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Biomedical subjects

P R Foster

Publications and source records attributed to P R Foster.

At least 37 records · Page 2Linked to original sources
PubMed1987

The viral safety of intravenous immunoglobulin.

Human immunoglobulin for intravenous (IV) use has an established safety record with regard to transmission of hepatitis B virus. The bulk of available evidence also suggests that the human immunodeficiency virus (HIV) is not transmitted by IV immunoglobulin. There has been one report, however, of isolation of HIV from two patients with hypogammaglobulinaemia who had been treated with several immunoglobulin products. Certain IV immunoglobulin products have transmitted non-A, non-B (NANB) hepatitis but careful clinical assessment of recipients of other products suggests that non-infective preparations can be made. Interpretation of available data most likely to be correct is that contamination with NANB is reduced but not eliminated by cold-ethanol fractionation and that the use of further virucidal procedures in the finishing of immunoglobulin products will confer a higher degree of safety.

Animals↗
PubMed1987

Studies on the effect of heat treatment on the thrombogenicity of factor IX concentrates in dogs.

This study examines the effects of heat treatment for 72 h at 80 degrees C on the potential thrombogenicity of lyophilized human coagulation factor IX concentrates. Since heating generated minor amounts of thrombin, concentrate was prepared with antithrombin III addition prior to heat treatment. Changes in coagulation parameters were followed prior to and after infusion of 100 iu/kg of heated and unheated concentrates to dogs. All batches produced a transient fall in platelet count during infusion and a delayed rise in plasma fibrinopeptide A, accompanied by a minor prolongation of the activated partial thromboplastin time. Such changes were less marked for heated batches. Control infusion of a 'failed' factor IX concentrate showed an additional fall in fibrinogen, rise in fibrin degradation products and a more rapid rise in fibrinopeptide A, while thrombin infusion caused an even more dramatic intravascular coagulation. These studies indicated no increase in the potential thrombogenicity of freeze dried factor IX concentrates as a result of heat treatment.

Albumins↗
PubMed1982

Control of large-scale plasma thawing for recovery of cryoprecipitate factor VIII.

Cryoprecipitation is commonly used as the primary step in the preparation of clinical factor VIII concentrates; yet recovery is usually very low. Much of this loss is due to poor temperature control and a process of continuous plasma thawing has been designed to overcome this. A substantial improvement has resulted, with an increase in both yield and purity of factor VIII:C of over 50% in comparison to a conventional batch thaw process.

Antigens↗
PubMed1981

Acute and chronic haemodynamic effects of prazosin in left ventricular failure.

We evaluated the acute and chronic effects of prazosin treatment in 11 patients with chronic congestive heart failure, NYHA functional class III and IV. Before treatment mean arterial pressure averaged 100 +/- 15 mmHg, left ventricular filling pressure 29 +/- 11 mmHg, and systemic vascular resistance 2372 +/- 1121 dynes s cm-5. Prazosin administration resulted in haemodynamic improvement in all but one patient with significant lowering of the mean arterial pressure, left ventricular filling pressure, and systemic vascular resistance. Nine patients completed a 10-week course of ambulatory treatment. Five patients remained improved while four developed significant fluid retention; two of these had transient exacerbation of congestive heart failure. This was controlled by increasing diuretic and/or prazosin treatment. After 10 weeks all nine patients had advanced to NYHA functional class II. Repeat haemodynamic measurements disclosed complete haemodynamic tolerance in one patient while three other patients showed partial tolerance with a lower cardiac output (CO) response to prazosin. The nine patients, however, still showed significant lowering of the mean arterial pressure, left ventricular filling pressure, as well as the systemic vascular resistance. Though pharmacodynamic tolerance was noted in four out of nine patients, beneficial clinical and haemodynamic effects could be demonstrated after 10 weeks of prazosin treatment in most patients. Further evaluation of the long-term effects of prazosin in chronic congestive heart failure is warranted.

Aged↗
PubMed1981

Changes in factor VIII complex activities during the production of a clinical intermediate purity factor VIII concentrate.

Samples taken at various stages of preparation of intermediate purity factor VIII concentrate were assayed for factor VIII coagulant activity (VIII:C), factor VIII coagulant antigen (VIIIC:Ag) and factor VIII related antigen (VIIIR:Ag). The antigen results were used to assess mechanical loss during fractionation as these markers are relatively stable. In contrast VIII:C is sensitive to both mechanical and inactivation losses. The major loss of factor VIII occurred during the cryoprecipitation and extraction step and was due to both mechanical loss and inactivation. Losses before and after this step were largely due to inactivation of the factor VIII. Assay of VIIIR:Ag in concentrates presented problems and a modified technique is suggested.

Antigens↗
PubMed1979

Atrial induction of ventricular tachycardia: reentry versus triggered automaticity.

Atrial stimulation induced a sustained ventricular tachycardia in two patients with mitral valve prolapse and in one patient who had mild hypertension without cardiac abnormalities. Exercise-induced sinus tachycardia also started the ventricular tachycardia in one patient. Evidence is presented to suggest that the mechanism of ventricular tachycardia in one patient was reentrant excitation and in another patient triggered automaticity. It is likely that the origin of the ventricular tachycardia was confined to a relatively protected small area near the posteroinferior portion of the left ventricle and was not due to macroreentry.

Adolescent↗
PubMed1979

Ventricular tachycardia and ventricular fibrillation in a young population.

In this study, we describe the findings in 18 young patients (age range 4 days to 24 years, mean 16.6 years) who had ventricular tachycardia and/or ventricular fibrillation and were followed for 4--70 months (mean 22.4 months). Patients had a variety of problems associated with their arrhythmia, including mitral valve prolapse, cardiomyopathy, myocarditis, prolonged QT syndrome and hypokalemia. Six patients had no clinically recognizable cardiac abnormality. The ventricular tachycardia showed a left bundle branch block contour in 10 of 17 patients, right bundle branch block in four, was multiform in two and had an indeterminate contour in one. Sustained ventricular tachycardia was initiated and terminated reproducibly by atrial and ventricular stimulation in three of seven patients who did not have spontaneous episodes of ventricular tachycardia during the electrophysiologic study. In one other patient, short bursts of ventricular tachycardia were induced. Patients who had ventricular fibrillation, those who died, and those who are still symptomatic with poorly controlled ventricular arrhythmias had significant heart disease. In one patient, a ventricular tachyarrhythmia that had required more than 100 electrical cardioversions spontaneously disappeared after requiring 1 year of antiarrhythmic therapy.

Adolescent↗
PubMed1977

Alterations in canine myocardial excitability during ischemia.

Changes in the ventricular diastolic excitability threshold following occlusion of the left anterior descending coronary artery (LAD) were studied in open-chest anesthetized dogs by using a new automatic threshold-following pacemaker (ATFP). The ATFP measures the diastolic excitability threshold by successively decreasing the duration of regularly occurring pacing stimuli until the ventricle fails to respond. Under control conditions, the threshold stimulus duration was 60 +/- 4 (mean +/- SEM) musec. In the first 1-3 minutes following occlusion of the LAD, the diastolic excitability threshold in the ischemic zone (IZ) decreased to 51 +/- 5 musec and then rapidly increased to 600 musec at 5 minutes. The initial decrease in excitability threshold at IZ could be abolished by elevating the serum K+ concentration prior to the LAD occlusion. These changes in excitability threshold at IZ could be prevented by infusing nonoxygenated solutions into the LAD at a site distal to the occlusion. As the excitability threshold increased in IZ during ischemia, the earliest time at which IZ could be reactivated by a stimulus with a voltage equal to twice the preligation diastolic voltage threshold was increased. In nine of 16 dogs, after 5 minutes of LAD ligation, the IZ to normal zone (NZ( activation time (when stimulating at IZ) exceeded the NZ to IZ activation time (when stimulating at NZ) by an average of 9 msec. We also found that in four dogs the NZ to IZ activation time exceeded the IZ to NZ activation time by an average of 10 msec. We conclude from these findings that a gradient of increasing excitability threshold exists as one moves from normally perfused toward more ischemic tissue, passing through a heterogenous border zone that manifests some areas which have a decreased excitability threshold and other areas which have an increased excitability threshold, and that these changes in excitability importantly influence the determination of refractory period durations and conduction times.

Animals↗
PubMed1977

Accelerated ventricular escapes induced in the intact dog by barium, strontium and calcium.

Accellerated ventricular escapes (AVE) were produced with infusion of BaCl2, SrCl2 and CaCl2. AVE demonstrated overdrive acceleration rather than overdrive suppression, i.e., faster pacing rates caused shorter escape intervals. BaCl2 (mean 20.2 mumol/kg) produced AVE in 18 of 23 dogs and a decrease in mean serum potassium (K+). SrCl2 alone (mean 2494 mumol/kg) did not produce AVE in 5 dogs and K+ was unchanged. When insulin and glucose were infused to lower K+ and SrCl2 was infused 30 minutes later, AVE was demonstrated in 7 of 10 dogs. CaCl2 alone (mean 1628 mumol/kg) produced AVE in 3 of 5 dogs and CaCl2 (mean 1733 mumol/kg) infused 30 minutes after insulin and glucose produced AVE in 4 of 4 dogs. This study demonstrates that AVE previously produced with cardiac glycosides can also be induced by infusion of barium, strontium and calcium.

Animals↗
PubMed1976

The kinetics of protein salting-out: precipitation of yeast enzymes by ammonium sulfate.

Protein solubility can be adequately represented by the classical Cohn equation for the salting-out of alcohol dehydrogenase and fumarase from clarified yeast homogenate with ammonium sulfate. However, the constant beta in this equation is a function of the contacting procedure employed. The kinetics of continuous salting-out were similar for alcohol dehydrogenase and fumarase. The overall rate equation for precipitation had a variable order which was high initially, up to 3.1, but approached unity on completion of precipitation. This was followed by a partial resolution stage which was first order with respect to the concentration driving force. Precipitate particle size was estimated as 0.5 to 5 mum with continuous flow precipitation producing the largest particles.

Alcohol Oxidoreductases↗
PubMed1976

Suppression of ouabain-induced ventricular rhythms with aprindine HCl. A comparison with other antiarrhythmic agents.

Three groups of dogs were given ouabain (mean 60 mug/kg) until an accelerated ventricular escape (AVE) and repetitive ventricular response (RVR) followed cessation of pacing. In a group of six control dogs, the AVE and RVR were found to occur at stable escape intervals for periods of at least three hours. A second group of dogs received various antiarrhythmic agents in an attempt to suppress the AVE and RVR. Quinidine, diphenylhydration, lidocaine, procainamide, and propranolol, were successful in only 0 to 33% of trials. Potassium canrenoate, 12 mg/kg was unsuccessful in three dogs. Verapamil, by bolus, suppressed RVR in 41% and AVE in 21% of trials. KCl, infused until AVE and RVR were suppressed, was successful when the mean serum potassium rose from 3.8 mEq/L to 7.2 mEq/L. Aprindine, 2.86 mg/kg, suppressed AVE and RVR in 14 of 14 dogs. In the third group of dogs, verapamil was infused continuously and suppressed RVR and AVE at a mean cumulative dose of 2.93 mg/kg. Calcium chloride reversed aprindine and verapamil-induced suppression of RVR and AVE. This study demonstrates that RVR and AVE resist suppression by available antiarrhythmic agents in clinically-used doses. Only aprindine was 100% successful at doses used in man. The ionic pathogenesis of RVR and AVE is unknown, but some data suggest the slow current may play an important role.

Animals↗
PubMed1975

Effects of aprindine HCL on cardiac tissues.

The effects of aprindine HCL on cardiac tissues were studied in anesthetized, open-chest dogs pretreated with atropine (0.8 mg/kg) and propranolol (1.0 mg/kg). Aprindine (10(-5)-10(-3) g/ml), injected into the sinus node artery, decreased the spontaneous sinus rate; when injected into the atrioventricular nodal artery, aprindine (10(-4) g/ml) prolonged the conduction time and functional refractory period of the atrioventricular node. Intravenous administration of aprindine (1.4, 2.8 and 4.2 mg/kg cumulative dose) prolonged atrial and ventricular conduction time and prolonged the effective refractory period of both tissues. The results from this study indicate that aprindine has a negative dromotropic effect on all cardiac tissue.

Animals↗