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Biomedical subjects

M F Wilson

Publications and source records attributed to M F Wilson.

At least 37 records · Page 2Linked to original sources
PubMed1997

Moderately obese, insulin-resistant women exhibit abnormal vascular reactivity to stress.

To define the hemodynamic implications of insulin resistance (IR), we compared 10 normotensive, insulin-resistant women who had abnormal glucose tolerance tests with 10 age-matched healthy normotensive women with normal glucose tolerance tests with respect to mental arithmetic and handgrip responses. Hemodynamic variables obtained at baseline and during stress included heart rate, blood pressure, cardiac output, and systemic vascular resistance. The IR group weighed more (84 versus 66 kg). Screening BP was similar (123/72 versus 120/68 mm Hg, P=NS) between groups although baseline diastolic BP at testing day was higher in the IR group than control group (75 versus 65 mm Hg, P<.05). The IR group showed a significantly greater increase in systolic (18% versus 10%, P<.O1) and diastolic (24% versus 12%, P<.01) blood pressure responses to mental stress than the control group. During mental stress, the control group demonstrated increased cardiac output (1.4 L/min) and decreased systemic vascular resistance (-120 dyne x s x cm[-5]), whereas IR subjects demonstrated increased systemic vascular resistance (119 dyne x s x cm(-5); group difference, P<.02) with only a small increase in cardiac output (0.5 L/min). Handgrip also caused a greater increase in systemic vascular resistance in the IR group (252 versus 64 dyne x s x cm(-5), P<.05), with a correspondingly greater increase in blood pressure than control subjects. Baseline blood pressure was correlated with weight (r=.41, P<.02) and stress blood pressure with fasting insulin (r=.51, P<.001) and glucose-to-insulin ratio (r= -.55, P<.001). We conclude that insulin resistance is associated with an exaggerated blood pressure response to stress; an enhanced vasoconstriction to stress may mediate this response. This hyperreactivity may be a marker for future hypertension in obese, normotensive, hyperinsulinemic individuals.

Adult↗
PubMed1996

Acute blood pressure elevations with caffeine in men with borderline systemic hypertension.

Whether the vasoconstrictive actions of caffeine are enhanced in hypertensive persons has not been demonstrated. Thus, caffeine (3.3 mg/kg) versus placebo was tested in 48 healthy men (aged 20 to 35 years) selected after screening on 2 separate occasions. Borderline hypertensive men (n = 24) were selected with screening systolic blood pressure (BP) of 140 to 160 mm Hg and/or diastolic BP 90 to 99 mm Hg. Low-risk controls (n = 24) reported no parental history of hypertension and had screening BP < 130/85 mm Hg. Participants were then tested on 2 occasions after 12-hour abstinence from caffeine in each of 2 protocols; this required a total of 4 laboratory visits. Caffeine-induced changes in diastolic BP were 2 to 3 times larger in borderline subjects than in controls (+8.4 vs +3.8 mm Hg, p < 0.0001), and were attributable to larger changes in impedance-derived measures of systemic vascular resistance (+135 vs +45 dynes.s.cm-5, p < 0.004). These findings were consistent and reached significance in both protocols. The percentage of borderline subjects in whom diastolic BP changes exceeded the median control response was 96%. Consequently, whereas all participants exhibited normotensive levels during the resting predrug baseline, 33% of borderline subjects achieved hypertensive BP levels after caffeine ingestion. Thus, in borderline hypertensive men, exaggerated responses to caffeine were: selective for diastolic BP, consistent with greater vasoconstriction, replicated in 2 protocols, and representative of nearly all borderline hypertensives. We suspect that the potential for caffeine to stabilize high resistance states in susceptible persons suggests that its use may facilitate their disease progression, as well as hinder accurate diagnosis and treatment.

Adult↗
PubMed1996

Stress-like adrenocorticotropin responses to caffeine in young healthy men.

The effects of oral caffeine (3.3 mg/kg, equivalent to 2-3 cups of coffee) on plasma adrenocorticotropin (ACTH) and cortisol (CORT) were tested in 47 healthy young men at rest in a double-blind, placebo-controlled, crossover study. Following caffeine, ACTH was significantly elevated at all times from 30 min to 180 min, and CORT was elevated from 60 min to 120 min (Fs > or = 8.4, ps < 0.01). Peak increases relative to placebo were: ACTH, 33% (+5.2 pg/ml) and CORT, 30% (+2.7 micrograms/dl) at 60 min postcaffeine. The results suggest that caffeine can activate important components of the pituitary-adrenocortical response in humans during the resting state. Caffeine's known ability to increase CORT production appears at least partly due to an increase in ACTH release at the pituitary.

Administration, Oral↗
PubMed1996

Caffeine and behavioral stress effects on blood pressure in borderline hypertensive Caucasian men.

Caffeine in dietary amounts raises blood pressure (BP), and its use increases during work stress; however, caffeine combined with behavioral stress has not been tested in borderline hypertensive (BH) men. Accordingly, this study tested a psychomotor stressor plus caffeine (3.3 mg/kg, equivalent to 2-3 cups of coffee) using a double-blind, crossover design in 24 BH men (140/90 mmHg < or = BP < or = 160/95 mmHg) and 24 controls (BP < or = 135/85 mmHg). BH men had modestly larger BP increases to the task and showed a greater combined effect of caffeine plus the task (+15/+11 mmHg) than controls (+10/+6 mmHg). BH men maintained response to the stressor in the face of an exaggerated BP response to caffeine, suggesting that use of caffeine during behavioral stress may elevate BP in BH individuals to a clinically meaningful degree.

Adult↗
PubMed1996

Dose-response effect of in vivo administration of endotoxin on polymorphonuclear leukocytes oxidative burst.

In vitro, endotoxin primes polymorphonuclear leukocytes (PMNs) to respond with a greater oxidative burst. The purpose of the present study was to investigate the in vivo effect of a wide range of single endotoxin bolus doses using a rat model. PMNs were subsequently challenged in vitro with phorbol ester to produce reactive oxygen intermediates (ROI). Flow cytometric determination of ROI production by large doses induced a decrease in ROI production by the few PMNs that remained in the circulation. By 6 h after injection, ROI production had returned to basal levels after a high dose, and was still increasing after a low dose. Neutropenia occurred immediately after endotoxin injection. After 6 h, PMN counts returned to almost normal levels with a high dose, but rebound neutrophilia occurred with a small dose. In contrast to in vitro studies, in vivo injection showed a response pattern that varied widely with dose and time of observation.

Animals↗
PubMed1995

Effect of aging on atenolol pharmacokinetics and pharmacodynamics.

A study was conducted to characterize and compare the pharmacodynamics and pharmacokinetics of atenolol in young and elderly men. Six young (mean +/- SD, 25.0 +/- 3.0 years) and six elderly (63.0 +/- 3.2 years) healthy men took atenolol 100 mg orally once daily for 6 days. Heart rate response to submaximal exercise was measured at selected times for 48 hours, and plasma and urine samples were collected over the same time interval. The Sigmoid Emax model was fit to percent reductions in exercise heart rate and atenolol plasma concentrations. The younger men had significantly lower values for area under the steady-state plasma concentration-time curve and higher values for systemic clearance/F and renal clearance. EC50 values showed a trend toward greater sensitivity to the negative chronotropic effects of atenolol among the elderly men. Model-derived percent reductions in heart rate were greater at all concentrations among the elderly men. These data suggest that group differences in atenolol pharmacokinetics were likely a result of age-related decline in renal function, and that the elderly subjects were at least as sensitive as, and maybe even more sensitive than, the younger subjects to the negative chronotropic effects of atenolol.

Adrenergic beta-Antagonists↗
PubMed1995

Caffeine elevates blood pressure response to exercise in mild hypertensive men.

The present study examined the effects of caffeine on blood pressure (BP) regulation in hypertensive men during exercise. Twenty unmedicated, mild hypertensives (HT, BP = 140/90 to 160/105 mm Hg) and 12 age-matched, normotensives (NT, BP < 130/80 mm Hg) performed 30 min of extended bicycle exercise following a single dose of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) and placebo in a double-blind, cross-over design. Hemodynamic measurements were made at predrug, 40-min postdrug and during exercise. At predrug baseline, HT had significantly higher HR (67 v 57 beats/min) and BP (141/96 v 118/72 mm Hg) than NT. At postdrug baseline, caffeine increased systolic and diastolic BP, and peripheral vascular resistance (P < .01 in all cases), decreased HR (P < .05) and did not significantly change stroke volume and cardiac output for both groups. During exercise, HR response was greater on caffeine day than placebo day in HT (P < 0.05) only. Systolic BP was consistently elevated on caffeine day compared to placebo day in both groups (P < .001). Diastolic BP was elevated in HT for 30 min of exercise on caffeine day, but this pressor effect disappeared at 15 min of exercise in NT. As a result, rate-pressure products were significantly higher on caffeine days in HT at postdrug and during exercise. On caffeine day, 7 (39%) HT and 1 (8%) NT showed an excessive BP response (> 230 for systolic or > 120 for diastolic) during exercise. In conclusion, caffeine has significant hemodynamic effects on mild hypertensives at rest and during exercise. The increased rate-pressure products following caffeine during exercise place a greater workload on the heart, and abstinence from caffeine, especially before exercise, may be beneficial for persons with hypertension.

Adult↗
PubMed1995

Insulin attenuates norepinephrine-induced venoconstriction. An ultrasonographic study.

To directly assess insulin-related venomotor changes objectively and quantitatively, we used a modified ultrasonographic technique to measure venous diameter. Ten healthy men and women were studied by use of an Acuson 128 XP ultrasonograph with a linear 7.5-MHz ultrasonographic transducer (sensitivity, +/- 0.1 mm). Venous diameter was measured with the arm kept at 30 degrees elevation and with a pneumatic cuff above the elbow inflated at 40 mm Hg for the last 2 minutes of each 5-minute observation period. Norepinephrine was infused at incremental concentrations of 12.5, 25, 50, and 100 ng/min (75, 150, 300, and 600 pmol/min, respectively) for 5 minutes each. Maximal venoconstriction was achieved by the dose of 100 ng/min norepinephrine, which was then combined with insulin doses of 8, 16, 24, and 32 microU/min (60, 120, 180, and 230 fmol/min, respectively) for 5 minutes each. In six different subjects, methylene blue, an inhibitor of guanylate cyclase, was infused simultaneously with 32 microU/min insulin and 100 ng/min norepinephrine. Mean resting diameter of the vein (1.8 +/- 0.6 mm [mean +/- SD]) increased (to 3.0 +/- 1.0 mm) after cuff inflation. Incremental doses of norepinephrine caused highly reproducible dose-dependent decrease in venous diameter (to 1.8 +/- 0.6 mm, P < .001). Incremental doses of insulin, when combined with the maximum dose of norepinephrine, caused highly reproducible dose-dependent increases in mean venous diameter (P < .001) compared with norepinephrine alone. Methylene blue, which had no independent effect on venous diameter, inhibited the venodilator effect of insulin (P < .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Adrenocortical effects of caffeine at rest and during mental stress in borderline hypertensive men.

We examined the effect or dietary doses of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) on adrenocortical responses to behavioral stress in borderline hypertensive (BH) men using a randomized, double-blind, caffeine-placebo crossover design. Cortisol levels were assessed in BH men and matched normotensive (NT) controls at rest and in response to 35 min of continuous work on a psychomotor task alternating with mental arithmetic. Caffeine at rest elevated cortisol among BHs hut not among NTs. Both groups showed significant cortisol responses to caffeine combined with the tasks. These findings may have implications for the dietary use of caffeine in persons at risk for hypertension when faced with stressful situations.

Journal Article↗
PubMed1995

New directions for research in prevention and treatment of delinquency: a review and proposal.

The past century has witnessed a number of approaches to the prevention and treatment of delinquency. Some approaches have emphasized physiological, psychological, and other individual characteristics; others have focused on the structure of the family; and still others have considered the structure of social relations within the broader society. More recent approaches have attempted to conceptualize an integrated complex of factors which includes community characteristics. This article reviews the various approaches which have dominated the field over the last few decades and concludes with a methodological proposal which may facilitate the systematic consideration of these various factors.

Adolescent↗
PubMed1994

Comparison of Staphylococcus aureus and Escherichia coli infusion in conscious rats.

The purpose of this study was to compare the pathophysiology of bacteremia produced by intravenous infusion of either a Gram-positive (Staphylococcus aureus) or a Gram-negative (Escherichia coli) organism. Conscious, unrestrained, instrumented rats received S. aureus, E. coli, or sterile saline over 120 min, followed by a 240-min monitoring period. The infusates produced 90% (S. aureus,) 80% (E. coli), and 0% (saline) mortality at 24 hr. Neither bacterial group produced hypotension during the entire 360-min study period. E. coli produced early tachycardia and increased glucose, followed by decreased stroke volume and increased lactate and pO2. S. aureus caused early tachycardia followed by decreased pH, stroke volume, and cardiac output and increased lactate and systemic vascular resistance. Respiration rate and central venous pressure were not affected by either bacterial infusion. Compared to E. coli, S. aureus produced decreased pH, glucose, pO2, heart rate, and cardiac output and increased lactate, hematocrit, pCO2, and systemic vascular resistance. These data document quantitative differences in the acute response of the conscious rat to bacteremia caused by these isolates of E. coli and S. aureus.

Animals↗
PubMed1994

Prolonged increase in blood pressure by a single oral dose of caffeine in mildly hypertensive men.

Caffeine is known to raise blood pressure (BP). We examined a single oral dose of caffeine (3.3 mg/kg, equivalent to 2 to 3 cups of coffee) on BP in 18 hypertensive (HTN) and 12 age-matched, normotensive (NT) men for 3 h. Systolic BPs were significantly higher after caffeine for both groups (P < .001) for the entire 3 h. The HTN group showed persistent elevation in diastolic BP for 3 h, whereas the increment of diastolic BP became smaller in the NT group 90 min after caffeine ingestion. Our results suggest that caffeine consumption may affect both diagnosis and treatment of hypertension and abstinence from caffeine may be beneficial, especially for hypertensive individuals.

Administration, Oral↗
PubMed1994

Procalcitonin increase after endotoxin injection in normal subjects.

As procalcitonin concentrations have been shown to be elevated in patients with septicemia and gram-negative infections in particular, we proceeded to investigate the effect of endotoxin, a product of gram-negative bacteria, on procalcitonin concentrations in normal human volunteers. Endotoxin from Escherichia coli 0113:H10:k, was injected i.v. at a dose of 4 mg/kg BW into these healthy volunteers. Blood samples were obtained before and 1, 2, 4, 6, 8, and 24 h after injection of the endotoxin. Each patient's cardiovascular and overall clinical status was monitored over this period. The patients developed chills and rigors, myalgia, and fever between 1-3 h. Tumor necrosis factor-alpha levels increased sharply at 1 h and peaked at 90 min, reaching the baseline concentration thereafter by 6 h. Interleukin-6 levels increased more gradually, peaking at 3 h and reaching the baseline concentration at 8 h. The procalcitonin concentration, which was undetectable (< 10 pg/mL) at 0, 1, and 2 h, was detectable at 4 h and peaked at 6 h, maintaining a plateau through 8 and 24 h (4 ng/mL). There was no elevation of calcitonin concentrations, which remained below 10 pg/mL, the lowest sensitivity of the assay. Procalcitonin was measured by a two-antibody immunoradiometric assay specific for this peptide, with no cross-reactivity with calcitonin, katacalcin, or calcitonin gene-related peptide. We conclude that endotoxin induces the release of procalcitonin systemically, that this increase is not associated with an increase in calcitonin, and that the increase in procalcitonin associated with septicemia in patients may be mediated through the effect of endotoxin described here. Whether procalcitonin participates in the mechanisms underlying inflammation remains to be investigated.

Adult↗
PubMed1994

Dose- and time-dependent cardiovascular responses induced by ethanol.

Four groups of male Sprague-Dawley rats (10/group) were instrumented to permit access to venous and arterial blood and comprehensive cardiovascular measurements for 4 h after intragastric administrations of water or 2, 4 or 6 g/kg of ethanol. Maximum blood concentrations for each increasing dose occurred within 45 min after ethanol attaining peaks of 63 +/- 8, 103 +/- 11 and 221 +/- 33 mg/d, respectively. Cardiac outputs were significantly lower than the control group beginning at 15 min for 4 and 6 g/kg and at 120 mins for 2 g/kg with similar effects on stroke volume for the three doses. Systemic vascular resistance and heart rate were consistently increased throughout the 4 h for the 6 g/kg group. There was a delayed mean arterial blood pressure decrease in the 6 g/kg group beginning at 120 min after ethanol with significant effects in the 4 g/kg group at 60 and 120 min. Decreased central venous pressure and respiration rate prevailed during the 4 h after 6 g/kg. Blood glucose concentrations were elevated at 60 min after 6 g/kg and at 240 min for all doses. However, blood temperatures were consistently lower than the control group after all three doses beginning 45 min after the drug. These data demonstrate that ethanol evokes cardiovascular, respiratory and metabolic changes that are both dose- and time-dependent. Cardiac output and systemic vascular resistance are significantly affected suggesting a marked alteration of peripheral blood flow.

Animals↗