Biomedical subjects

J R Randall

Publications and source records attributed to J R Randall.

6 recordsLinked to original sources

PubMed1995

Heparin-induced increase in the international normalized ratio. Responses of 10 commercial thromboplastin reagents.

A clinician's concern about an erratic response to oral anticoagulation in a patient treated concurrently with heparin and warfarin led the authors to investigate the effect of heparin on INR values obtained with various commercial thromboplastin reagents. Studies conducted with pooled normal plasma and with pooled plasma from patients treated long-term with oral anticoagulants demonstrated a wide range of sensitivities to heparin of these reagents as characterized by prolongation of INR values. Innovin was unaffected by concentrations of heparin as high as 1 U/mL. In contrast, Ortho thromboplastin showed the greatest increase in INR values over the range of heparin concentrations studied. Three other thromboplastins including Neoplastine CI, Dade thromboplastin, and Simplastin A demonstrated only limited sensitivity to heparin. Prolongation of the INR by heparin was reversed by protamine in a dose-related manner and also by preincubation of the plasma with heparinase. Some patients treated with warfarin while on the authors' institutional protocol for heparin had plasma concentrations greater than 0.8 U/mL. When thromboplastin reagents sensitive to heparin were used with such specimens, the INR values obtained were falsely elevated. The authors suggest that reagents insensitive to heparin be employed to avoid this difficulty.

Blood Coagulation↗

PubMed1995

Adaptation of a functional assay for protein S to a Cobas Fara II centrifugal analyzer.

An adaptation of the manual Staclot protein S functional assay (American Bioproducts, Parsippany, NJ) for the Cobas FARA II centrifugal analyzer is described. This automated method is based on determining the clotting time by measuring the change in turbidity of the specimen as clotting progresses. The accurate and precise pipetting of the analyzer combined with its enhanced data acquisition and rapid parallel processing features result in a markedly improved procedure compared to the less accurate and reproducible manual method. The assay is linear over the range of protein S concentrations encountered clinically (0% to 150%); has a limit of detection of 3% protein S; within and between day precision (CV) at a level of 50% protein S is 4.7 and 12.6%, respectively; and results agree closely with those obtained on the STA automated hemostasis analyzer (slope = 0.98, intercept 3.92, and r = 0.98). Protein S values obtained with this assay for specimens from 20 normal males and 20 normal females were 115% +/- 22.31% (mean +/- standard deviation [SD]) and 98% +/- 18.2%, respectively. In 14 patients on chronic stable treatment with Coumadin (DuPont Pharmaceuticals, Wilmington, DE) the mean functional protein S activity was 16.2% and the SD 11.7%. The method for determination of protein S activity on the centrifugal analyzer yields results comparable to data reported with a variety of other techniques.

Anticoagulants↗

PubMed1985

Adenosine antagonist aminophylline attenuates pacing-induced coronary functional hyperemia.

The role of adenosine in pacing-induced hyperemia was examined in 10 dogs. Left coronary blood flow (LCBF), left ventricular O2 extraction [(a-v)O2], and myocardial O2 consumption (MVO2) were monitored. Heart rate (HR) was initially paced at 120 beats/min and then increased to 180 beats/min to elicit a hyperemic response (delta LCBF). During the hyperemia, the vasodilatory response to exogenous adenosine (FAd) was tested. HR was then returned to the initial level, and 20 min after injection of aminophylline (100 mg iv) HR was again increased to 180 beats/min. The response to adenosine was again tested. The pacing-induced increase in MVO2 (delta MVO2) was not affected by aminophylline (P greater than 0.05). However, after aminophylline, the flow response slope delta LCBF/delta MVO2 was decreased by about 20% (P less than 0.05), and the extraction-response slope delta (a-v)O2/delta MVO2 was increased by 100% (P less than 0.05). FAd was also decreased by aminophylline, and the magnitude of the reduction was correlated with the decrease in the flow-response slope (r = 0.82). These results suggest that endogenous adenosine may play an important role in coronary functional hyperemia induced by increases in heart rate.

Adenosine↗

PubMed1983

Optical urethrotomy--a 3-year experience.

One hundred and thirty-seven patients underwent optical urethrotomy and have been followed up over a period of 3 years. The overall improvement rate was 66%. The results were unrelated to the length of history, the number of previous dilatations or the site of the lesion. However, traumatic strictures did significantly less well than the others. Although the procedure can be repeated, the chance of failure following the third or subsequent urethrotomy was much greater than after the first or second procedure. Urethrotomy for post-prostatectomy membranous strictures was followed by incontinence in 31% of patients. Otherwise the procedure was safe and should be the first choice of treatment for most patients with urethral strictures.

Adolescent↗

PubMed1982

Effect of aminophylline on coronary functional hyperemia and myocardial adenosine.

The role of adenosine in coronary functional hyperemia was tested using the adenosine antagonist aminophylline. In 11 dogs left coronary blood flow (LCBF) and left ventricular oxygen extraction [(a-v)O2] were monitored. Myocardial oxygen consumption (MVO2) was calculated. Before aminophylline was administered, intracoronary infusion of 6.8 micrograms/min norepinephrine increased LCBF and MVO2 by 40-80%. Simultaneous infusion of adenosine further increased LCBF. Fifteen minutes after injection of 100 mg aminophylline, norepinephrine still increased LCBF, and the ratio delta LCBF/delta MVO2 was unchanged (P greater than 0.05). Although the functional hyperemia was not blunted, the response to infused adenosine was abolished by aminophylline. In 20 additional dogs myocardial adenosine was determined. Before norepinephrine infusion myocardial adenosine with and without aminophylline was 12.7 and 14.3 nmol/g dry wt, respectively (P greater than 0.05). During norepinephrine infusion an increase in adenosine correlated well with increases in MVO2 and LCBF, but the increase in adenosine was not greater after aminophylline. Thus the failure of aminophylline to blunt functional hyperemia was not due to a higher adenosine level after aminophylline. These results do not support a role for adenosine in functional hyperemia elicited by norepinephrine.

Adenosine↗

PubMed1982

Reduced oxygen and blood flow demands in the chronically sympathectomized heart.

Using an anesthetized, open-chest preparation, seven 3-week sympathectomized (CS) and eight 3-week sham operated (SO) dog hearts were studied. Circumflex blood flow per 100-g heart (CBF), left ventricular oxygen extraction [(a-v)O2], maximal dP/dt, and tension-time index (TTI) were measured at constant heart rate while aortic pressure (AoP) was changed by aortic constriction or hemorrhage. Left ventricular myocardial oxygen consumption (MVO2) was calculated from (a-v)O2 and CBF. The MVO2, CBF, (a-v)O2, and maximal dP/dt were related to TTI at each level of AoP by regression analyses. Over a wide range of TTI, MVO2 and CBF in CS were only about 50% of those in SO; (a-v)O2 was not different between the groups. These data indicate that the chronically sympathectomized heart operates at reduced oxygen and blood flow demands. Also, since (a-v)O2 and the regression of CBF on MVO2 were not different between the two groups, the data suggest that the reduced CBF in CS was secondary to a metabolic vasocontriction resulting from the reduced MVO2. Analyses of maximal dP/dt did not indicate that the reduced MVO2 in CS was as a result of reduced contractility.

Adrenergic Fibers↗