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Biomedical subjects

V Gillard

Publications and source records attributed to V Gillard.

26 records · Page 2Linked to original sources
PubMed1989

Angiotensin II and phorbol-esters potently down-regulate endothelin (ET-1) binding sites in vascular smooth muscle cells.

[125I]ET-1 binding to vascular smooth muscle cells showed an apparent single class of high affinity recognition sites with a Kd of 2.12 +/- 0.46 nM and a Bmax of 81.2 +/- 5.2 fmol/10(6) cells. The specific binding was equally and totally displaced by ET-1 and ET-2 whereas ET-3 presented a different pattern. We investigated heterologous regulation of ET-1 binding sites by preincubating the cells with angiotensin II (AII), Arg-vasopressin, bradykinin, enkephalins, serotonin, norepinephrine and carbachol, for 18 h at 37 degrees C. Only AII pretreatment resulted in an important and dose-dependent decrease of ET-1 binding capacity. Sar1-Ile8-AII inhibited the regulatory effect of AII. Furthermore, preexposure of the cells with phorbol-12,13 dibutyrate but not with phorbol-12,13 didecanoate also resulted in a concentration-dependent diminution of ET-1 binding sites. These findings suggest that AII may selectively down-regulate ET-1 binding sites in vascular smooth muscle cells by a mechanism involving protein kinase C.

Angiotensin II↗
PubMed1989

Vascular mechanism of action of endothelin-1: effect of Ca2+ antagonists.

The vasoconstrictive properties of the endothelium-derived peptide, endothelin-1 (ET-1), were investigated on rat isolated aorta and on cultured rat aortic smooth muscle cells. In rat isolated aorta, endothelin-1 induced a slow and sustained contraction in a Ca2+-free medium; after calcium readmission, an additional sustained contraction was elicited. In vascular smooth muscle cells, endothelin-1 provoked a dose-dependent Ca2+ influx that was not inhibited by calcium entry blockers (nifedipine, D 600, or diltiazem). In these cells, [125I]-endothelin-1 bound to a specific, saturable, and high affinity recognition site (Kd about 10(-9) M and Bmax = 52 +/- 2 fmol/10(6) cells). The binding was not reversible and not affected by calcium antagonists. These data do not support the hypothesis that endothelin-1 acts as an endogenous agonist of the voltage-dependent Ca2+ channels. The action of endothelin-1 can be separated into two components: one dependent on Ca2+ influx but insensitive to calcium antagonists and another independent of extracellular Ca2+. The irreversible binding of endothelin-1 may reflect an internalization of the ligand inside the cell membrane, leading to multiple contractile events.

Animals↗
PubMed1987

[Effects of sotalol on blocked suprahepatic pressure in cirrhotic patients].

With the use of two balloon catheters inserted in the right jugular vein, the following parameters were measured before and after injection of sotalol (1.5 mg/kg): cardiac output with the thermodilution method, hepatic output with the indocyanin green perfusion method, free sub-hepatic pressure, blocked sub-hepatic pressure recorded at rest and during coughing. After 30 minutes, the following modifications were recorded: the cardiac output goes from 6.8 +/- 2.1 to 5.9 +/- 1.9 L/min (NS), the hepatic output goes from 1.9 +/- 1.1 to 1.5 +/- 0.6 L/min (NS), the hepatic pressure gradient goes from 18.2 +/- 6.1 to 11.5 +/- 5.4 mmHg (p less than or equal to 0.0005); the blocked sus-hepatic pressure at rest goes from 25.0 +/- 7.8 to 19.8 +/- 8.0 mmHg (p less than or equal to 0.025); the blocked sus-hepatic pressure during coughing goes from 92 +/- 32 to 82 +/- 39 mmHg (NS). This study demonstrates: a) that the drop in the hepatic pressure gradient induced by a dose of sotalol is more important than that observed by Westaby et al. with propranolol: 37% vs 31% (NS); b) that sotalol cannot lower the blocked sub-hepatic pressure during coughing. This result suggests that the potential protective effect of sotalol toward esophageal varices rupture disappears during coughing.

Aged↗
PubMedDate not supplied

Evaluation of polyps by endoscopic ultrasonography (eus): implication for endotherapy.

UNLABELLED: EUS is the single best imaging modality in precise visualization of the five layers structure of G.I. tract wall, space occupying lesion and surrounding structures. In case of "protruding lesion" into the G.I. lumen, the site of origin of the tumor can be easily determined by EUS, and then its nature can be presumed (1). However, despite of these tiny details of the G.I. wall obtained by EUS, histology is still mandatory, especially when dealing with lesion suspected of malignancy (2). In case of sessile malignant "polypoid" lesion, Endoscopic Mucosal Resection (EMR) guided by EUS, could be considered in specific cases of selected patients. Conventional EUS transducer (7.5 and 12 Mhz) employed for this purpose is not sufficient for differentiating cancers invading the muscularis mucosae from those invading the sub-mucosa. A Miniature Ultrasonic Probe (20 and 30 Mhz) which can be used through the biopsy channel of an endoscope has recently been developed and is accurate in measuring such a superficial infiltration and in assessing regional lymph nodes allowing then an exact pre-treatment staging. In patient not fitted for surgery, with a lesion less than 2 cm and involving less than half circumference of the lumen, EMR could be performed according to the parietal infiltration (T), the nodal involvement (N) and the related involved organs (Esophagus, Stomach, Colo-rectum). CONCLUSIONS: EUS may be usefull and sometimes is mandatory for assessing the G.I. tract polyps before resection.

Endosonography↗