and peaked at 1371 +/- 530 IU/liter in 10.9 +/- 1.9 hr. Within the first 4 hr after coronary occlusion, MMA consistently comprised more than 20% of plasma MM CK activity despite insignificant increase of total CK. Changes in isoform proportions were consistent and independent of peak total CK activity and of cumulative CK release over a 10-fold range. Thus initial CK release indicative of infarction is detectable within 1 hr after the onset of ischemia by quantification of plasma MM CK isoforms.

Animals↗
PubMed1985

Efflux of metabolized and nonmetabolized fatty acid from canine myocardium. Implications for quantifying myocardial metabolism tomographically.

It has generally been assumed, from assessment of myocardial metabolism with [1(-11)C]palmitate and positron emission tomography, that clearance of the radiolabel from the myocardium is attributable solely to efflux of the products of oxidative metabolism. However, interpretations would differ if this assumption were unfulfilled. Furthermore, efflux of metabolized and nonmetabolized tracer has not been quantified. Accordingly, in this study, myocardium was perfused extracorporeally in 21 open-chest anesthetized dogs, and the extraction and clearance of [1(-11)C]palmitate were characterized under baseline conditions (normoxia, n = 21), and, again, with ischemia (n = 6), with hypoxia (n = 9), or under control conditions (n = 6). After intracoronary bolus injection of [1(-11)C]palmitate, myocardial time activity curves were measured with a beta-probe, and the products of oxidative metabolism (11CO2) and efflux of extracted but nonmetabolized fatty acid ("back-diffusion" of [1(-11)C]palmitate) were measured directly from analysis of arterial and regional coronary venous blood. Under control conditions, 45.2 +/- 3.8% (mean +/- SD) of initially extracted [1(-11)C]palmitate was metabolized to 11CO2, whereas 6.2 +/- 2.6% back-diffused in unaltered form in 1-10 minutes. In contrast, with ischemia (perfusion of 26% of baseline), only 16.9 +/- 9.8% of administered tracer evolved as 11CO2 (P less than 0.001 compared with control) but 15.6 +/- 8.9% (i.e., almost half of the total amount cleared) evolved unaltered as [1(-11)C]palmitate (P less than 0.05). Similarly, with hypoxia, 15.1 +/- 8.4% evolved as 11CO2 (P less than 0.0001) and 18.8 +/- 11.7% back-diffused (P less than 0.001). Overall, from 1-40 minutes after intracoronary injection of tracer, back-diffusion of [1(-11)C]palmitate contributed 40.6% of total radioactivity in the effluent with ischemia, 48.7% with hypoxia, but only 8.9% under control conditions. Despite the increased back-diffusion of [1(-11)C]palmitate seen with ischemia and hypoxia, the overall residue of 11C activity in myocardium increased, consistent with the diminished clearance observed in the myocardial time-activity curves and the increase in the tissue content of triglyceride and nonesterified fatty acid. Our results indicate that estimates of oxidative metabolism based upon clearance of radiolabeled fatty acid must take into account the efflux of initially extracted but nonmetabolized fatty acid. The findings apply to external determination of oxidative metabolism of the heart with any imaging modality that delineates retention and clearance of labeled fatty acids or their analogs.

Animals↗
PubMed1984

Effect of whole-body hypothermia on myocardial blood flow and infarct salvage during coronary artery occlusion in dogs.

The effect of moderate whole-body hypothermia on blood flow to acutely ischemic and nonischemic myocardium and on the relationship between blood flow and necrosis after 5 hours of left anterior descending (LAD) coronary artery occlusion was investigated in 20 dogs. Blood flow to ischemic myocardium was not significantly increased or decreased by hypothermia. However, much less myocardial necrosis (shown by nitro blue tetrazolium staining) was observed in the hypothermia-treated animals. Therefore, this protective effect of hypothermia is not a result of improved blood flow to the ischemic region, but is more likely due to decreased metabolic requirements. Nearby noninfarcted myocardium had slightly higher blood flow than homologous tissue in the corresponding controls under both normothermic and hypothermic conditions. This tissue, which must compensate for the loss of contractility in the ischemic region, appears to maintain its ability to respond to increased demand for blood flow even during moderate hypothermia. Blood pressure and cardiac output data indicate that hypothermia did not interact with myocardial infarction to produce or exacerbate cardiogenic shock. Consequently, whole-body hypothermia may prove to be a safe and effective emergency pretreatment which may significantly decrease the amount of necrotic myocardium when initiated prior to emergency coronary artery bypass surgery.

Animals↗
PubMed1984

Creatine kinase MM isoenzyme subforms in myocardium, cardiac lymph and blood after coronary artery occlusion in dogs.

A time-varying pattern of creatine kinase MM (CK-MM) isoenzyme subforms has been found in the blood of patients after acute myocardial infarction, but the site of enzyme modification has not been identified. Therefore, we studied the CK-MM subform patterns in myocardium, cardiac lymph and blood of dogs after coronary artery occlusion. In five conscious dogs, serial blood samples were taken for 72 h after occlusion of the left anterior descending coronary artery. Samples of non-infarcted and infarcted myocardium were taken after 72 h. In five other anaesthetised, open-chest dogs, cardiac lymph and blood samples were taken for 6 h after coronary artery occlusion. CK-MM subforms were quantitated by an isoelectric focusing method. Before coronary occlusion, 64% of the total CK activity in blood appeared as the anodal subform CK-MM 1 (pI 6.3); 20% and 9% as the cathodal subforms CK-MM 2 (pI 6.6) and CK-MM 3 (pI 6.9), respectively. However, after 2 h of coronary occlusion CK-MM 2 and CK-MM 3 were increased (38% and 17% of total activity respectively) compared with CK-MM 1. Between 4 h and 10 h, CK-MM 2 and CK-MM 3 decreased as CK-MM 1 increased restoring the control relative activities of subforms. In contrast to the subform changes in blood, CK-MM 3 was the predominant subform in both non-infarcted and infarcted myocardium after 72 h of coronary occlusion and in cardiac lymph during 6 h of coronary occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Serum creatine kinase MM isoenzyme sub-bands after acute myocardial infarction in man.

Using an isoelectric-focusing (IEF) method developed to quantitate MM isoenzyme-creatine kinase (CK) sub-band activity, we identified a reproducible time-varying pattern of these sub-bands in the serum of eight patients with acute myocardial infarction (MI). Our observations are consistent with the view that MM3-CK (the M2-CK dimer, the pure gene product) is converted intravascularly to MM2-CK, and then to MM1-CK (the M1-CK dimer, the pure postsynthetic sub-band). The MM3-CK reaches a peak first, 16 hours after infarction, followed by MM2-CK, and then by MM1-CK. The MM3-CK is the dominant sub-band in normal myocardium; there is much less MM2-CK and virtually no MM1-CK. The MM3-CK sub-band peak may indicate the time at which enzyme ceases to be released from the injured myocardium. The ratio MM3-CK:MM1-CK rises within 6 hours after onset of chest pain from a baseline of 0.38 and peaks 10 hours after MI. The peak ratio was between 1.1 and 4.2, and the value correlated with the time when total CK activity peaked after MI. The 10-fold change in the MM3:MM1 ratio after MI, as well as the early period at which this ratio peaks (10 hours), makes this an earlier and more sensitive indicator of enzyme release.

Aged↗
PubMed1982

Myocardial blood flow during acute isovolumic anemia and treadmill exercise in dogs.

We examined whether submaximal treadmill exercise during acute isovolumic anemia altered the distribution of myocardial blood flow and thus caused subendocardial ischemia in unsedated dogs. Myocardial blood flow (determined by the microsphere method) and left ventricular function (indicated by pressures, volumes, and contractile indices) were measured in five dogs at rest and during exercise before and after equal volume exchange of blood and 6% dextran 70, which lowered hematocrit from 36 +/- 4 to 18 +/- 2% (SD). Total myocardial blood flow increased from 175 +/- 65 to 296 +/- 151 ml . min-1 . 100 g-1 (69%) during exercise before anemia and from 329 +/- 61 to 599 +/- 126 (82%) during exercise after anemia. The distribution of blood flow to the left and right ventricles and interventricular septum as well as the subendothelial-to-subepicardial blood flow ratio in these areas did not change during exercise either before or after anemia. Left ventricular function was not impaired during exercise after anemia. We conclude that subendocardial ischemia does not occur when dogs exercise during acute isovolumic anemia.

Acute Disease↗
PubMed1981

Continuous positive-pressure ventilation does not alter ventricular pressure-volume relationship.

To determine whether alterations in the mechanical properties (i.e., stiffening) of the right and left ventricles contribute to the decrease in right and left ventricular end-diastolic volumes during continuous positive-pressure ventilation (CPPV), we studied six dogs anesthetized with chloralose urethane and ventilated with a volume ventilator. We varied ventricular volumes by withdrawing or infusing blood. Pressure-volume curves, constructed by plotting transmural ventricular end-diastolic pressures against ventricular end-diastolic volumes, did not change during CPPV (12 cmH2O positive end-expiratory pressure) compared to intermittent positive-pressure ventilation (IPPV, 0 cmH2O end-expiratory pressure). We conclude that decreased ventricular end-diastolic volumes during CPPV result primarily from a decrease in venous return. Alterations in the mechanical properties of the ventricles do not play a significant role in this response.

Animals↗
PubMed1980

Continuous positive-pressure ventilation decreases right and left ventricular end-diastolic volumes in the dog.

We investigated the mechanism(s) responsible for the decreased cardiac output during continuous positive-pressure ventilation (CPPV). Seven dogs were anesthetized with chloralose-urethane, intubated, and ventilated using a volume ventilator. We measured heart rate, stroke volume, and the determinants of stroke volume: left and right ventricular end-diastolic volumes, isovolumic and ejection phase indices of myocardial contractility, and pulmonary and systemic arterial pressures. Myocardial blood flow was estimated using radioactive microspheres. Variables were measured during a control period of intermittent positive-pressure ventilation (IPPV), 8-20 minutes after the initiation of CPPV using 12 cm H2O positive end-expiratory pressure (PEEP), and 8-20 minutes after the removal of PEEP. CPPV decreased cardiac output but did not affect total or regional myocardial blood flow or the ratio of subendocardial to subepicardial blood flow. Isovolumic and ejection phase indices of myocardial cointractility, heart rate, and systemic arterial pressure did not change during CPPV. Right and left ventricular end-diastolic and end-systolic volumes decreased markedly during CPPV. We conclude that CPPV decreases cardiac output in accordance with Starling's law by decreasing preload.

Animals↗