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Biomedical subjects

R Roberts

Publications and source records attributed to R Roberts.

At least 595 records · Page 33Linked to original sources
PubMed1976

Two complications of diagnostic colonoscopy.

Two complications of diagnostic colonoscopy are reported. One patient had a perforation which was recognized immediately, and the other had a serosal tear discovered fortuitously at elective surgery. Previous reports of colonoscopic complications are reviewed, and factors predisposing to such complications are discussed.

Colon↗
PubMed1976

Radioimmunoassay for creatine kinase isoenzymes.

Creatine kinase has three isoenzymes designated MM, MB, and BB, with BB being the grain form and MM the muscle form. Antibodies to BB creatine kinase were obtained by immunization of rabbits with human BB creatine kinase. The antibodies demonstrated specificity for BB and MB creatine kinase (myocardial isoenzyme) but no cross-reactivity with MM creatine kinase. With the use of this antibody, a highly sensitive radioimmunoassay capable of measuring picomolar amounts of MB creatine kinase has been developed. Clinical application of this method should provide a sensitive and specific test for the diagnosis of myocardial infarction.

Brain↗
PubMed1976

Estimation of infarct size from serum MB creatine phosphokinase activity: Applications and limitations.

Results of enzymatic estimates of infarct size have been verified under defined experimental conditions, and close correlations have been obtained between enzymatically and morphologically estimated infarct size in patients. Nevertheless, to provide a basis for improved enzymatic estimates we explored several aspects of the original model. The first order disappearance rate of creatine phosphokinase (CPK) was verified by observed high correlation coefficients of the logarithm of CPK versus time after myocardial infarction in patients or intravenous injection of purified myocardial CPK in dogs. Selected hemodynamic interventions simulating derangements accompanying myocardial infarction including acceleration of heart rate, diminution of cardiac output and reduction of renal or hepatic perfusion in conscious dogs did not markedly alter CPK disappearance. To exclude contributions from noncardiac CPK to enzymatic estimates we performed studies with the MB CPK isoenzyme. Under standard assay conditions, MB CPK was found virtually exclusively in myocardium. Serial serum MB CPK curves paralleled those of total CPK from patients with uncomplicated infarction. Similar MB curves were obtained even in patients whose noncardiac CPK values distorted the total CPK curve after intramuscular injections. The correlation coefficient between infarct size estimated from total CPK and MB CPK was 0.97 in 12 patients with hemodynamically uncomplicated infarction. Thus, hemodynamic perturbations associated with infarction are unlikely to affect CPK disappearance and hence should not lead to spurious enzymatic estimates of infarct size. Furthermore, improved enzymatic estimates can be obtained by quantitative assay of MB CPK, a more specific myocardial marker, avoiding spurious estimates due to contributions from noncardiac enzyme.

Animals↗
PubMed1976

[Laboratory standardization and quality control in anticoagulant therapy].

Standardisation and quality control are now available for the laboratory tests which are needed to control the blood levels of anticoagulants. The most important cause for variation in results between different laboratories is the use of different types of thromboplastin. The British standards are based on the use of a national reagent with a national system of reporting supported by quality control with lyophilised plasma and thromboplastin preparations. It offers a model which has been adopted at Tygerberg Hospital, and could be used to standardise anticoagulant therapy in this country. Human brain thromboplastin is preferred to the commercially available rabbit preparations. For the first time, as far as we know, a phenol-saline extract of baboon brain thromboplastin was examined. Preliminary results indicate that it compares well with human brain extracts.

Animals↗
PubMed1976

Determination of the origin of elevated plasma CPK after cardiac catheterization.

Episodes of chest pain are not common in patients undergoing cardiac catheterization. The diagnostic implications of this symptom may be complicated by the occasional appearance of electrocardiographic changes mimicking those seen in acute myocardial infarction, and by the frequent elevation of conventionally measured serum enzymes. Exclusion of infarction is particularly important when coronary revascularization is contemplated. Since the MB CPK isoenzyme is relatively specific to myocardium, we assayed CPK isoenzymes in plasma samples from 184 patients undergoing cardiac catheterization to determine whether CPK elevations accompanying catheterization can be distinguished from those associated with myocardial infarction. Samples were obtained every 2 hr for 24 hr, and CPK isoenzymes quantified by a kinetic fluorometric method. Total plasma CPK increased in all patients (mean peak 0.238 +/- 0.042 (SD) IU/ml) but MB CPK remained normal in 181 patients (less than 0.005 IU/ml). In three remaining patients, MB CPK was elevated and myocardial infarction was confirmed by 99mTc (SN) pyrophosphate scan. Twelve patients after catheterization, in whom no intramuscular premedication was given, exhibited only minimal elevation of total plasma CPK. In contrast, 100 control patients with acute myocardial infarction exhibited peak total CPK activity averaging 0.833 +/- 0.037 (SD), and MB CPK was elevated in all cases (0.078 +/- 0.027 (SD) IU/ml). Thus, CPK elevations after catheterization reflect release of enzyme from noncardiac sources rather than from injured myocardium. Furthermore, increased plasma MB CPK activity may be considered a reliable index of myocardial infarction in patients undergoing cardiac catheterization.

Adolescent↗
PubMed1976

Improved detection of myocardial infarction with technetium-99m stannous pyrophosphate and serum MB creatine phosphokinase.

The relative sensitivity and combined value of myocardial technetium-99m stannous pyrophosphate imaging and determinations of serum MB creatine phosphokinase (the "myocardial" CPK isoenzyme) in detecting acute myocardial infarction were evaluated in 41 patients with suspected infarction and 23 patients recovering from cardiac surgery. In the patients with suspected infarction, myocardial infarction was confirmed in 25 and was consistently associated with increased serum MB CPK. Abnormal radionuclide images were obtained in 23 of 25 patients (92 percent) with definite myocardial infarction and in 2 of 16 patients without confirmed infarction. Although the localization of infarction by imaging correlated well with the localization by electrocardiogram, infarct size estimated by imaging did not correlate well with estimates based on peak total serum CPK activity or serial changes in CPK activity. Serum MB CPK activity increased after cardiac surgery in 6 patients undergoing valve replacement and in 17 patients undergoing coronary arterial bypass surgery. However, no patient with valve replacement and only 1 of the 17 with bypass surgery had an abnormal radionuclide image. These results suggest that (1) abnormal radionuclide images in patients without infarction can be distinguished from abnormal images indicative of ischemic necrosis by consideration of MB CPK activity and (2) interpretation of elevated MB CPK activity, particularly in particularly in patients undergoing cardiac surgery, is facilitated by evaluation with imaging.

Adult↗
PubMed1976

Paradoxical endogenous synthesis of a coronary dilating substance from arachidonate.

Isolated bovine, canine, and human coronary arteries exhibited dose dependent contractions to prostaglandin (PG) E2 and F2alpha (50 ng/ml to 10mug/ml). The ED50 value for both PGE2 and PGF2alpha was 500 ng/ml in the bovine and human coronary arteries. Paradoxically, although PGE2 and gf2alpha are vasoconstrictors, administration of their precursor, arachidonate (100 ng/ml to 10 mug/ml) caused relaxation of the bovine, canine and human coronary arteries. This observation suggests that arachidonate is not being converted by the coronary PG synthetase to PGE2 or PGF2alpha. However, the arachidonate induced coronary relaxation was inhibited by pretreatment with PG synthetase inhibitors, indomethacin, meclofenemate and aspirin. Indomethacin addition to the strips previously relaxed by arachidonate caused contraction. In contrast to other PGs (E2 and F2alpha), PGE1 (10 ng/ml to 10 mug/ml) caused dose dependent relaxation of the bovine coronary arteries (ED50 = 100 ng/ml). Indomethacin induced further relaxation of the blood vessels previously relaxed by PGE1. Since PGE1 cannot arise from arachidonate, the arachidonate coronary dilation and reversal by indomethacin must be independent of PGE1 formation. Linolenate (100 ng/ml to 10 mug/ml) and oleate (100 ng/ml to 10 mug/ml) also caused relaxation of the bovine coronary blood vessels both before and after indomethacin, thereby eliminating a direct non-specific fatty acid effect as the cause of the arachidonate relaxation. These results suggest that in isolated coronaries, arachidonate undergoes a novel conversion, possibly by PG synthetase, to a dilating substance which exerts different contractile effects than exogenously administered PGE2, PGF2alpha and PGE1.

Animals↗
PubMed1976

CPK isoenzymes in evaluation of myocardial ischemic injury.

Enzymatic criteria for diagnosis of myocardial infarction have suffered from a lack of specificity, since enzyme elevations also occur in noncardiac disorders. The MB isoenzyme of creatine phosphokinase has provided a way out of this difficulty. Not only is it specific to injured myocardium but a recently developed plasma assay makes possible both diagnosis and, in many cases, measurement of the extent of damage.

Clinical Enzyme Tests↗
PubMed1976

Serial radionuclide determinations of the electron fraction with 99mTc-labeled red blood cells.

The reproducibility of area/length ejection fraction determinations was evaluated in 21 subjects using 99mTc-labeled red blood cells (99mTc-RBCs). The ejection fraction was determined within 30 minutes and 3-5 hours after a single injection of 99mTc-RBCs. The mean absolute difference between the initial and subsequent ejection fractions was 7% (maximum, 15%) (r = 0.90). 99mTc-RBCs offer a reproducible method of determining the ejection fraction which is suitable for serial noninvasive evaluations of left ventricular function.

Cardiac Output↗
PubMed1976

The association of increased plasma MB CPK activity and irreversible ischemic myocardial injury in the dog.

To evaluate the concordance between elevated plasma MB CPK and irreversible myocardial ischemic injury, coronary occlusion was induced for 10 minutes to 48 hours in 21 open chest dogs and 13 conscious animals. Results of plasma CPK and MB CPK assayed in samples obtained serially ofr 24 hours were compared to microscopic changes in hearts from the same animals examined 48 hours after occlusion. Twelve of the 34 dogs died within two hours after coronary occlusion. Among the surviving 22 dogs, one failed to exhibit gross of electrocardiographic evidence of ischemia and was therefore excluded. Twelve had coronary occlusion maintained for 30 minutes or longer and in 11 of these peak plasma MB CPK activity exceeded thenormal range (mean +/- 2 SD) and baseline values by at least 100%. Necrosis was present in the hearts from each manifested by nuclear pyknosis, eosinophilia, shrinkage of cytoplasm, and leukocytic infiltration. In the remaining nine dogs with occlusion for less than 30 minutes, peak plasma MB CPK activity was not elevated and necrosis was not detected. The close concordance between plasma MB CPK elevations and myocardial necrosis was significant (chi2 = 14.5, P less than 0.001), and thus, increased plasma MB CPK activity reflected irreversible myocardial ischemic injury.

Animals↗
PubMed1976

Relations between enzymatically estimated myocardial infarct size and early ventricular dysrhythmia.

The relation between ventricular dysrhythmia during the first 20 hours after hospitalization for acute myocardial infarction and enzymatically estimated infarct size was studied prospectively. The duration of dyshythmia was measured by the total time during which the average premature ventricular depolarization (PVC) rate was above 25 PVCs/hr. This index was significantly correlated with infarct size index (ISI) and the strength and significance of the correlation increased when patients with previous, remote myocardial infarction were excluded. An initially expected correlation between PVC frequency and average heart rate was not observed. In a subset of patients selected to include the entire range of ISI, median PVC coupling interval did not correlate with ISI or heart rate. Our results confirm the general reduction of PVC frequency with time after hospital admission. An analysis of total lidocaine administered for therapeutc purposes and dysrhythmia evaluated by retrospective computer analysis disclosed a moderately strong and significant correlation. These findings indicate that persistence and severity of ventricular dysrhythmia in the first 20 hours after hospitalization for myocardial infarction are related to enzymatically estimated infarct size.

Adult↗
PubMed1976

Elevated plasma MB creatine phosphokinase activity. A specific marker for myocardial infarction in perioperative patients.

Plasma MB creatine phosphokinase (CPK) activity is consistently elevated following myocardial infarction (MI). To determine whether elevations of plasma MB CPK activity is a specific index of myocardial injury, CPK and isoenzymes were assayed by a quantitative kinetic fluorometric technique in fresh organs obtained at surgery. Analysis of CPK isoenzymes showed myocardium to be essentially the only organ with MB CPK. Operative procedures included thoracic, neck, genitourinary, and orthopedic surgery. Total plasma CPK activity increased in all patients; however, MB CPK activity was not elevated. Thus, (1) the heart appears to be the only organ that is capable of liberating substantial amounts of MB CPK into plasma; (2) in spite of notably increased CPK activity after cardiac surgery, MB CPK activity is not elevated; and (3) increased MB CPK activity is a reliable index of MI in postoperative patients.

Acute Disease↗