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Biomedical subjects

J B Warren

Publications and source records attributed to J B Warren.

At least 73 records · Page 4Linked to original sources
PubMed1986

Systemic absorption of inhaled epinephrine.

To determine the systemic absorption of epinephrine when it is given by inhalation, six normal volunteers were given 15 puffs, followed by 30 puffs, of epinephrine from a pressurized aerosol (160 micrograms epinephrine/puff). The peak mean (+/- SE) plasma epinephrine levels were 1.50 (+/- 0.61) and 4.22 (+/- 1.93) nmol/L 1 minute after each dose, respectively. The effect on physiologic finger tremor correlated with the plasma epinephrine level and returned to baseline 20 minutes after taking the higher dose. There was a small fall in mean plasma potassium levels of 0.45 mmol/L and a small rise in plasma glucose levels of 0.81 mmol/L. On a separate occasion an injection of 0.3 ml of 1/1000 (300 micrograms) epinephrine was given subcutaneously to the same individuals. This caused a peak plasma epinephrine level of 2.43 (+/- 0.47) nmol/L at 10 minutes, and this was still raised at 2.05 (+/- 0.41) nmol/L after 40 minutes. The maximum fall in the mean plasma potassium level was 0.43 mmol/L after the injection.

Absorption↗
PubMed1986

Effect of infused vasoactive intestinal peptide on airway function in normal subjects.

Vasoactive intestinal peptide, one of the putative neurotransmitters of non-adrenergic inhibitory nerves in human airways, is a potent relaxant of human airways in vitro. Previous in vivo studies of infused vasoactive intestinal peptide in asthmatic subjects have shown only a small bronchodilator effect, which may have been secondary to the cardiovascular effects of the peptide. The effect on airway function of infused vasoactive intestinal peptide was studied in normal subjects, who readily develop bronchodilation in response to a beta agonist. Separate experiments were designed to assess whether there is any synergy between this peptide and the beta agonist isoprenaline. Incremental doses of 1, 3, and 6 pmol/kg/min of vasoactive intestinal peptide were infused for 15 minutes. At 6 pmol/kg/min it caused a mean fall in systolic blood pressure from 108 to 88 mm Hg and a rise in heart rate from 71 to 95 beats/min. There was no significant change in specific airways conductance (sGaw) at any dose of vasoactive intestinal peptide. No significant changes were found with placebo. Isoprenaline (400 microgram) given by inhalation at the end of the infusion produced a mean increase in sGaw of 50%. Infused peptide caused no significant change in the cumulative dose-response curve for inhaled isoprenaline. The lack of effect of vasoactive intestinal peptide on airway responses in vivo may be due to rapid enzymatic breakdown of the peptide or to the fact that dosage has to be limited by the cardiovascular effects.

Adult↗
PubMed1986

Calcium channel blockers and treatment of hypertension.

Over the past years, research efforts have been focused on the pathophysiologic role of calcium ions, and the implication for the potential role of calcium channel blockers in the management of essential hypertension. Numerous studies have shown that nifedipine and verapamil are effective antihypertensive agents, initial experience with diltiazem is also encouraging. The magnitude of blood pressure reduction with these drugs is related to the pre-treatment blood pressure. In refractory hypertension, combination with other antihypertensive agents provide additive effect. In the elderly population and in patients with ischemic heart disease, supraventricular arrhythmia, bronchospastic disease, peripheral vascular disease or diabetes mellitus, the calcium channel blockers offer potential advantages over other antihypertensive agents. Experimental studies also suggest that these drugs may reverse ventricular hypertrophy. When long-term safety with these drugs is documented from well-controlled clinical trials, the calcium channel blockers may be our first line of therapy for the management of hypertension.

Antihypertensive Agents↗
PubMed1985

Association of chronic cystic mastopathy, xeromammographic patterns, and cancer.

The Breast Cancer Demonstration and Detection Project in Louisville (BCDDP-L) screened 10,128 women for cancer. From this screening, another project evolved wherein those patients diagnosed as having chronic cystic mastopathy (CCM) were followed over a 10-year period to evaluate any association between CCM and breast cancer. In all, 1396 breast biopsies were performed, with 165 cancers being diagnosed either on initial screening or during subsequent years. Three of these are excluded, since histopathologic slides could not be obtained for central review. Of this group, cancer was associated with CCM in 116 specimens and without CCM in 46 specimens. One subset of 355 patients with biopsy-proven CCM but no breast cancer was followed for 6 to 12 years, for a total of 2443.5 woman-years of observation. Within this subset, a total of only four cancers occurred (4 cancers/2443.5 woman-years for 0.00164 cancers/woman-years). This incidence is not significantly different from the expected value. However, an estimate is provided as to the power of the test that could be obtained from a larger sample size derived from other BCDDPs. This group of 355 women was sorted into subsets by establishing a matrix matching ten histopathologic subdivisions of CCM against six subdivisions of Wolfe's xeromammographic (XM) patterns. The numbers of cancers in each cell of this matrix is reported. The results found no concentration of these four cancers in this matrix.

Adult↗
PubMed1985

Posture and theophylline kinetics.

The effect of posture on theophylline kinetics was examined in six healthy men who took 450 mg slow-release aminophylline orally at the same time of day on two separate occasions. On one day they remained standing and on the other supine throughout. Plasma theophylline was measured hourly for 6 h from ingestion. Mean theophylline levels were significantly higher in the standing position at all times (P less than 0.01). We conclude that diurnal variation in theophylline kinetics can be explained, at least in part, by differences in posture.

Adult↗
PubMed1985

Particles and macrophages in murine Peyer's patches.

Mice were given 1% suspensions of 5 insoluble particles (chrysotile asbestos, quartz, carmine, carbon, and iron oxide) in drinking water for 3 months. The particles were subsequently sought in intestinal Peyer's patches by light microscopy. Carbon and iron oxide particles were visible in Peyer's patch macrophages, particularly in the subepithelial region, but the other particles could not be detected. The findings suggest that particle surface properties as well as particle size govern accumulation in Peyer's patches. The cytochemistry of subepithelial, mid-dome, tingible-body, and serosal macrophages of control mice indicated diversity of macrophages within the patch. Macrophages of asbestos-fed mice contained more lysosomes than macrophages of controls. Macrophage abundance in the dome apex was not significantly altered by asbestos ingestion. The other particles did not produce detectable alterations in macrophage morphology.

Animals↗
PubMed1985

Theophylline.

Explore the source record for details and available documents.

Adolescent↗
PubMed1984

Protective effect of circulating epinephrine within the physiologic range on the airway response to inhaled histamine in nonasthmatic subjects.

The specific airway conductance response of six normal subjects to increasing doses of inhaled histamine was studied on two occasions. On each occasion either epinephrine (0.025 micrograms/kg/min) or saline was infused intravenously during the histamine challenge. This dose of epinephrine, when it was administered to seated normal subjects, produces plasma levels similar to those found at the end of strenuous exercise. Epinephrine caused a significant elevation in the concentration of histamine required to cause a 35% fall in specific airway conductance (PC35), although this was in part caused by a small airway dilator effect. The mean (+/-SD) PC35 rose from 21 mg/ml (+/-6) during saline infusion to 58 mg/ml (+/-27) during epinephrine infusion, p less than 0.05. Levels of circulating epinephrine, similar to those found during exercise in normal subjects, appear to be capable of protecting against bronchoconstrictor stimuli.

Administration, Intranasal↗
PubMed1984

Effect of penbutolol and propranolol on normal airway response to salbutamol.

The specific airway conductance (sGaw) response of eight normal men to inhaled salbutamol, 200, 600, and 1800 micrograms, was measured on 3 separate days. On each occasion subjects received either placebo, long-acting propranolol (160 mg), or penbutolol (40 mg) orally in a double-blind manner after baseline lung function determination. After placebo, mean sGaw rose from a baseline of 2.07 +/- 0.15 to 2.81 +/- 0.25 kPa-1 X sec-1 after 200 micrograms salbutamol. There was little further airway dilation with higher doses of salbutamol. With long-acting propranolol, there was no significant airway dilation after 200 micrograms salbutamol but there was after 600 and 1800 micrograms inhaled salbutamol; baseline sGaw rose from 2.02 +/- 0.17 to 2.70 +/- 0.28 and 2.95 +/- 0.32 kPa-1 X sec-1. Penbutolol prevented any significant airway dilation with all doses of salbutamol. Penbutolol at the doses used appears to be a more potent blocker of beta 2-receptors than does propranolol.

Adult↗
PubMed1984

Effect of adrenergic and vagal blockade on the normal human airway response to exercise.

Ten normal, non-asthmatic subjects performed an 18 min graduated exercise test on a static exercise bicycle on 3 separate days. They received either no medication, or propranolol 80 mg orally 2 h before, or ipratropium bromide 0.216 mg by inhalation 30 min before, the start of exercise. With no medication, transpulmonary index (TPI), a measure of airway resistance, fell linearly during exercise from a resting value of 0.269 +/- 0.024 to 0.170 +/- 0.014 kPa X 1(-1) X s by the end of exercise. This returned to baseline between 2 and 4 min after stopping exercise. Propranolol elevated baseline TPI slightly from 0.270 +/- 0.024 to 0.294 +/- 0.024 before exercise and during exercise this fell linearly to 0.185 +/- 0.016 kPa X 1(-1) X s. The fall in TPI during exercise after propranolol was not significantly different from the fall seen with no medication. Six minutes after exercise stopped TPI rose to 0.336 +/- 0.035 kPa X 1(-1) X s after propranolol. All values for TPI from 4 min to 16 min after exercise were significantly higher after propranolol than the corresponding values found after no medication (P less than 0.05). Ipratropium bromide decreased baseline TPI from 0.264 +/- 0.024 to 0.163 +/- 0.013 kPa X 1(-1) X s (P less than 0.001) and this did not change significantly further either during or after exercise. Normal subjects show considerable airway dilatation during exercise and this appears to result from inhibition of resting vagal tone. The sympathetic system does not appear to mediate the airway dilatation during exercise, but it may be important in protecting against post-exercise bronchoconstriction.

Adult↗
PubMed1984

Adrenaline secretion during exercise.

By studying six normal subjects during graduated treadmill exercise, we have confirmed that there is very little rise in venous plasma adrenaline levels during mild or moderate exercise. During a second study, adrenaline was infused intravenously in six resting subjects at a rate of 0.025 micrograms min-1 kg-1. This elevated the basal plasma adrenaline level from 0.28 +/- 0.04 nmol/l to 0.92 +/- 0.16, 1.16 +/- 0.20 and 1.28 +/- 0.19 nmol/l at 3, 5 and 7 min after the start of the infusion. The same adrenaline infusion was repeated in the same subjects 7 min after they started moderate exercise at a constant rate on a static exercise bicycle. Just before the start of the infusion, 7 min after the onset of exercise, plasma adrenaline had risen to 0.36 +/- 0.07 nmol/l. This rose to 1.86 +/- 0.30, 1.98 +/- 0.26 and 2.19 +/- 0.29 nmol/l at 3, 5 and 7 min after the start of this second infusion. Five minutes after the end of the infusion, while the subjects were still exercising, the mean level was 0.56 +/- 0.04 nmol/l. The venous plasma level of adrenaline is the result of a balance between the secretion of adrenaline by the adrenal medulla and the clearance of adrenaline from plasma. Our results suggest that the lack of any significant rise in plasma adrenaline during moderate exercise does not result from an accelerated clearance of adrenaline by exercising tissue. The clearance rate of adrenaline from plasma is reduced during exercise. There is no significant increase in secretion by the adrenal medulla in response to the stimulus of mild or moderate exercise.

Adult↗