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Biomedical subjects

S W Rabkin

Publications and source records attributed to S W Rabkin.

At least 19 recordsLinked to original sources
PubMed1992

Dynorphin A (1-13) in the brain suppresses epinephrine-induced ventricular premature complexes and ventricular tachyarrhythmias.

The objectives of this study were to test the hypothesis that dynorphin in the central nervous system modulates epinephrine-induced cardiac arrhythmias and that central cholinergic mechanisms are operative in this action of dynorphin. Cardiac arrhythmias were produced by continuous intravenous infusion of epinephrine, in Wistar rats, previously instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Epinephrine produced ventricular premature complexes and later the development of fatal ventricular fibrillation. Dynorphin A (1-13), 5 or 20 micrograms (3 or 12 nM) administered into the lateral cerebral ventricle (ICV), significantly (P less than 0.05) increased the threshold for development of cardiac arrhythmias. Dynorphin A (1-13), 20 micrograms, increased the epinephrine dose at the occurrence of ventricular premature beats to 171 +/- 8 (mean +/- 1 S.E.M.) compared to 120 +/- 5 micrograms epinephrine/kg in the control group and increased the dose at the onset of fatal arrhythmias to 186 +/- 8 compared to 141 +/- 10 micrograms epinephrine/kg in the control group. The action of dynorphin was significantly (P less than 0.05) antagonized by the kappa opioid antagonist MR2266. Atropine sulfate, administered ICV or intravenously, produced a dose dependent antagonism of this action of dynorphin A (1-13). This was not due to the peripheral effects of atropine, as atropine methylnitrate, which does not cross the blood brain barrier, did not oppose the effects of dynorphin A (1-13). These data indicate (i) dynorphin A (1-13) increases the threshold for or suppresses the manifestations of epinephrine-induced ventricular arrhythmias, (ii) dynorphin's action on cardiac arrhythmias is mediated through central cholinergic rather than peripheral parasympathetic mechanisms (iii) dynorphin may play a role as an endogenous opioid within the brain that modulates cardiac arrhythmias in circumstances of elevated circulating epinephrine concentration.

Animals↗
PubMed1992

Prevalence, control and awareness of high blood pressure among Canadian adults. Canadian Heart Health Surveys Research Group.

OBJECTIVE: To estimate the prevalence and distribution of elevated blood pressure (BP) among Canadian adults and to determine the level of control, treatment, awareness and prevalence of other risk factors among adults with high BP. DESIGN: Population-based cross-sectional surveys. SETTING: Nine Canadian provinces, from 1986 to 1990. PARTICIPANTS: A probability sample of 26,293 men and women aged 18 to 74 years was selected from the health insurance registers in each province. For 20,582 subjects, BP was measured at least twice. Nurses administered a standard questionnaire and recorded two BP measurements using a standardized technique. Two further BP readings, anthropometric measurements and a blood specimen for lipid analysis were obtained from those subjects who attended a clinic. OUTCOME MEASURES: Mean values of systolic and diastolic BP, prevalence of elevated BP using different criteria, and prevalence of smoking, elevated blood cholesterol, body mass index, physical activity and presence of diabetes by high BP status are reported. MAIN RESULTS: Sixteen percent of men and 13% of women had diastolic BP of 90 mm Hg or greater or were on treatment (or both). About 26% of these subjects were unaware of their hypertension, 42% were being treated and their condition controlled, 16% were treated and not controlled, and 16% were neither treated nor controlled. Use of non-pharmacologic treatment of high BP with or without medication was low (22%). Hypertensive subjects showed a higher prevalence of elevated total cholesterol, high body mass index, diabetes and sedentary lifestyle than normotensive subjects. Most people with elevated BP were in the 90 to 95 mm Hg range for diastolic pressure and 140 to 160 mm Hg range for systolic pressure. Prevalence of high isolated systolic BP sharply increased in men (40%) and women (49%) 65 to 74 years old. CONCLUSIONS: The relatively low level of control of elevated BP calls for population and individual strategies, stressing a non-pharmacologic approach and addressing isolated systolic hypertension in the elderly.

Adult↗
PubMed1992

Obesity and its relation to cardiovascular disease risk factors in Canadian adults. Canadian Heart Health Surveys Research Group.

OBJECTIVE: To describe the distribution of weight and abdominal obesity among Canadian adults and to determine the association of obesity with other risk factors for cardiovascular disease. DESIGN: Population-based cross-sectional surveys. Survey nurses administered a standard questionnaire and recorded two blood pressure measurements during a home visit. At a subsequent visit to a survey clinic two further blood pressure readings were made, anthropometric measurements recorded and a blood specimen taken for plasma lipid determination. SETTING: Nine Canadian provinces, from 1986 to 1990. PARTICIPANTS: A probability sample of 26,293 men and women aged 18 to 74 years was selected from the health insurance registration files of each province. Anthropometry was performed on 17,858 subjects. OUTCOME MEASURES: Body mass index (BMI), ratio of waist to hip circumference (WHR), mean plasma lipid levels, prevalence of high blood pressure (diastolic greater than or equal to 90 mm Hg or patient on treatment) and self-reported diabetes mellitus. MAIN RESULTS: The prevalence of obesity (BMI greater than or equal to 27) increased with age and was greater in men (35%) than in women (27%). Abdominal obesity was likewise higher in men and increased with both age and BMI. The prevalence of high blood pressure was greater in those with higher BMI, especially in those with a high WHR. Although total plasma cholesterol levels increased only modestly with BMI, levels of low density lipoprotein (LDL) cholesterol and triglycerides and the ratio of total cholesterol to high density lipoprotein (HDL) cholesterol increased steadily, while HDL-cholesterol decreased consistently with increasing BMI. High total cholesterol levels (greater than or equal to 5.2 mmol/L) were more prevalent among people with high BMI, especially those with a high WHR. The prevalence of diabetes increased with BMI among those 35 years or older, especially those with abdominal obesity. About half of men and two-thirds of women who were obese were trying to lose weight. CONCLUSION: Obesity remains common among Canadian adults. There is a need for broad-based programs that facilitate healthy eating and activity patterns for all age groups. Health professionals should incorporate measurement of BMI and WHR into their routine examinations of patients to enhance their evaluation of health risk.

Adult↗
PubMed1992

The calcium antagonist diltiazem has antiarrhythmic effects which are mediated in the brain through endogenous opioids.

The purpose of this study was to examine the hypothesis that the calcium channel blocker, diltiazem, modulates catecholamine-induced arrhythmias through CNS mechanisms. Rats, that had catheters previously inserted into the lateral cerebral ventricle and femoral artery, received diltiazem, 10 or 50 micrograms/kg or the diluent, into the lateral cerebral ventricle (i.c.v.). Epinephrine was infused to produce arrhythmias. The onset of ventricular arrhythmias, premature ventricular complexes, occurred at a significantly (P less than 0.05) greater dose of epinephrine, after diltiazem, compared to the control group and in a dose-dependent manner, with the mean (+/- 1 SEM) dose of epinephrine being 198 +/- 5, 175 +/- 13 and 115 +/- 15 micrograms/kg in the groups treated with 50 and 10 micrograms/kg of diltiazem and the control groups, respectively. The development of fatal arrhythmias, mainly ventricular tachyarrhythmias, occurred at significantly (P less than 0.05) greater concentrations of epinephrine with diltiazem, 50 and 10 micrograms/kg, 225 +/- 5 and 183 +/- 13 micrograms/kg, respectively, compared to controls, 131 +/- 15 micrograms/kg. Endogenous opioids of the mu-type were implicated in this action of diltiazem, because the mu opioid antagonist naloxone, 1 mg/kg (i.v.), significantly (P less than 0.05) antagonized the antiarrhythmic effects of centrally administered diltiazem and the mu opioid agonist DAGO (i.c.v.), did not further enhance the suppression of epinephrine-induced arrhythmias, produced by diltiazem, 50 micrograms/kg. Atropine sulfate, which crosses the blood-brain barrier and atropine methylnitrate, which does not enter the brain, each at 1 mg/kg (i.v.), produced an equal and significant antagonism of the effect of diltiazem, 50 micrograms/kg, that was less than that of naloxone. The combination of naloxone plus atropine sulfate completely prevented the effect of diltiazem, 50 micrograms/kg, on arrhythmias. The antiarrythmic action of diltiazem could not be explained by alteration of the blood pressure or heart rate response to epinephrine. The results suggest that: (a) calcium channels on neurons in the CNS play an important role in the modulation of epinephrine-induced cardiac arrhythmias, (b) diltiazem can suppress arrhythmias through CNS mechanisms, (c) activation of the parasympathetic nervous system mediates some of the effect of diltiazem, but (d) the mechanism of action of diltiazem is modulated through endogenous opioids.

Acetylcholine↗
PubMed1992

Effect of antiarrhythmic drugs on choline uptake in cardiac cells in culture.

OBJECTIVE: The aim was to examine the effect on choline uptake of various antiarrhythmic drugs: lignocaine, tocainide, encainide, flecainide, propafenone, procainamide, N-acetylprocainamide, bretylium, and amiodarone. METHODS: Cardiac ventricular myocytes from 7 d old chick embryos were exposed in culture to these drugs, at concentrations ranging from 10(-6) to 10(-4) M, for 24 h. Myocyte choline uptake was assessed by the addition of methyl [3H] choline to media. After 120 min, media were removed, the cells were harvested, and intracellular [3H] actively was counted. RESULTS: Lignocaine and tocainide produced a significant (p less than 0.05) dose dependent increase in intracellular [methyl 3H] choline. Encainide produced a small increase and flecainide a small decrease in choline, neither of which was dose dependent. Propafenone significantly (p less than 0.05) altered choline uptake: at 10(-6) M and 10(-5) M choline uptake was increased and at 10(-4) M it was decreased. Amiodarone produced a marked and significant (p less than 0.05) dose dependent reduction in choline uptake. Bretylium, procainamide, and N-acetylprocainamide did not alter myocyte choline. CONCLUSIONS: Choline incorporation into cardiac myocyte is altered by some antiarrhythmic drugs, suggesting this may be part of their antiarrhythmic properties.

Amiodarone↗
PubMed1992

Cilazapril and captopril accelerate recovery from hypoxia in myocardial cell aggregates in culture.

We wished to determine whether angiotensin-converting enzyme (ACE) inhibition alters the effect of hypoxia and reoxygenation directly on the cardiac myocyte; to compare two different ACE inhibitors, one with and one without a sulfhydryl group (i.e., captopril and cilazapril), and to examine the potential interaction of these ACE inhibitors with agents that purportedly prevent the deleterious action of oxygen-derived free radicals. Ventricular myocytes were obtained from 7-day-old chick embryo hearts and were maintained in culture for 96 h before study. Hypoxia produced a significant (p less than 0.05) and marked reduction in cardiac contractile frequency that was not influenced by captopril 10(-6) and 10(-7) M or cilazapril 10(-6) or 10(-7) M. During the reoxygenation period, cardiac contractile frequency gradually returned to normal. Both ACE inhibitors, captopril and cilazapril, were associated with a similar significant (p less than 0.05) enhancement of restoration of contractile frequency. Angiotensin II (ANGII) reversed the effect of these ACE inhibitors. Two agents that reduce reoxygenation-induced myocardial damage, perhaps through alteration in production or degradation of oxygen-derived free radicals, i.e., allopurinol and superoxide dismutase (SOD), significantly (p less than 0.05) accelerated recovery of cardiac myocytes during reoxygenation. There was no additive effect with either captopril or cilazapril plus allopurinol or SOD. Conclusions about the actions of these ACE inhibitors must be tempered by the evidence that substrates other than ANGI, particularly bradykinin, are processed by the enzyme and inhibited by ACE inhibitors so that some of the observed effects may have been due to accumulation of other substrates.(ABSTRACT TRUNCATED AT 250 WORDS)

Allopurinol↗
PubMed1992

Morphine and the endogenous opioid dynorphin in the brain attenuate digoxin-induced arrhythmias in guinea pigs.

The effects of the opioid receptor agonists morphine and dynorphin on digoxin-induced arrhythmias were examined in guinea pigs that had received intravenous digoxin (50 mu/kg bolus plus 500 mu/kg/hr intravenously). Animals received either morphine (50 or 100 micrograms/kg) or dynorphin A(1-13) (50 or 100 micrograms/kg) or saline (the diluent) into the lateral cerebral ventricle (intracerebroventricularly) prior to digoxin. Morphine and dynorphin produced significant (P < 0.05) dose-dependent increases in the threshold of digoxin-induced arrhythmias. The mean digoxin dose at the development of fatal arrhythmias was 775 +/- 42 micrograms/kg in the control group but was significantly higher namely 958 +/- 45 micrograms/kg after 100 micrograms/kg of morphine ICV, and 984 +/- 47 micrograms/kg after 100 micrograms/kg of dynorphin A (1-13) intracerebroventricularly. In the absence of digoxin, the highest doses of each of these opioids did not produce arrhythmias. Changes in blood pressure and heart rate were unlikely explanations for the observed actions of these opioids as morphine accentuated the increase in blood pressure that accompanied digoxin while dynorphin was associated with a lower blood pressure with digoxin, despite similar effects on arrhythmias. In the control group, fatal digoxin-induced arrhythmias were ventricular tachyarrhythmias in two-thirds of cases and complete heart block in the rest. Morphine and dynorphin reduced the development of ventricular tachyarrhythmias. The role of the cholinergic system was explored, with morphine, utilizing atropine sulfate which crosses the blood brain barrier and atropine methylnitrate which does not enter the CNS. Atropine sulfate but not atropine methylnitrate reversed the effects of morphine on digoxin-induced arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Angiotensin II-induced protein phosphorylation in the hypertrophic heart of the Dahl rat.

Angiotensin II-induced phosphorylation of proteins was examined in isolated myocytes from hearts of Dahl rats. A high salt diet induced cardiac hypertrophy in Dahl salt-sensitive rats. Angiotensin II-induced phosphorylation of a 42-kd protein (pp42) was detected by two-dimensional electrophoresis in hypertrophic but not normal ventricular myocytes. Angiotensin II stimulation was time-dependent, with a peak effect at 30 minutes. The half-maximal and maximal concentrations of angiotensin II that stimulated pp42 phosphorylation were 1 and 10 nM, respectively. Phosphorylation of pp42 was a function of cardiac hypertrophy. Phorbol 12-myristate 13-acetate-induced phosphorylation of pp42 indicates the possibility of an association between protein kinase C and the signal transduction pathway of angiotensin II-induced pp42 phosphorylation. Ionomycin and A23187 (both at 1 microM) did not stimulate phosphorylation of pp42. Angiotensin II produced a small increase in the synthesis of myocyte proteins in both normal and hypertrophic cells as shown by [35S]methionine incorporation. However, this increase could not account for the increase in the phosphate content of pp42. This protein was not an isoform of actin nor was it of platelet origin. These results raise the possibility that angiotensin II may play a role in the activation of factors in hypertrophic myocytes; however, further study is required to define a link between phosphorylation of pp42 and the hypertrophic process.

Angiotensin II↗
PubMed1991

Regulation by angiotensin II of phosphate transport in cardiac myocytes.

The purpose of this study was to test the hypothesis that angiotensin II (ang II) affects the transport of inorganic phosphate in adult ventricular myocytes. Ventricular myocytes were isolated from Dahl rats and allowed to take up 32P inorganic phosphate (32P-Pi). The intracellular 32P concentration increased rapidly and reached a peak at 5 min. Ang II, 10(-10) to 10(-5) M, produced a significant (P less than 0.05) and concentration-dependent reduction in 32P-Pi uptake that plateaued at 0.1 to 1.0 microM. Ang II at 1 microM produced a 30% reduction in Vmax and a slightly greater reduction in the Km of 32P-Pi uptake, compared to myocytes that were not exposed to ang II. The ang II receptor antagonist saralasin (Sar1-Val5-Ala8-angiotensin II), significantly (P less than 0.05) antagonized the action of ang II on 32P-Pi uptake. TPA (12-O-tetradecanoylphorbol-13-acetate) also produced a significant (P less than 0.05) reduction of 32P-Pi uptake, suggesting that protein kinase C is involved in the transduction of ang II effects on intracellular Pi. 32P Efflux from myocytes, pulsed with 32P-Pi and chased with Pi-free medium, was accentuated markedly by ang II; this effect was blunted by saralasin. These data suggest that ang II is capable of regulating total intracellular Pi in the heart via two actions: (i) by inhibiting uptake of Pi into the myocyte, and (ii) by increasing the efflux of phosphates out of the cell.

Amino Acid Sequence↗
PubMed1991

Angiotensin in the brain suppresses epinephrine-induced cardiac arrhythmias through CNS opioid mechanisms.

To test the hypothesis that angiotensin II (Ang II) in the central nervous system modulates catecholamine-induced cardiac arrhythmias and to determine whether endogenous opioids are operative in this action, arrhythmias were produced in male Wistar rats, by continuous infusion of epinephrine at incremental doses until the development of fatal arrhythmias that were usually ventricular fibrillation. Rats were instrumented with catheters in the lateral cerebral ventricle, femoral vein and femoral artery. Ang II, 0.5 microgram, in the lateral cerebral ventricle (ICV) markedly and significantly (p less than 0.05) increased the epinephrine dose, at the occurrence of ventricular premature beats compared to the control group 228 +/- 11 (SEM) vs 116 +/- 7 micrograms epinephrine/kg and at the onset of fatal arrhythmias 225 +/- 13 vs 185 +/- 9 micrograms epinephrine/kg. Ang II, 0.5 microgram i.v., did not affect arrhythmia threshold. The angiotensin converting enzyme inhibitor captopril, 1 mg/kg, decreased arrhythmia threshold as ventricular arrhythmias were first noted at 106 +/- 4 and fatal arrhythmias occurred at 118 +/- 4 micrograms epinephrine/kg. The Ang II receptor antagonist saralasin 150 micrograms/kg ICV, blunted and 300 micrograms/kg ICV reversed the effect of Ang II. The mu opioids antagonist naloxone and the kappa opioid antagonist MR 2266, 50 micrograms/kg ICV, prevented the effect of Ang II on fatal arrhythmias. The action Ang II on arrhythmias could not be explained by the effects of Ang II on blood pressure or heart rate. These data indicate a role for Ang II within the CNS to modulate cardiac arrhythmias and that this is mediated in part, by endogenous opioids.

Angiotensin II↗
PubMed1991

D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin in the nucleus tractus solitarius of the rat produces cardiorespiratory depression.

1. The synthetic Met-enkephalin, D-Ala-2-Me-Phe-4-Met-(O)-ol-enkephalin (FK 33-824). 1 or 2 micrograms, after its injection into the nucleus tractus solitarius (NTS) of Wistar rats, anesthetized with pentobarbital and breathing spontaneously, produced a transient increase in blood pressure followed by sustained and significant (P less than 0.05) hypotension and bradycardia. This occurred in a dose dependent manner. 2. FK 33-824 in the NTS, 1 or 2 micrograms, also produced a marked respiratory depression. 3. In anesthetized rats, in which hypoventilation was prevented by mechanical ventilation, there was a definite reduction in blood pressure and heart rate that was considerably and significantly (P less than 0.05) less than that observed in spontaneously breathing rats. 4. Blood pressure fluctuations occurred after NTS injection that were more marked in spontaneously breathing animals but still occurred in animals that were ventilated mechanically. 5. FK 33-824, 1 and 2 micrograms in the NTS was fatal within 100 min for all animals but was prevented by mechanical ventilation. Higher doses of FK 33-824, 10 micrograms in the NTS, however, induced fatal ventricular arrhythmias even in the mechanically ventilated rat. 6. Thus, FK 33-824 in the NTS decreases blood pressure and heat rate in spontaneously breathing as well as mechanically ventilated rats, but much of the effect on blood pressure and heart rate is due to the profound respiratory depression in the spontaneously breathing rat.

Animals↗
PubMed1991

Reversal of angiotensin II effect on the cyclic adenosine 3',5' monophosphate response to isoprenaline in cardiac hypertrophy.

STUDY OBJECTIVE: The aim was to examine the effect of angiotensin II on the response of hypertrophic cardiac myocytes to the beta adrenergic receptor agonist isoprenaline. DESIGN: Viable ventricular myocytes were isolated from hypertrophic hearts of Dahl S rats and hearts of Dahl R rats. Myocytes were stimulated with isoprenaline. cAMP content was measured by competitive binding radioimmunoassay. MEASUREMENTS AND MAIN RESULTS: Hypertrophic Dahl S myocytes had smaller cAMP response to isoprenaline than Dahl R myocytes (p less than 0.05). Angiotensin II inhibited cAMP stimulation in Dahl R myocytes. In contrast, angiotensin II increased cAMP accumulation in hypertrophic Dahl S myocytes compared to the effect of isoprenaline alone (p less than 0.05). Enhancement of isoprenaline stimulation of cAMP accumulation by angiotensin II was positively related to the degree of cardiac hypertrophy. Angiotensin II treatment in the absence of isoprenaline had no effect on cAMP levels. CONCLUSION: The reversal of the normal inhibitory action of angiotensin II is evidence of a unique alteration in the signal transduction of beta receptor stimulation and is of potential importance in defining the role of angiotensin II in cardiac hypertrophy.

Angiotensin II↗
PubMed1991

Diltiazem and verapamil lower blood pressure in the unanaesthetized rat through CNS mechanisms involving endogenous opioids.

1. To evaluate and compare the effects of the calcium channel blockers, diltiazem and verapamil, on CNS modulation of blood pressure, unanaesthetized and unrestrained rats with catheters previously inserted into the lateral cerebral ventricle and femoral artery received intracerebroventricular (i.c.v.) administration of diltiazem or verapamil, 10 or 50 micrograms/kg, or their diluent. 2. Diltiazem, at both 10 and 50 micrograms/kg i.c.v., produced significant (P less than 0.05) decreases in systolic and diastolic blood pressure and heart rate. Verapamil, at 50 micrograms/kg but not at 10 micrograms/kg i.c.v., produced a significant (P less than 0.05) decrease in blood pressure, while both doses significantly (P less than 0.05) decreased heart rate. 3. To examine the endogenous opioid systems as potential modulators of the effects of these calcium antagonists, the mu opioid antagonist naloxone, 20 micrograms/kg, was administered i.c.v. either before or after each calcium antagonist. Naloxone reversed and prevented the reduction in blood pressure produced by both agents. The decrease in heart rate produced by verapamil but not diltiazem was reversed by naloxone. 4. The results suggest that: (1) calcium channels in neuron membranes in the CNS play a role in blood pressure regulation; (2) at least part of the blood pressure reduction produced by calcium blockers may be effected in the CNS; and (3) central opioid mechanisms modulate part of the action of the calcium antagonists verapamil and diltiazem on blood pressure.

Animals↗
PubMed1979

Preoperative electrocardiography: its cost-effectiveness in detecting abnormalities when a previous tracing exists.

In 812 patients who underwent routine preoperative electrocardiography a mean of 24.6 months after undergoing electrocardiography at the same institution, the frequency of new abnormalities was estimated to evaluate the cost-effectiveness of this procedure prior to an operation. New abnormalities were judged to be either relevant or irrelevant to the assessment of operative risk, depending upon their previously demonstrated correlation with operative and postoperative morbidity and mortality. Since new abnormalities, especially new relevant abnormalities, were found to be relatively infrequent, the cost-effectiveness of routine preoperative electrocardiography was considered to be low. The evidence suggested that when a previous tracing exists preoperative electrocardiography is most clearly indicated for patients who are 60 years of age or older or whose previous tracing exhibited abnormalities. However, further research is required to develop more sensitive and specific protocols, and to evaluate the role of repeat electrocardiography in clinical decision-making.

Cost-Benefit Analysis↗
PubMed1979

DEAE-cellulose chromatography of creatine kinase isoenzymes--effect of pH and serum.

DEAE-cellulose chromatography (pH 7.0) of human heart extracts revealed the presence of three creatine kinase isoenzymes. The CK3 (skeletal muscle) isoenzyme was not retained on the column under these conditions. The CK2 (heart) and CK1 (brain) isoenzymes eluted at a conductivity of 5.5 +/- 0.6 m omega-1 and 11.4 +/- 1.2m omega-1, respectively. When DEAE-cellulose chromatography was performed at pH 8.0, CK2 eluted at a slightly higher conductivity, 6.5 m omega-1, whereas CK1 eluted as before 12.0 m omega-1. DEAE-cellulose chromatography of CK2 and CK1 isoenzymes in the presence of serum protein, and serum albumin had no significant effect on the elution of CK2 at pH 7.0 and 7.4, and on the elution of CK1 at pH 7.0 and 8.0 However, serum and serum albumin decreased the affinity of CK2 for DEAE-celluose at pH 8.0, and caused this isoenzyme to elute at a conductivity of 3.0-3.5 m omega-1. The decreased affinity of CK2 for DEAE-cellulose was not due to aggregation of CK2 with albumin or some other serum protein, but was related to the amount of albumin applied to the column.

Blood↗