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Biomedical subjects

A Martinsson

Publications and source records attributed to A Martinsson.

At least 37 records · Page 2Linked to original sources

Altered cardiovascular responsiveness to adrenaline in endurance-trained subjects.

The influence of physical training on responses to i.v. adrenaline infusions and to exercise were investigated in 10 endurance-trained men (mean age: 35 y; VO2max: 61.9 ml kg-1 min-1) and 10 age-matched and sedentary controls (36 y, 37.5 ml kg-1 min-1). The untrained subjects were reinvestigated after a 4 month training period which increased their VO2max by 18%. Resting heart rate and diastolic blood pressure were significantly lower in the trained state. The venous plasma adrenaline concentrations attained during infusions (4 dose levels, 8 min each) were lower in the well-trained than in the untrained subjects (2.15 vs. 3.59 nmol l-1 at the highest dose level, P less than 0.01). The adrenaline-induced increases in heart rate and in plasma cAMP and decreases in pre-ejection period (PEP) and PEP/LVET ratio were not dependent on the training state. The adrenaline-induced decrease in diastolic blood pressure was more pronounced (P less than 0.05) in the well-trained than in the untrained group and tended (0.05 less than P less than 0.1) to be enhanced by training in the latter group. The increases in systolic blood pressure were greater in the well-trained subjects (P less than 0.01) but training did not alter this response in the untrained subjects. The plasma noradrenaline response to maximal cycle ergometer exercise (VO2max test) was significantly greater in the well-trained than in the untrained subjects, while no difference was seen for adrenaline. The submaximal exercise systolic blood pressure was similar in all training conditions when related to the absolute rate of work. In summary, the present results indicate that both the vasodilator and systolic pressor responses to adrenaline are enhanced in endurance-trained subjects. The cardiac chronotropic and inotropic effects of adrenaline seem, however, to be independent of the training state.

Adult↗

Temperature-induced changes in metabolic and hormonal responses to intensive dynamic exercise.

Seven male subjects performed intensive cycle exercise to exhaustion at subnormal muscle temperature (Tm, 29 +/- 2.8 degrees C). Exercise at exactly the same rate of exercise and duration (370 +/- 34 W, 1.5 +/- 0.15 min) was then repeated with normal Tm (35 +/- 0.9 degrees C). During exercise both the arterial (a) and femoral venous (fv) contents of oxygen were significantly higher at subnormal than at normal Tm, because of the higher haemoglobin concentration, but the a-fv oxygen difference was the same in the two situations. The rate of increase in lactate concentration in both arterial and venous blood during exercise was the same in two situations. During exercise the plasma concentrations of adrenaline and noradrenaline in arterial and venous blood were significantly higher at subnormal than at normal Tm. At rest and after exercise the calf blood flow was significantly reduced at subnormal Tm. At the end of exercise the concentrations of glucose-6-phosphate and lactate in the muscle were significantly higher at subnormal Tm than in the muscle of normal temperature. These findings suggest that there was a greater increase in glycolysis in the muscle of subnormal temperature during exercise, possibly as a result of impaired work efficiency and/or reduced blood flow in the cold muscle.

Adult↗

Influence of circulating alpha adrenoceptor agonists on lung function in patients with exercise induced asthma and healthy subjects.

The influence of circulating noradrenaline (in this context primarily a non-selective alpha agonist) and the alpha 1 selective agonist phenylephrine on bronchial tone, blood pressure, and heart rate was studied in eight patients with exercise induced asthma and eight age and sex matched controls. All subjects refrained from taking treatment for at least one week before the trial. The agonists were infused intravenously in stepwise increasing doses of 0.04, 0.085, 0.17, and 0.34 micrograms/kg a minute for noradrenaline and 0.5, 1.0, 2.0, and 4.0 micrograms/kg a minute for phenylephrine. At the highest dose the plasma concentration of noradrenaline was about 30 nmol/l, resembling the concentrations found during intense exercise, and that of phenylephrine was about 400 nmol/l. Both agonists caused dose dependent and similar increases in blood pressure in the two groups. Despite clearcut cardiovascular effects (systolic and diastolic blood pressure increased by about 40-50/25-30 mm Hg), neither agonist altered lung function, as assessed by measurements of specific airway compliance (sGaw), peak expiratory flow (PEF), or end expiratory flow rate, in either group. It is concluded that circulating alpha agonists, whether alpha 1 selective (phenylephrine) or non-selective (noradrenaline), fail to alter basal bronchial tone in patients with exercise induced asthma or in healthy subjects.

Adolescent↗

Beta-adrenoceptor function in white blood cells from newborn infants: no relation to plasma catecholamine levels.

The maturity of beta-adrenoceptors in newborn infants was studied in relation to the catecholamine surge during labor. Umbilical blood was collected at birth from 12 infants delivered vaginally and 13 infants delivered by elective cesarean section. Granulocytes and lymphocytes were isolated. Receptor numbers and binding affinity were determined in the granulocytes by incubation with 125I-iodohydroxybenzylpindolol. Receptor responsiveness was tested by assessing isoproterenol-induced cyclic AMP accumulation in lymphocytes. Significantly higher plasma noradrenaline, adrenaline, and dopamine concentrations were found in infants born vaginally (108; 8.9; 0.9 nmol/liter, liter, respectively, median values) as compared with those delivered by cesarean section (11.0; 2.4; 0.2 nmol/liter). No significant differences in beta-adrenoceptor binding sites (receptor number: 39.2 +/- 2.6 versus 44.7 +/- 5.9 fmol/mg protein and binding affinity: 66.6 +/- 7.8 versus 65.0 +/- 6.2 pM) or responsiveness (maximal isoprenaline induced cAMP formation 52.4 +/- 10.3 versus 40.6 +/- 8.9 pmol/10(6) cells) were found between the two groups of infants. Lymphocyte beta-adrenoceptor sensitivity was similar to that found in adults. The beta-adrenoceptors on whole blood cells seem to be mature at birth and have the same responsiveness as in adults. The higher catecholamine surge during vaginal delivery as compared to elective cesarean section does not seem to affect beta-adrenoceptor function. Our results do not support the idea that reduced beta-adrenoceptor function is the cause of the previously observed inappropriately small cardiovascular and metabolic responses to the exceptionally high plasma catecholamine concentrations at birth.

Binding Sites↗

Co-release of neuropeptide Y and catecholamines during physical exercise in man.

Venous plasma levels of neuropeptide Y-like immunoreactivity (with chromatographic properties of synthetic neuropeptide Y) increased in parallel with catecholamines, heart rate and blood pressure during graded physical exercise in man. The plasma levels of neuropeptide Y correlated better with the levels of noradrenaline than adrenaline, suggesting release of a neural origin. Taken together with previous results, this suggests that neuropeptide Y is released together with noradrenaline upon sympathetic activation during physiological conditions in man. Determinations of plasma neuropeptide Y may therefore be valuable in the assessment of sympathetic nerve activity.

Adult↗

Ethanol dependent interaction between prostaglandins and lipoxygenase products in human peripheral lymphocytes.

The effect of lipoxygenase products, 12-L-HETE and 15-L-HPETE, on cyclic AMP levels in human peripheral lymphocytes was examined in the absence and in the presence of a prostaglandin of the E-type (0.6-3.0 microM) or isoprenaline (33 microM). The studies were performed either in the absence or in the presence of 6 per cent ethanol. For comparison the effect of arachidonic acid and linolenic acid were studied. In the absence of ethanol 12-L-HETE and 15-L-HPETE had no significant effect on cyclic AMP accumulation. However, in the presence of ethanol 12-L-HETE (above 1 microM) inhibited prostaglandin E1 but not isoprenaline induced cyclic AMP accumulation. 15-L-HPETE had a biphasic effect on prostaglandin E2 induced cyclic AMP accumulation. Concentrations below 1 microM stimulated, those above inhibited. Virtually complete inhibition was seen at 15 microM. The two other fatty acids inhibited both prostaglandin E2 and isoprenaline induced cyclic AMP accumulation in the presence, but not in the absence of ethanol. The results show that lipoxygense products have little or no effect on cyclic AMP accumulation in human peripheral lymphocytes unless ethanol is present. In the presence of ethanol both 12-L-HETE and 15-L-HPETE appeared to selectively affect the cyclic AMP accumulation stimulated by PGE.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Reduced beta 2-adrenoceptor responsiveness in exercise-induced asthma.

Beta-adrenoceptor responsiveness was studied both in vivo and in vitro in patients with exercise-induced asthma (EIA), asthmatic patients without EIA (NEIA), and control subjects. All subjects were age- and sex-matched and without medication at least one week prior to the tests. In vivo, beta-adrenoceptor responsiveness was evaluated by plasma concentration-effect studies for intravenously infused isoprenaline (0.02-0.1 micrograms X kg-1 X min-1). Mainly beta 2-adrenoceptor mediated responses to isoprenaline, ie, decreases in diastolic blood pressure and increases in plasma cyclic AMP, were reduced in EIA patients but not in NEIA patients. Heart rate and plasma glycerol responses to isoprenaline did not differ between the groups. In vitro, the beta 2-adrenoceptor mediated accumulation of cyclic AMP in lymphocytes stimulated by isoprenaline was attenuated (p less than 0.05) in EIA patients, whereas the beta 2-adrenoceptor responsiveness of lymphocytes from NEIA patients was normal. Thus, beta 2-adrenoceptor mediated responses were reduced both in vivo and in vitro in EIA patients, but not in NEIA patients. This finding that beta 2-adrenoceptor responsiveness was reduced only in a subgroup of asthmatic patients could explain some of the controversies in the literature concerning beta-adrenoceptor function in asthma.

Adolescent↗

Comparison of the effects of different arachidonic acid metabolites on cyclic nucleotide accumulation in human peripheral lymphocytes.

The effect of PGE1, PGE2, PGD2, PGF2 alpha, PGI2, PGG2, PGA1, 12L-HETE, arachidonic acid, 15- HPETEa and linolenic acid on the accumulation of cyclic AMP in human peripheral lymphocytes was studied. PGE1, PGE2 and PGD2 were essentially equipotent as stimulators of cyclic AMP accumulation (threshold at about 10(-8)M and EC50 about 0.15 microM), PGF2 alpha was about 20 times less potent, while PGG2, 12L-HETE, 15-HPETE, PGA1 and linolenic acid were inactive. PGI2 caused a weak stimulation between 5 and 600 nM and a secondary stimulation above 3 microM. Arachidonic acid had no effect on cyclic AMP levels up to 100 microM. PGE1, PGD2, PGI2 and PGF2 alpha increased cyclic GMP in the concentrations that produced a rise in cyclic AMP, but the cyclic GMP increase was of smaller magnitude. Exogenous arachidonic acid was converted mainly to 12L-HETE, HHT and thromboxane B2 by lymphocyte suspensions. This conversion could be accounted for by contamination with blood platelets. The results show that the degree of cyclic AMP accumulation in human lymphocytes following stimulation of arachidonic acid metabolism will be critically dependent upon which prostaglandins are in fact formed by cells surrounding the lymphocytes.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

Sympathoadrenal reactivity in exercise-induced asthma.

The possibility that sympathoadrenal activity is altered in asthma was examined in eight patients with a history of exercise-induced asthma (EIA), eight matched patients with nonexercise induced asthma (NEIA), and eight matched healthy control subjects. No medication was allowed for at least one week before examination. In a pretrial exercise test diagnosis of EIA was confirmed and each individual's work capacity (Vo2 max) was determined. The trial consisted of an orthostatic test and a standardized exercise test at 80 to 90 percent of VO2 max on a treadmill. The trial exercise test caused a decrease in FEV1 in EIA patients only, whereas measurements of Sgaw revealed a significant but less pronounced postexercise bronchoconstriction in NEIA-patients as well. Basal plasma catecholamine levels were similar in all groups. Noradrenaline and adrenaline levels were approximately doubled by the orthostatic test and increased approximately ten-fold following exercise, with no differences between the groups. Plasma cAMP levels were approximately doubled by the exercise test. In the EIA patients there was an inverse correlation between increases in plasma cAMP and decreases in Sgaw. Our study does not support earlier claims that exaggerated catecholamine response to exercise causes postexercise bronchoconstriction by alpha-adrenoceptor stimulation in EIA. Differences in study results appear to have methodologic explanations.

Adolescent↗