Bo Brantmark - Academia.edu (original) (raw)
Papers by Bo Brantmark
Clinical pharmacology and therapeutics, 1977
This paper presents a self-adjusting randomization plan which is thought to be useful in controll... more This paper presents a self-adjusting randomization plan which is thought to be useful in controlled stratified randomized clinical trials. The method assures an optimal balance of treatments within each subgroup of patients. An imbalance caused by a high number of dropouts in one treatment group will be counteracted by the self-adjusting nature of the method. The method has been tested in computer-simulated trials and has been shown to produce better results than conventional plans for stratified randomized clinical trials. The method does not involve any complicated calculations and its use in a running clinical trial has shown that it is easy to handle.
American journal of obstetrics and gynecology, Jan 15, 1975
Pregnant, habitually smoking women were studied during the last trimester when smoking a standard... more Pregnant, habitually smoking women were studied during the last trimester when smoking a standard cigarette, smoking a nontobacco cigarette, or chewing a piece of chewing gum containing 2 or 4 mg. of nicotine. The effects of the experimental interventions were followed on the concentration of nicotine and the percentage of carboxyhemoglobin (COHb) in maternal blood, on the amount and pattern of the fetal breathing movements, and on the maternal heart rate, breathing rate, and blood glucose level. The maternal blood concentration of nicotine was increased by the standard cigarette, the 4 mg. nicotine chewing gum, and the 2 mg. nicotine chewing gum in descending order. The COHb percentage in maternal blood was increased by the standard cigarette and to a lower degree by the nontobacco cigarette. A significant increase of apnea and periodic breathing movements in the fetus followed the smoking of a standard cigarette; a similar but nonsignificant change occurred in a dose-related way a...
European Journal of Clinical Pharmacology, 1973
Lidoflazine, a new coronary vasodilator, has been tested in 31 cases of angina pectoris in a doub... more Lidoflazine, a new coronary vasodilator, has been tested in 31 cases of angina pectoris in a double-blind cross-over study. It diminished significantly the frequency of attacks and nitroglycerine consumption of the more severe cases, but its effects were less marked in milder cases. The results are discussed in relation to other anti-anginal drugs. The necessity for a preliminary run-in period
Methods of Biochemical Analysis, 1966
Analytical Biochemistry, 1965
Psychopharmacologia, 1973
Chewing gum containing nicotine or placebo was given to smokers attending an anti-smoking clinic.... more Chewing gum containing nicotine or placebo was given to smokers attending an anti-smoking clinic. During a one week double-blind study subjects receiving nicotine smoked less and chewed less gum than those receiving placebe. The difference in tobacco consumption between the two treatment groups was most apparent among previous heavy smokers. During a 6 month follow-up phase all subjects were offered nicotine-containing chewing gum; the number of nonsmokers then remained fairly constant in the "initial-nicotine group" while it increased in the "initial-placebo group".
European Journal of Clinical Pharmacology, 1981
A high-pressure liquid chromatographic technique was developed which allowed concurrent measureme... more A high-pressure liquid chromatographic technique was developed which allowed concurrent measurement of acetylsalicylic acid (ASA) and salicylic acid (SA) in plasma. ASA was extensively deacetylated to SA not only in vivo but also in vitro, even in frozen plasma. The in vitro conversion could be prevented by physostigmine. In vivo, ASA was eliminated within few hours, whereas SA was continuously present following daily administration of conventional doses of ASA. A slight modification of a similar method, originally developed for naproxen determination [9], was found appropriate for measurement of the SA derivative diflunisal, of two non-SA antiinflammatory agents, indomethacin and indoprofen, and of a related anti-platelet agent, indobufen.
European Journal of Clinical Pharmacology, 1982
Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses... more Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses this activity following first-pass deacetylation to salicylic acid (SA). In order to compare the bioavailability of unchanged ASA from rapid- and slow-release formulations, the single-dose concentration profiles of ASA and SA were studied in healthy volunteers following intake of two different rapid-release (conventional and effervescent tablets) and three different slow-release (microencapsulated ASA in tablets and in capsules, and enteric-coated tablets) formulations of ASA, and of one slow-release formulation of sodium salicylate. Since anti-platelet therapy with ASA is often combined with dipyridamol, the influence of this drug was also examined. The concentrations of ASA and SA were measured by high-pressure liquid chromatography. While the bioavailability of SA from the 5 ASA formulations was essentially equal and similar to that of the salicylate formulation, the bioavailability and peak concentrations of ASA appeared to be the much greater after rapid-release than after slow-release formulations. Indeed, ASA was only rarely detected in systemic blood following intake of slow-release ASA. Co-administered dipyridamol did not significantly influence the kinetics of ASA or SA. It appears that rapid-release formulations of ASA should be prefered in anti-platelet therapy, either alone or in combination with dipyridamol.
European Journal of Clinical Pharmacology, 1984
Acetylsalicylic acid (ASA) is increasingly employed in the secondary prophylaxis of thromboemboli... more Acetylsalicylic acid (ASA) is increasingly employed in the secondary prophylaxis of thromboembolic diseases, due to its capacity to inhibit platelet aggregation. The anti-aggregatory effect of ASA on platelets can be inhibited in vitro by a high concentration of salicylic acid (SA). SA is generated in vivo upon ASA administration, and the SA thus formed might impair the antiplatelet effect of ASA. To assess this possibility, the platelet response to ASA was tested in healthy volunteers before and after medication for 1 week with ASA 1 g t.i.d., with SA 1 g t. i.d., and with the SA derivative diflunisal 0.5 g b.i.d. Pre-medication test doses of 1 g ASA always inhibited platelet aggregation in vivo. Neither treatment with SA nor diflunisal, producing plasma steady-state concentrations of about 1.0 and 0.35 mmol/1, respectively, inhibited platelet aggregation. Nor did administration of SA, diflunisal or ASA itself impair the anti-aggregatory effect of a fresh test dose of ASA. ASA inhibited platelet aggregation in vitro at 0.03 mmol/1, whereas SA and diflunisal failed to impair platelet aggregation until concentrations exceeding 2.0 and 0.5 mmol/1, respectively, were reached. These findings make it unlikely that SA formed upon administration of ASA would impair the anti-aggregating capacity of ASA.
Clinical pharmacology and therapeutics, 1977
This paper presents a self-adjusting randomization plan which is thought to be useful in controll... more This paper presents a self-adjusting randomization plan which is thought to be useful in controlled stratified randomized clinical trials. The method assures an optimal balance of treatments within each subgroup of patients. An imbalance caused by a high number of dropouts in one treatment group will be counteracted by the self-adjusting nature of the method. The method has been tested in computer-simulated trials and has been shown to produce better results than conventional plans for stratified randomized clinical trials. The method does not involve any complicated calculations and its use in a running clinical trial has shown that it is easy to handle.
American journal of obstetrics and gynecology, Jan 15, 1975
Pregnant, habitually smoking women were studied during the last trimester when smoking a standard... more Pregnant, habitually smoking women were studied during the last trimester when smoking a standard cigarette, smoking a nontobacco cigarette, or chewing a piece of chewing gum containing 2 or 4 mg. of nicotine. The effects of the experimental interventions were followed on the concentration of nicotine and the percentage of carboxyhemoglobin (COHb) in maternal blood, on the amount and pattern of the fetal breathing movements, and on the maternal heart rate, breathing rate, and blood glucose level. The maternal blood concentration of nicotine was increased by the standard cigarette, the 4 mg. nicotine chewing gum, and the 2 mg. nicotine chewing gum in descending order. The COHb percentage in maternal blood was increased by the standard cigarette and to a lower degree by the nontobacco cigarette. A significant increase of apnea and periodic breathing movements in the fetus followed the smoking of a standard cigarette; a similar but nonsignificant change occurred in a dose-related way a...
European Journal of Clinical Pharmacology, 1973
Lidoflazine, a new coronary vasodilator, has been tested in 31 cases of angina pectoris in a doub... more Lidoflazine, a new coronary vasodilator, has been tested in 31 cases of angina pectoris in a double-blind cross-over study. It diminished significantly the frequency of attacks and nitroglycerine consumption of the more severe cases, but its effects were less marked in milder cases. The results are discussed in relation to other anti-anginal drugs. The necessity for a preliminary run-in period
Methods of Biochemical Analysis, 1966
Analytical Biochemistry, 1965
Psychopharmacologia, 1973
Chewing gum containing nicotine or placebo was given to smokers attending an anti-smoking clinic.... more Chewing gum containing nicotine or placebo was given to smokers attending an anti-smoking clinic. During a one week double-blind study subjects receiving nicotine smoked less and chewed less gum than those receiving placebe. The difference in tobacco consumption between the two treatment groups was most apparent among previous heavy smokers. During a 6 month follow-up phase all subjects were offered nicotine-containing chewing gum; the number of nonsmokers then remained fairly constant in the "initial-nicotine group" while it increased in the "initial-placebo group".
European Journal of Clinical Pharmacology, 1981
A high-pressure liquid chromatographic technique was developed which allowed concurrent measureme... more A high-pressure liquid chromatographic technique was developed which allowed concurrent measurement of acetylsalicylic acid (ASA) and salicylic acid (SA) in plasma. ASA was extensively deacetylated to SA not only in vivo but also in vitro, even in frozen plasma. The in vitro conversion could be prevented by physostigmine. In vivo, ASA was eliminated within few hours, whereas SA was continuously present following daily administration of conventional doses of ASA. A slight modification of a similar method, originally developed for naproxen determination [9], was found appropriate for measurement of the SA derivative diflunisal, of two non-SA antiinflammatory agents, indomethacin and indoprofen, and of a related anti-platelet agent, indobufen.
European Journal of Clinical Pharmacology, 1982
Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses... more Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses this activity following first-pass deacetylation to salicylic acid (SA). In order to compare the bioavailability of unchanged ASA from rapid- and slow-release formulations, the single-dose concentration profiles of ASA and SA were studied in healthy volunteers following intake of two different rapid-release (conventional and effervescent tablets) and three different slow-release (microencapsulated ASA in tablets and in capsules, and enteric-coated tablets) formulations of ASA, and of one slow-release formulation of sodium salicylate. Since anti-platelet therapy with ASA is often combined with dipyridamol, the influence of this drug was also examined. The concentrations of ASA and SA were measured by high-pressure liquid chromatography. While the bioavailability of SA from the 5 ASA formulations was essentially equal and similar to that of the salicylate formulation, the bioavailability and peak concentrations of ASA appeared to be the much greater after rapid-release than after slow-release formulations. Indeed, ASA was only rarely detected in systemic blood following intake of slow-release ASA. Co-administered dipyridamol did not significantly influence the kinetics of ASA or SA. It appears that rapid-release formulations of ASA should be prefered in anti-platelet therapy, either alone or in combination with dipyridamol.
European Journal of Clinical Pharmacology, 1984
Acetylsalicylic acid (ASA) is increasingly employed in the secondary prophylaxis of thromboemboli... more Acetylsalicylic acid (ASA) is increasingly employed in the secondary prophylaxis of thromboembolic diseases, due to its capacity to inhibit platelet aggregation. The anti-aggregatory effect of ASA on platelets can be inhibited in vitro by a high concentration of salicylic acid (SA). SA is generated in vivo upon ASA administration, and the SA thus formed might impair the antiplatelet effect of ASA. To assess this possibility, the platelet response to ASA was tested in healthy volunteers before and after medication for 1 week with ASA 1 g t.i.d., with SA 1 g t. i.d., and with the SA derivative diflunisal 0.5 g b.i.d. Pre-medication test doses of 1 g ASA always inhibited platelet aggregation in vivo. Neither treatment with SA nor diflunisal, producing plasma steady-state concentrations of about 1.0 and 0.35 mmol/1, respectively, inhibited platelet aggregation. Nor did administration of SA, diflunisal or ASA itself impair the anti-aggregatory effect of a fresh test dose of ASA. ASA inhibited platelet aggregation in vitro at 0.03 mmol/1, whereas SA and diflunisal failed to impair platelet aggregation until concentrations exceeding 2.0 and 0.5 mmol/1, respectively, were reached. These findings make it unlikely that SA formed upon administration of ASA would impair the anti-aggregating capacity of ASA.