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Biomedical subjects

A D Sniderman

Publications and source records attributed to A D Sniderman.

At least 127 records · Page 7Linked to original sources
PubMed1978

Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs.

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.

Animals↗
PubMed1977

Differences between the effects of practolol and propranolol on the diastolic properties of the left ventricle.

To elucidate the mechanism by which left ventricular and diastolic pressure (LVEDP) is reduced by practolol, ventricular volumes, hemodynamics, and diastolic elastic stiffness were determined before and 10 min after intravenous practolol (400 mug/kg) in 12 patients. Heart rate decreased in all patients after practolol (avg., --9/min, p less than 0.02). There was an insignificant increase in stroke work index and decrease in cardiac index attributable to the fall in rate. Practolol did not change and diastolic volume or ejection fraction, but the average LVEDP fell from 21 to 15 mm Hg (p less than 0.01) which was sustained even with atrial pacing to prepractolol heart rates. Diastolic elastic stiffness was also reduced after practolol (0.665 to 0.593, p less than 0.0025). The data indicate that practolol exerts a negative chronotropic effect on the intact heart and, in contrast to other beta blockers such as propranolol, appears to decrease diastolic stiffness in the left ventricle.

Adult↗
PubMed1977

Predictable changes in low density lipoprotein composition after acute myocardial infarction.

Acute changes in low density lipoprotein cholesterol levels may be due to both a change in the number of LDL particles/ml of plasma and an alteration in the amount of cholesterol per LDL particle. Since LDL cholesterol levels are known to alter abruptly after myocardial infarction, the composition of LDL was determined in nine patients who suffered an uncomplicated transmural myocardial infarction. In six of these, LDL cholesterol levels fell whereas in three LDL cholesterol rose during the first nine days in hospital. The contents of B protein, free cholesterol, phospholipid, cholesterol ester and triglyceride in LDL were determined in the initial sample and the subsequent sample showing the greatest changes in LDL cholesterol level. The proportion of the LDL molecule contributed by B protein, free cholesterol and phospholipid did not differ significantly between the two samples. In contrast, when LDL cholesterol fell, the decrease in the proportion of cholesterol ester was disproportionately greater than in triglyceride. The opposite was observed when LDL cholesterol rose. This inverse relation between changes in LDL cholesterol ester and triglyceride could be expressed by Y = -1.02 X -0.17 (r = -0.94). These data are consistent with a pseudomicellar model of LDL in which the surface components are present in fixed amounts but the interior shell of cholesterol ester and triglyceride varies in an inverse relation depending on the absolute LDL concentration.

Cholesterol↗
PubMed1977

Experience with bretylium tosylate by a hospital cardiac arrest team.

The effect of bretylium tosylate (BT) was determined in 27 consecutive cases of resistant ventricular fibrillation (VF) encountered by a hospital cardiac arrest team. The VF was sustained and completely resistant to multiple injections of lidocaine, sequential DC shocks at 400 watt-sec and one or a combination of intravenous propranolol, diphenylhydantoin or procainamide. Following 30 min of sustained cardiac massage, BT (5 mg/kg i.v.) was administered. In 20 patients, VF was terminated within 9-12 min after DC shock. Eight of these patients failed to recover while 12 (44%) of all patients resuscitated survived to be discharged from hospital. Eleven out of 20 (55%) of all patients who had a cardiac arrest outside the CCU were survivors; only one out of seven in the CCU were successfully resuscitated. While receiving maintanance BT post-resuscitation (5 mg/kg i.m. q 8-12 hrs x 48 hrs), half the patients developed hypotension and three required vasopressors and/or fluid replacement. The data indicate that BT is a useful agent in patients with sustained VF refractory to repeated lidocaine injections, some other antiarrhythmic agents, and multiple DC shocks.

Bretylium Compounds↗
PubMed1977

Microencapsulated charcoal hemoperfusion: a possible therapeutic adjunct in digoxin toxicity.

Attempts to remove substantial quantities of digoxin by either peritoneal or hemodialysis, have been unsuccessful due to their low clearance rate. The present study determined the in-vivo clearance rate for digoxin of a single microcapsule of 300 gm of activated charcoal. The clearance rate was 55 +/- 5 ml/min (mean +/- SEM) in the first hour and 48.4 +/- 4 ml/min in the second; these values are approximately five-fold higher than with other dialysis techniques. No evidence of a post-dialysis rebound increase in serum digoxin levels was found, implying that peripheral tissues can rapidly release digoxin to the diminishing serum pool. Preliminary data obtained suggest a beneficial effect on arrhythmias and lowering of the myocardial to serum rate of digoxin after hemoperfusion.

Animals↗
PubMed1976

Possible mechanisms of normal amylase activity in hyperlipemic pancreatitis.

Lipemic serum from three patients with acute pancreatitis and type IV hyperlipemia was fractionated into very-low-density lipoproteins and clear serum. Amylase activity (determined by the Phadebas method) in the component fractions did not exceed that in the original lipemic serum. Addition of these fractions or VLDL and chylomicrons from asymptomatic patients with hyperlipemia to nonlipemic serum from patients with "routine acute pancreatitis" did not inhibit amylase activity or alter the electrophoretic mobility of amylase isoenzymes. Therefore the normal amylase activity often observed in hyperlipemic pancreatitis does not result from an inhibition of amylase activity by serum lipoproteins.

Acute Disease↗
PubMed1975

Turnover and tissue distribution of 125-I-labeled low density lipoprotein in swine and dogs.

Swine plasma low density lipoprotein (LDL) isolated ultracentrifugally (d 1.019-1.063) was labeled with 125-I, dialyzed, and reisolated by centrifugation at d 1.063. Over 96% of the radioactivity was shown to be associated with the apoprotein. After reinjection into the donor animal, disapperance of 125-I was followed for up to 122 hr. At all time intervals examined, over 95% of the total plasma 125-I was recovered in LDL (D 1.006-1.063), i.e., there was apparently no transfer of radioactivity to high density or very low density lipoproteins. The disappearance curve was biexponential, with half-lives of 0.83 plus or minus 0.06 and 22.5 plus or minus 1.7 hr for the first and second phases, respectively (13 studies). The mean calculated fractional catabolic rate was 0.041 plus or minus 0.003 hr-minus 1. Similar results were obtained in three dogs using autologous LDL of density 1.020-1.050; fractional catabolic rates were 0.031, 0.031, and 0.029 hr-minus 1. Tissue distribution of 125-I was determined in swine killed at various time intervals after [125-I]LDL injection with corrections for radioactivity in trapped plasma. Of the tissues examined, the liver showed by far the highest concentration. Total hepatic radioactivity, expressed as a percentage of total plasma radioactivity, was rather constant and independent of the time of killing from 3 to 122 hr (15.8 plus or minus 1.9%). The total extravascular LDL pool calculated from analysis of the plasma disappearance curves was about 20-30% of the size of the plasma LDL pool. These data are consistent with the conclusion that the liver accounts for a very large fraction of the total extravascular LDL pool. These data are consistent with the conclusion that the liver accounts for a very large fraction of the total extravascular LDL pool and that it is infairly rapid equilibrium with the plasma pool. To what extent the liver is involved in irreversible degradation cannot be inferred from these findings.

Animals↗
PubMed1974

Paradoxical increase in rate of catabolism of low-density lipoproteins after hepatectomy.

It has been suggested that the liver may be a major site for irreversible degradation of low-density lipoprotein (LDL). The disappearance of autologous (125)I-labeled LDL from plasma was compared in intact and in hepatectomized swine. Contrary to expectations, the rate of irreversible removal of LDL from plasma was increased rather then decreased by hepatectomy. These studies suggest that the liver is not a major site for LDL removal. We propose further that the liver (or some function requiring an intact liver) may affect the metabolism of LDL in a manner that prolongs its lifetime in the plasma compartment.

Animals↗
PubMedDate not supplied

In vitro interactions between low density lipoprotein from hyperapobetalipoproteinemic plasma and arterial wall proteoglycans.

OBJECTIVE: To examine the interactions of low density lipoprotein-B (LDL-B) with proteoglycans (PG) in vitro. DESIGN: The PG were isolated from human aortas, removed at autopsy by a combination of extraction with 4M guanidine-Tris buffer containing protease inhibitors and fractionation on a DEAE-Sephacel ion-exchange chromatography column. LDL and LDL-B from healthy or hyperapobetalipoproteinemic sera, respectively, were isolated by standard density flotation techniques followed by radioiodination. Radiolabelled lipoproteins (LP) were incubated with proteoglycans at 4 or 37 degrees C in a low ionic strength buffer with or without addition of polyethylene glycol (PEG) which was used to enhance precipitation of the resulting LP-PG complexes. MAIN RESULTS: Data revealed that a specific ratio of LP to PG is a prerequisite for optimal interactions between these macromolecules. Further, it was observed that LDL-B forms fewer precipitable complexes than normal LDL at 4 degrees C. However, at physiological temperature or with the addition of PEG, precipitation of the two LDLs was equal. CONCLUSION: LDL and LDL-B showed equal reactivity with PG in terms of precipitable complexes.

Aorta↗
PubMedDate not supplied

Regression of left ventricular hypertrophy in dialysis patients following correction of anemia with recombinant human erythropoietin.

Left ventricular hypertrophy is an independent determinant of survival in patients with end-stage renal disease, and anemia is one determinant of hypertrophy in such patients. Accordingly, the authors studied 22 dialysis patients by echocardiography before and after correction of their anemia with recombinant human erythropoietin. Observers were blinded to patient identity and order of studies. Hemoglobin increased from 63 +/- 8 g/L (mean +/- standard deviation) to 114 +/- 15 g/L; an increase of at least 30 g/L over baseline was maintained for eight months in all patients. Left ventricular mass decreased from 253 +/- 77 to 215 +/- 71 g (2P = 0.0004) and left ventricular end diastolic volume fell from 173 +/- 60 mL to 138 +/- 48 mL (P less than 0.0001). The reduction in mass and decrease in end diastolic volume, however, were seen only in those with significant hypertrophy at the onset of therapy. The authors conclude that partial regression of left ventricular hypertrophy is possible within a short time period through correction of anemia in dialysis patients. Whether this will improve survival in end-stage renal disease remains to be determined.

Adolescent↗