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Biomedical subjects

B Cercek

Publications and source records attributed to B Cercek.

At least 91 records · Page 5Linked to original sources
PubMed1986

Usefulness of residual plasma fibrinogen after intravenous streptokinase for predicting delay or failure of reperfusion in acute myocardial infarction.

The relation between the level of residual plasma fibrinogen and coronary artery reperfusion after 750,000 IU of intravenous (i.v.) streptokinase (SK) was examined in 76 patients with acute myocardial infarction. Both the frequency and rapidity of reperfusion were greater in the 53 patients in whom the residual fibrinogen level was 50 mg/dl or less (low fibrinogen) than in the 23 patients in whom it was more than 50 mg/dl (high fibrinogen). Reperfusion occurred in all 53 patients in the low-fibrinogen group, compared with only 15 patients in the high-fibrinogen group (p less than 0.001). The interval from initiation of SK to clinical signs of reperfusion was 50 +/- 34 minutes in the low-fibrinogen group and 110 +/- 54 minutes in the high-fibrinogen group (p less than 0.001). A high fibrinogen level occurred in 58% of patients who weighed more than 85 kg and in 25% of patients who weighed 85 kg or less (p less than 0.05). No patient who weighed 60 kg or less had a high fibrinogen level. The high-fibrinogen group also had a greater incidence of a high anti-SK antibody titer: 8 of 13 patients (62%) tested, compared with none of the 8 patients tested in the low-fibrinogen group (p less than 0.01). Our data indicate that a high residual fibrinogen level after administration of i.v. SK identifies patients in whom SK is relatively ineffective, probably because of inadequate dosage of inactivation of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Coronary Circulation↗
PubMed1986

Interaction of SK-human plasmin, SK-dog plasmin complexes with alpha 2-antiplasmin and alpha 2-macroglobulin.

In patients treated with streptokinase there is a rapid and significant decrease in the level of fibrinogen in the circulation. In dogs given streptokinase there is no such change in circulating fibrinogen. To find an explanation for this species difference in response to streptokinase, the inhibition of SK-human plasmin and SK-dog plasmin by soybean trypsin inhibitor, alpha 2-antiplasmin and alpha2-macroglobulin were compared in this study. Soybean trypsin inhibitor completely blocked the hydrolysis of S-2251 substrate (D-val-L-leu-lys-p-nitroanilide) by SK-dog plasmin and had no effect on SK-human plasmin. Alpha 2-Antiplasmin, the physiologically important regulator of fibrinolysis, inhibited S-2251 hydrolysis by SK-dog plasmin but not the activity of SK-human plasmin. alpha 2-Macroglobulin showed 100% inhibition of proteolytic activity and 50% inhibition of S-2251 activity of SK-dog plasmin, and had no effect on SK-human plasmin. Studies with fresh human and dog plasma also showed that the SK-dog plasmin is rapidly inactivated by the alpha 2-antiplasmin present in the plasma. The inactivation of SK-dog plasmin and not SK-human plasmin by plasma inhibitors explains the differences in the response of dog and humans to the administration of streptokinase.

Animals↗
PubMed1986

Elevated serum D dimer: a degradation product of cross-linked fibrin (XDP) after intravenous streptokinase during acute myocardial infarction.

D dimer, a degradation product of cross-linked fibrin, is generated by lysis of fibrin but not by lysis of fibrinogen and can be reliably detected by specific monoclonal antibody techniques. The generation of D dimer after intravenous streptokinase in acute myocardial infarction was studied with the use of a semiquantitative latex agglutination immunoassay. This assay utilizes the monoclonal antibody DD-3B6/22, raised by conventional hybridoma technology, against a highly purified preparation of human D dimer and is adjusted to give a positive agglutination at a D dimer serum concentration of greater than 200 ng/ml (upper limit of normal). Twenty-one patients with acute transmural myocardial infarction of less than 3 hours' duration were studied. Fifteen patients received 0.75 to 1.5 million U intravenous streptokinase and 6 patients were treated conventionally without thrombolytic therapy. An elevated serum level of D dimer was detected before treatment in only 1 of 15 patients receiving intravenous streptokinase and within 2 hours of treatment in the remaining 14 patients who received streptokinase. In contrast, an elevated serum D dimer level was not detected during the first 24 hours in any of the six conventionally treated patients, including two patients who manifested the clinical syndrome of spontaneous reperfusion. The data suggest that in patients with acute myocardial infarction, an elevated serum level of D dimer, a cross-linked fibrin degradation product occurs early after administration of a large dose of streptokinase, but is infrequent during the first 24 hours in conventionally treated patients with acute infarction. Measurement of D dimer may be potentially useful for monitoring thrombolysis in patients with acute myocardial infarction.

Aged↗
PubMed1986

Enhancement of thrombolysis with tissue-type plasminogen activator by pretreatment with heparin.

The effect of pretreatment with heparin on lysis of arterial thrombi by tissue-type plasminogen activator (rt-PA) was studied in 19 dogs. Copper coil-induced carotid artery thrombi were weighed, inserted into the femoral arteries, and exposed to a 15 min infusion of rt-PA at 10 micrograms/kg/min either with (n = 6 thrombi) or without pretreatment with a 200 unit/kg bolus of heparin (n = 6 thrombi). The infusion of rt-PA without pretreatment reduced the thrombus weight by 27.6 +/- 7.4%, while infusion of rt-PA with pretreatment reduced it by 79.1 +/- 12.3% (p less than .0001). To test the hypothesis that heparin enhanced thrombolysis by preventing continued incorporation of new fibrin into the thrombus during thrombolysis we repeated the experiments using pretreatment with 8 U/kg of ancrod, which rapidly depletes fibrinogen. Pretreatment with ancrod (n = 6 thrombi) depleted fibrinogen and enhanced the lytic effect of rt-PA to a similar degree as pretreatment with heparin, resulting in a 67.6 +/- 12.3% (NS) decrease in thrombus weight. We conclude that heparin significantly enhances the thrombolytic effect of rt-PA, probably by preventing new fibrin formation and its incorporation into the thrombus during lysis.

Ancrod↗
PubMed1985

Arrhythmias with brief, high-dose intravenous streptokinase infusion in acute myocardial infarction.

Cardiac arrhythmias are described during the first 2 h after brief, high-dose, intravenous streptokinase infusion in 23 patients with evolving myocardial infarction was given. A control group consisted of 22 similar patients with acute myocardial infarction not treated with streptokinase infusion. On the basis of an early peak of creatine kinase activity successful reperfusion was achieved in 60.9% of patients. Significantly more ventricular premature complexes (P less than 0.01) and paroxysms of idioventricular rhythm (P less than 0.05) were noticed in the treated group. Premature ventricular complexes did not predict any severe ventricular arrhythmia. Accelerated idioventricular rhythm appears to be the most specific arrhythmia encountered with thrombolytic therapy of acute myocardial infarction. We propose that in routine clinical work it can be used as a bedside sign of successful reperfusion.

Adult↗
PubMed1985

The effects of the rate of intravenous infusion of streptokinase and the duration of symptoms on the time interval to reperfusion in patients with acute myocardial infarction.

We studied the influence of the following variables on the time interval from initiation of an intravenous infusion of 750,000 U of streptokinase until reperfusion (reperfusion time) in 140 consecutive patients with an evolving acute myocardial infarction: (1) the rate of infusion of streptokinase, (2) the duration of chest pain before initiation of treatment, (3) patient age, (4) patient sex, (5) location of infarction, (6) history of previous myocardial infarction, and (7) pretreatment pathologic Q waves. The time of reperfusion was recognized by clinical criteria that were completely concordant with the anatomic findings in all 119 patients in whom patency or occlusion of the artery of infarction was established at delayed angiography (n = 116) or at postmortem examination (n = 3). The mean reperfusion time for the 129 patients for whom data were available was 49 +/- 36 min. The reperfusion time was inversely related to the rate of infusion of streptokinase (r = .41, p less than .001), but this effect of infusion rate appeared to plateau at rates of greater than 500 U/kg/min. In the 64 patients receiving infusions at rates of 500 U/kg/min or less, the mean reperfusion time was 60 +/- 40 min, whereas in the 58 patients receiving the drug at rates greater than 500 U/kg/min it was 35 +/- 22 min (p less than .001). The duration of chest pain before treatment was the only other studied variable found to influence the reperfusion time, but only at infusion rates of less than 250 U/kg/min (r = .6, p less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1985

The hypotensive effect of intravenous streptokinase in patients with acute myocardial infarction.

We studied the hypotensive effect of a rapid intravenous infusion of high-dose streptokinase in 98 patients with an acute myocardial infarction. The systolic blood pressure fell from 132 +/- 20 (range 90 to 174) to 97 +/- 21 mm Hg (range 58 to 152) at 15 +/- 8 min (range 4 to 40) after the commencement of the streptokinase infusion (p less than .001). A fall in diastolic blood pressure from 80 +/- 16 (range 51 to 105) to 61 +/- 15 mm Hg (range 32 to 92) accompanied the fall in systolic pressure (p less than .001). The fall in blood pressure was associated with an increase in heart rate (73 +/- 14 to 78 +/- 17 beats/min, p less than .001), preceded the appearance of clinical signs of reperfusion by 37 +/- 38 min and was similar in magnitude and timing in patients with anterior and inferior infarction. There were direct relationships between the rate of infusion of streptokinase and both the magnitude (r = .49, p less than .001) and the rate of fall of systolic blood pressure (r = .67, p less than .001) as well as both the magnitude and rate of fall of diastolic blood pressure. In most patients, the fall in blood pressure was transient (9 +/- 6 min, range = 2 to 30) and easily managed by slowing or stopping the infusion, placing the patient in the Trendelenburg position, or by administering an infusion of low-dose norepinephrine or dopamine. However, in four patients with severe left ventricular dysfunction, severe hypotension persisted for more than 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Thrombolytic therapy with intracoronary or intravenous streptokinase during acute myocardial infarction.

This report compares the results of intracoronary (IC) and intravenous (IV) streptokinase in a sequential series of 200 patients (IC = 81 and IV = 119) admitted within 3 hours of the onset of an acute myocardial infarction. Reperfusion was achieved in 71 of 81 (88%) patients in the IC group and in 113 of 119 (95%) patients in the IV group (p = NS) 35 +/- 27 and 42 +/- 33 minutes after commencement of treatment respectively (p = NS). The interval from onset of symptoms to reperfusion was significantly longer in the IC than in the IV group, 235 +/- 62 versus 175 +/- 61 minutes (p less than 0.001). Mean values of peak creatine kinase-MB were 152 +/- 117 IU/L in the IC group and 117 +/- 79 IU/L in the IV group (p less than 0.05). Three patients in the IC group and 16 patients in the IV group suffered major hemorrhagic complications. In-hospital mortality was 7 of 81 (8.7%) in the IC group and 10 of 119 (8.4%) in the IV group (p = NS). We conclude that IV administration of streptokinase in patients with an acute myocardial infarction is at least as efficacious as IC administration.

Aged↗
PubMed1984

Sotalol-induced torsade de pointes.

A case of sotalol-induced polymorphous ventricular tachycardia (torsade de pointes) is presented. The patient had moderately prolonged Q-T interval before medication with sotalol with further prolongation after application of this drug. Electrophysiological study during rechallenge with sotalol demonstrated a uniform ventricular tachycardia with a somewhat polymorphous onset; whether or not this tachycardia represented replication of the patient's spontaneous arrhythmia is questionable. Without antiarrhythmic drugs and during medication with pindolol ventricular tachycardia was not inducible.

Aged↗
PubMed1983

Heterogeneity of cyclic nucleotide phosphodiesterases in liver endoplasmic reticulum.

A microsomal fraction from rat liver was subfractionated into three rough endoplasmic reticulum fractions RIII, RII and RI, together with a smooth endoplasmic reticulum plus Golgi fraction. Cyclic nucleotide phosphodiesterase activity was found in all fractions. Subsequently it was shown that Golgi fractions were essentially devoid of cyclic AMP phosphodiesterase activity and the activity resided in the smooth endoplasmic reticulum fraction. The activity of the endoplasmic reticulum constituted some 20% of the homogenate activity, with the major fraction of this being associated with the RII fraction and the least with the RI fraction. With the exception of the activity of the RI fraction, which was a peripheral enzyme, all of the other enzyme activities were integral, requiring detergent or repeated freeze-thawing to effect solubilization. All of the activities appeared to be exposed at the external surface of the endoplasmic reticulum, as they were inactivated by trypsin under conditions where glucose 6-phosphatase was not. All of these activities displayed distinct sensitivities to both thermal and trypsin inactivation, yielding activity decays consistent with a single enzyme species being present in each case. The freeze-thaw-solubilized enzymes yielded single symmetrical peaks on sucrose-density-gradient centrifugation and polyacrylamide-gel electrophoresis. The sedimentation coefficients for the enzymes in the smooth-endoplasmic-reticulum-plus-Golgi, RIII, RII and RI fractions were 3.2S, 4.2S, 4.5S and 4.5S respectively. Whereas the activity in the smooth-endoplasmic-reticulum-plus-Golgi fraction exhibited normal Michaelis kinetics, those in the other fractions yielded kinetics indicative of apparent negative co-operativity. All of the enzymes exhibited low Km values towards cyclic AMP. The enzymes did not appear to be regulated by Ca2+ or calmodulin. ZnCl2 was found to be a potent non-competitive inhibitor of the enzyme in all fractions. NaF was a weak non-competitive inhibitor. The bilayer fluidizing agent benzyl alcohol exerted dissimilar effects on the enzyme activities. It is concluded that the endoplasmic reticulum displays lateral heterogeneity, with single, rather distinct, cyclic AMP phosphodiesterases being found in the different fractions.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1982

Submitochondrial localization and asymmetric disposition of two peripheral cyclic nucleotide phosphodiesterases.

There are two distinct cyclic AMP phosphodiesterases associated with the liver mitochondrion: one with the outer membrane and one with the inner membrane. No activity is associated with the lysosomal fraction. Both of the enzymes are peripheral proteins and can be released from the membranes by high-ionic-strength treatment. Treatment of intact mitochondria with trypsin and insoluble trypsin localizes these enzymes to the cytosol-facing surface of their respective membranes. The enzymes differ in regard to sedimentation coefficient, thermostability and susceptibility to inactivation by trypsin. Both enzymes degrade cyclic AMP and cyclic GMP. Whereas the outer-membrane enzyme displays Michaelis kinetics and appears to be a low-affinity enzyme, the inner-membrane enzyme displays kinetics indicative of apparent negative co-operativity.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Involvement of mitochondria in changes in fluorescein excitation and emission polarization spectra in living cells.

The comparison of fluorescein polarization spectra in living cells and in isolated subcellular structures identified the mitochondria as the cytoplasmic domain in which on excitation at 470 nm the sharp fluorescein emission polarization peak at 510 nm is formed. Changes in the emission polarization peak during the cell cycle or those induced by growth stimulators and inhibitors reflect structural changes in the mitochondria on their transition from the resting, orthodox into the active, ATP-generating, condensed conformation and vice versa. Possible mechanisms for the formation of the sharp emission polarization peak are discussed.

Animals↗
PubMed1978

Fluorescein excitation and emission polarization spectra in living cells: changes during the cell cycle.

Changes in the fluorescein fluorescence emission and excitation polarization spectra in synchronized cultured S3 fibroblasts at G1, mid-S, and mitosis, as well as in human lymphocytes before and after stimulation with mitogens, were studied. In contrast to those measured in aqueous solutions the emission and excitation polarization spectra in living cells exhibit a wavelength dependence characteristic for the state of the cell cycle. Changes in the temperature and in the amount of intracellular water result in quantitative wavelength-independent changes in the polarization spectra. Possible mechanisms for the qualitative wavelength-dependent changes in the fluorescein emission and excitation polarization spectra during the cell cycle are discussed.

Cell Cycle↗