Biomedical subjects

L J Verschueren

Publications and source records attributed to L J Verschueren.

23 records · Page 2Linked to original sources

PubMed1980

Stabilization of whole molecules of gastropodan haemocyanins by chlorhexidine.

Chlorhexidine diacetate 0.01% stabilized the whole molecules of Helix pomatia alpha-haemocyanin under dissociating conditions; in 1 M NaCl and in 1.42 M sucrose. Dissociation at low ionic strength (10 mM) of the haemocyanin of Pila leopoldvillensis was likewise prevented by chlorhexidine. After dissociation into half molecules of H. pomatia alpha-haemocyanin in 1.42 M sucrose and of P. leopoldvillensis haemocyanin by lowering the ionic strength, whole molecules were formed on introduction by dialysis of chlorhexidine diacetate to a concentration of 0.01%. This stabilization points to the binding of the two chlorophenyl groups in hydrophobic regions of the protein and an ensuing cross-linking of the half molecules of gastropodan haemocyanins. Chlorguanide, which almost corresponds to one half chlorhexidine, even at a concentration of 0.1%, only slightly stabilized the whole molecules.

Animals↗

PubMed1980

Fragmentation of crystalline beta-haemocyanin of Helix pomatia with plasmin and trypsin. Location of the fragments in the polypeptide chain.

The action of plasmin on tenth molecules of beta C-haemocyanin of Helix pomatia at pH 8.2 yielded first a three-domain fragment P3 and a five-domain fragment P1 (present as a dimer at pH 8.2). Fragment P1 was further split by plasmin into a four-domain fragment P2 and a one-domain fragment P4 (also present as a dimer at pH 8.2). Trypsinolysis of P2 yielded T2 and fragment X, which was further split into T1C and T3. Fragments P3 and P4 corresponded respectively to the tryptic fragments T1A and T1B, also by their circular dichroic spectra. The determination of the N-terminal groups and the order of splitting allowed the location of the fragments in the polypeptide chain: P3 (a--c), P2 (d--g), P4 (h); T1A (a--c), T3 (d), T1C (e--f), T2 (g), T1B (h).

Amino Acids↗

PubMed1980

Acute changes in the renin-angiotensin-aldosterone system, catecholamines and prostaglandins during captopril in man.

The acute hypotensive effect of 25 mg captopril was investigated in 26 hypertensive patients (11 essential and 15 with renal arterial disease). Intra-arterial blood pressure was recorded continuously and arterial blood was sampled for renin, angiotensin I and II, aldosterone, kininase II, catecholamines and prostaglandins. Captopril provoked increases in plasma renin activity, active and total plasma renin concentration and angiotensin I; decreases in plasma kininase II activity, angiotensin II, aldosterone, prostaglandins E2 and F2 alpha and no changes in plasma (nor)adrenaline, dopamine and inactive renin concentration.

Adult↗

PubMedDate not supplied

Effect of aspirin on renal function and the prostaglandin-kallikrein systems early after myocardial infarction.

Using a double-blind procedure, 29 patients with a recent myocardial infarction were randomly allocated to a placebo group (n = 14) and to a group receiving aspirin, 300 mg three times a day (n = 15) over 7 days. No change in renal function was observed in either treatment group. Compared with the placebo group, the 24-h urinary excretion of prostaglandin E2 (PGE2) was significantly suppressed in the aspirin group, but the urinary kallikrein activity was unchanged. These results contrast with our previous study of similar patients, in which sulfinpyrazone decreased renal function, as well as the urinary PGE2 and kallikrein excretions. These divergent effects of aspirin and sulfinpyrazone on urinary kallikrein activity could explain the different trends in renal function observed early after myocardial infarction.

Aged↗

PubMedDate not supplied

Prostaglandin-kallikrein-renin system during acute sulphinpyrazone administration in healthy volunteers.

Sulphinpyrazone administered acutely to 8 healthy male volunteers decreased the urinary (U) excretion of prostaglandin (PG)E2 (p less than 0.01)( but not of PGF2 alpha. Also, the ratio U-PGE2/U-PGF2 alpha and the urinary excretion of kallikrein declined (p less than 0.001 and p less than 0.05 respectively). Sulphinpyrazone therapy caused a significant inhibition of PRA (p less than 0.05). Renal function, as assessed by serum creatinine and creatinine clearance, remained constant in these normal men, possibly related to the fact that both the vasodilatory PG-kallikrein-kinin system and the vasoconstrictive renin-angiotensin system were inhibited by sulphinpyrazone. However, it is conceivable that in clinical situations where vasoconstrictive stimuli are enhanced, sulphinpyrazone can disturb the balance between those systems and can lead to an impaired renal function.

Adult↗