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Dive into the research topics where Derrick A. Pulliam is active.

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Featured researches published by Derrick A. Pulliam.


American Journal of Cardiology | 1993

Aortic dimensions in tall men and women

Carl M. Reed; Phyllis A. Richey; Derrick A. Pulliam; Grant W. Somes; Bruce S. Alpert

Abstract Subjects with the Marfan syndrome are at risk for sudden death from aortic regurgitation, dissection or rupture. The severity of aortic regurgitation correlates with the degree of aortic root dilation, not annular dilation.1,2 The risk of aortic dissection increases with aortic enlargement.1,2 Aortic dissection may occur with only moderate aortic root dilation.1 Because Marfan patients with nonenlarged aortic roots are thought to be at low risk for aortic dissection and rupture,1 it is critical to define an enlarged aortic root. Nomograms that have been published for normal aortic root dimensions have not included a sufficient number of healthy subjects whose height exceeds the 95th percentile,3–7 usually present in Marfan patients. Thus, we do not know the normal aortic root dimensions for subjects whose body size is equivalent to those with the Marfan syndrome. This study examines the acceptable upper limit of normal for the aortic root in healthy subjects taller than the 95th percentile. The data were sought for use in determining which Marfan patients have aortic roots of greater than normal size, thus warranting pharmacologic intervention and activity restriction.


Hypertension | 1991

Sodium excretion and racial differences in ambulatory blood pressure patterns.

Gregory A. Harshfield; Bruce S. Alpert; Derrick A. Pulliam; Elaine S. Willey; Grant W. Somes; F B Stapelton

The influence of Na+ excretion and race on casual blood pressure and ambulatory blood pressure patterns was examined in a biracial sample of healthy, normotensive children and adolescents (10–18 years; n=140). The slopes relating 24-hour urinary Na+ excretion to systolic blood pressure were different for both black and white subjects for casual blood pressure (p<0.001) and blood pressure during sleep (p<0.03). For casual blood pressure, the slope was significant for black subjects (β=0.17;p<0.001) but not for white subjects. For blood pressure during sleep, the slope was again significant for black subjects (β=0.08; p<0.0l) but not for white subjects. Na+ excretion was also related to awake levels of systolic blood pressure for black subjects (β=0.08, r=0.36; p<0.01), although the slopes for both black and white subjects were not significantly different. Further analyses indicated the results were not due to racial differences in 24-hour urinary K+ excretion. However, plasma renin activity was marginally related to Na+ excretion in white subjects (r=0.22; p<0.06) but not black subjects, a finding that is consistent with previous studies. Na+ excretion was not associated with diastolic blood pressure or heart rate in either group under any condition. The results of this study support research that has demonstrated a stronger relation between Na+ handling and casual blood pressure in black subjects and extend these findings to blood pressure while the subject is both awake and asleep.


Hypertension | 1994

Racial Differences in the Age-Related Increase in Left Ventricular Mass in Youths

Gregory A. Harshfield; David W. Koelsch; Derrick A. Pulliam; Bruce S. Alpert; Phyllis A. Richey; Judith A. Becker

We determined the factors related to left ventricular mass adjusted for body size in 60 black (mean age, 13 +/- 2 years) and 40 white (mean age, 14 +/- 2 years) normotensive youths. The factors examined included age, sex, systolic blood pressure, diastolic blood pressure, plasma renin activity, plasma aldosterone concentration, and sodium and potassium intake as determined by 24-hour excretion. Sex (beta = 13.3, P < .003), age (beta = 2.88, P < .001), and systolic blood pressure (beta = 0.41, P < .02) were independent predictors in the sample as a whole, accounting for 37% of the variance of left ventricular mass adjusted for height. Separate analyses were performed for black and white subjects. In the black subjects, age (beta = 4.4, P < .004) followed by sex (beta = 11.85, P < .02) were independent factors, accounting for 43% of the variance of left ventricular mass adjusted for height. In contrast, in white subjects systolic blood pressure (beta = 0.4, P < .003) followed by sodium excretion (beta = 0.13, P < .05) were independent factors, with gender (beta = 8.89, P < .07) tending to account for 36% of the variance. Similar results were observed for left ventricular mass adjusted for body surface area. In conclusion, the age-related increase in adjusted left ventricular mass in black but not white youths may in part account for the early development of cardiovascular disease among the black population.


Hypertension | 1991

Patterns of sodium excretion during sympathetic nervous system arousal.

Gregory A. Harshfield; Derrick A. Pulliam; Bruce S. Alpert

The purpose of this study was to examine Na+ handling and regulation during 1 hour of behaviorally induced sympathetic nervous system (SNS) arousal followed by 2 hours of recovery. Two patterns of response were observed among experimental subjects, despite similar changes in blood pressure and heart rate. In one group (n=19), Na+ excretion increased significantly during SNS arousal, which then decreased significantly during recovery (12.3 versus 16.0 versus 13.1 meq/hr, baseline, SNS arousal, recovery, respectively). Changes in Na+ excretion were correlated with changes in creatinine clearance from baseline to SNS arousal (r=0.54) and SNS arousal to recovery (r=0.58), and were accompanied by significant increases in plasma renin activity (1.5 versus 2.0 ng/ml/hr) and aldosterone (8.5 versus 10.3 ng/ml/hr) from baseline to SNS arousal. Na+ excretion decreased during SNS arousal in the other group of subjects (n=17) and remained below baseline levels during recovery (16.2 versus 12.7 versus 11.9 meq/hr). These changes were associated with significant decreases in creatinine clearance from baseline to recovery (138 versus 121 ml/min/1.73 m2) and significant increases in plasma renin activity from baseline to SNS arousal (1.3 versus 2.2 ng/ml/hr) but not in aldosterone. Control subjects in n=24) maintained baseline levels of each variable throughout the procedure. These results suggest that individuals differ in Na+ handling and regulation during behavioral arousal. Decreases in Na+ have been reported previously in humans and animals at risk for the development of hypertension.


Pediatrics | 1994

Ambulatory blood pressure recordings in children and adolescents

Gregory A. Harshfield; Bruce S. Alpert; Derrick A. Pulliam; Grant W. Somes; Dawn K. Wilson


American Journal of Obstetrics and Gynecology | 1994

Cardiac function in fetuses and newborns exposed to low-dose aspirin during pregnancy

Thomas G. Di Sessa; Michael L. Moretti; Aldo Khoury; Derrick A. Pulliam; Kristopher L. Arheart; Baha M. Sibai


American Journal of Hypertension | 1994

Ambulatory blood pressure and renal function in healthy children and adolescents

Gregory A. Harshfield; Derrick A. Pulliam; Bruce S. Alpert


American Journal of Hypertension | 1993

Ambulatory Blood Pressure Patterns in Youth

Gregory A. Harshfield; Derrick A. Pulliam; Grant W. Somes; Bruce S. Alpert


Pediatrics | 1991

Ambulatory blood pressure patterns in children and adolescents: influence of renin-sodium profiles.

Gregory A. Harshfield; Derrick A. Pulliam; Bruce S. Alpert; F. Bruder Stapleton; Elaine S. Willey; Grant W. Somes


American Journal of Hypertension | 1995

A30 - The renin-angiotensin-aldosterone system and salt sensitivity in the elderly

Grant W. Somes; Gregory A. Harshfield; Phyllis A. Richey; Derrick A. Pulliam; Cl Jones; Karen C. Johnson

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Bruce S. Alpert

University of Tennessee Health Science Center

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Grant W. Somes

University of Tennessee Health Science Center

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Phyllis A. Richey

University of Tennessee Health Science Center

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Cl Jones

University of Tennessee Health Science Center

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Karen C. Johnson

University of Tennessee Health Science Center

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Elaine S. Willey

University of Tennessee Health Science Center

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Aldo Khoury

University of Tennessee Health Science Center

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Baha M. Sibai

University of Texas Health Science Center at Houston

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Carl M. Reed

University of Tennessee Health Science Center

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