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Biomedical subjects

S Glasson

Publications and source records attributed to S Glasson.

7 recordsLinked to original sources
PubMed1983

[Monitoring amiodarone].

Serum levels of amiodarone (A) and desethylamiodarone (D) were determined by HPLC in 34 adults receiving loading (2 g) or maintenance doses (200 mg daily) of amiodarone. Serum levels of A after i.v. loading doses were much higher (1.35 micrograms/ml) than after equivalent oral doses (0.51 microgram/ml), suggesting low bioavailability. During maintenance therapy, very low levels of A were measured during the first 3 months of treatment (0.31 microgram/ml), after which they tended to rise (0.53 microgram/ml), as did the ratio of D/A. Among 4 children under maintenance therapy, one had high serum levels of A (1.50 micrograms/ml) and D (2.50 micrograms/ml) and showed nervous and cutaneous signs of toxicity.

Aged↗
PubMed1982

Multiple human serum binding of two thienopyridinic derivatives, ticlopidine and PCR 2362, and their distribution between HSA, alpha1-acid glycoprotein and lipoproteins.

The binding of two drugs, ticlopidine and PCR 2362, chemically related to thienopyridin, potent antiaggregant agents, was studied in vitro to serum and to the corresponding isolated proteins, HSA, alpha 1-AGP, VLDL, LDL and HDL, using equilibrium dialysis at pH 7.4 and 37 degrees. The binding of these drugs to HSA and lipoproteins was non-saturable. The binding capacity of the lipoproteins was much greater than that of HSA and appeared to be dependent on lipid content. The binding capacities of the apoproteins were less than 10% of that observed for the native lipoproteins suggesting that drug-lipoprotein binding involves drug solubilization in the lipid phase of lipoproteins rather than a classical binding to definite sites. However drug binding to alpha 1-AGP was saturable with n = 3 for both and K = 89,000 and 33,000 for ticlopidine and PCR 2362, respectively. At physiological concentration, alpha 1-AGP binding capacity represented 15% of total serum binding capacity which could double in pathological states, in which the level of this protein is increased.

Humans↗
PubMed1981

[Comparison of the effects of betablockers and captopril on the development of genetic hypertension in the rat].

The preventative effects of betablockers and captopril on the development of genetic hypertension in genetically hypertensive rats, were studied after long-term daily dosage by forced feeding, from the 5th to the 20th week of age of the animals. Of the drugs studied, captopril, atenolol and propranolol limited the development significantly, but pindolol only had a modest effect and acebutolol was ineffective. No correlation was found between the degree of prevention of genetic hypertension and the intensity of betablockade. Atenolol and propranolol prevent genetic hypertension by I) reducing cardiac output, a reduction which is not neutralised by the simultaneous change in peripheral resistance, 2) decreasing plasma renin concentrations, and 3) limiting the development of myocardial hypertrophy. Captopril is very effective in preventing the development of genetic hypertension and acts: 1) by causing an early and lasting fall in peripheral resistance related to the suppression of Angiotensin II, and possibly by potentialising the vasodilatation of bradykinins and, 2) by limiting myocardial hypertrophy.

Adrenergic beta-Antagonists↗
PubMed1980

Captopril and hypertension development in the SHR.

Captopril (100mg/kg) administered daily by gavage to young spontaneously hypertensive rats (SHRs) from their 6th to 20th weeks of age almost completely inhibited genetic hypertension development (GHD). This effect was correlated with an early and long-lasting limitation of the progressive increase in peripheral resistance which normally develops in SHRs during their growth. Heart rate, cardiac and systolic indexes remained unchanged, plasma renin concentration was significantly increased and heart weight/body weight ratio was significantly decreased. At last, captopril's GHD preventive effect persisted up to 12 weeks after treatment discontinuation.

Angiotensin II↗