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Biomedical subjects

G P Todd

Publications and source records attributed to G P Todd.

6 recordsLinked to original sources

Relation between changes in blood pressure and serum ACE activity after a single dose of enalapril and ACE genotype in healthy subjects.

1. The effects of a single oral dose of enalapril 10 mg on serum ACE activity and blood pressure in relation to the ACE genotype were studied in 27 healthy men, n = 9 each of genotype DD, ID and II, in a parallel group study design. 2. Before treatment serum ACE activity differed significantly between the genotypes, with serum ACE activity 56% higher in DD than II subjects, and the genotype explaining 40% of between-subject variance in serum ACE activity. 3. After oral enalapril 10 mg the absolute fall in serum ACE activity was significantly larger in DD than II subjects at 2, 4, and 6 h (by 9.0 (95% CI 0.7-17.2), 10.7 (3.8-17.6), and 9.7 (2.8-16.6) nmol ml-1 min-1 respectively), but not at 24 h (fall in II > DD by 1.1 (-8.9 to 6.7) nmol ml-1 min-1). 4. Serum ACE activity remained significantly related to the ACE genotype at each time-point after enalapril, with the genotype explaining 22-46% of between-subject variance in serum ACE. 5. Falls in mean arterial pressure in response to enalapril were not significantly related to the ACE genotype, with the average fall over 6 h in DD > II genotype by 0.7 mm Hg (95% CI -5.5 to 4.1). 6. Blood pressure responses to enalapril did not correlate significantly with the initial serum ACE, or the absolute or percent reductions in serum ACE activity after enalapril.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

Pressor effect of hyperventilation in healthy subjects.

Hyperventilation is an important feature of panic disorder, and an association has been reported between panic disorder and hypertension. We have examined the effect of hyperventilation on the blood pressure (BP) of healthy subjects. Twenty six subjects were randomised in a balanced two-period cross-over study to compare the effects of hyperventilation with that of normal breathing on sitting BP, heart rate and the electrocardiogram. Each study phase lasted 40 min, with 15 min of baseline observation, 5 min of hyperventilation or normal breathing, and 20 min of continued observation. Hyperventilation significantly increased SBP by 8.9 mm Hg (95% CI 3.8-13.8, P < 0.01), diastolic blood pressure by 8.2 mm Hg (95% CI 1.7-14.7, P < 0.05), mean arterial pressure by 10.0 mm Hg (95% CI 3.3-16.7, P < 0.01) and heart rate by 36 beats/min (95% CI 31-44, P < 0.01). The changes in diastolic and mean arterial pressure correlated significantly with the total volume of air expired during hyperventilation (r = 0.57, p < 0.01 and r = 0.50 P < 0.01, respectively), but not with the change in expired carbon dioxide. In the electrocardiogram, T wave changes occurred in the inferior leads in 10 of 26 subjects, but there were no significant changes in other measurements. Hyperventilation significantly increased the BP of healthy subjects, and the role of hyperventilation in the link between panic disorder and hypertension deserves further study.

Adult

General solution to the inverse problem of the differential equation of the ultracentrifuge.

Whenever experimental data can be simulated according to a model of the physical process, values of physical parameters in the model can be determined from experimental data by use of a nonlinear least-squares algorithm. We have used this principle to obtain a general procedure for evaluating molecular parameters of solutes redistributing in the ultracentrifuge that uses time-dependent concentration, concentration-difference, or concentration-gradient data. The method gives the parameter values that minimize the sum of the squared differences between experimental data and simulated data calculated from numerical solutions to the differential equation of the ultracentrifuge.

Kinetics