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Biomedical subjects

G Rorive

Publications and source records attributed to G Rorive.

At least 91 records · Page 5Linked to original sources
PubMed1985

Double-blind comparison of ketanserin with propranolol in hypertensive patients: interim report.

This double-blind study, which is still in progress, aims to compare ketanserin (K) and propranolol (P) during long-term treatment of hypertensive patients in general practice. After a run-in period on placebo, active treatment was initiated with 20 mg K or 40 mg P, b.i.d., during a 2-week period, whereafter the daily dose of either drug was doubled. Presently, 331 patients have been randomized, two-thirds to the K group (n = 221) and one-third to the P group (n = 110). Both groups were similar at randomization, with blood pressure (BP) averaging 171/105 mm Hg. The presently available data concerning the initial 3 months of the trial show that up to the 2nd month after randomization, systolic BP was significantly (p less than 0.05) higher in the K than in the P group, whereas the differences in diastolic BP were mostly not significant. The change in BP after 3 months on K treatment was positively and independently related to both the initial BP and the concurrent changes in body weight. Heart rate was lower (p less than 0.001) during P, whereas body weight was not statistically different between both groups. Differences in complaints between the K and P group were small. However, in the K group dry mouth was transiently more frequently reported at 1 month (p = 0.02) and multiple complaints at 3 months (p = 0.03).

Adult↗
PubMed1985

[Proliferative response of the arterial wall in arterial hypertension: hyperplasia versus polyploidy].

Proliferation changes are along with cell hypertrophy and extracellular deposit the major components of the hypertensive structural changes in large arteries. There is still some doubt about the nature of the proliferative changes: hyperplasia or polyploidization. The aorta and the tail artery of SHR and Goldblatt one-kidney, one clip hypertensive rats (RVHR) were studied at different ages and hypertensive stages. After enzymatic dispersion, cell relative DNA content was assayed by flow cytofluorimetry and by Feulgen microdensitometry. Tissue total DNA content was assayed by fluorimetry. The increase in diploid and tetraploid cells within the hypertensive arteries was further calculated. In the RVHR, hypertension is of very rapid onset and reaches a plateau within 20 days (compared to the normotensive Wistar, systolic BP is 32 mmHg at 15 days, 52 mmHg at 40 days, 45 mmHg at 90 days). An increase in total aortic DNA content (DNA: 32 micrograms at 15 days, 31 micrograms at 40 days, 40 micrograms at 90 days) is found before the development of a significant polyploidy (polyploidy in per cent: 2.3 p. 100 at 15 and 40 days; 12.0 p. 100 at 90 days). Proliferation changes in this model appears to be hyperplasia at the acute phase and polyploidy at the chronic phase. The course of hypertension is slower and less severe in the SHR (compared to the WKY, systolic BP: 0 mmHg in 4 weeks, 17 mmHg in 8 weeks old and 33 mmHg in 35 weeks old rats).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Kinetics of proliferation of rat aortic smooth muscle cells in Goldblatt one-kidney, one-clip hypertension.

Wistar female rats were made hypertensive by applying a silver clip to the left renal artery and removing the right kidney. In aortas, the proliferation fraction of smooth muscle cells, DNA synthesis and wet weight have been correlated with the blood pressure increase subsequent to the operation. A wave of proliferation of smooth muscle cells in the aortic media is triggered immediately after the highest increased rate of blood pressure. When blood pressure stabilizes at high values, the metabolism of nucleic acid within the aortic media resumes its normal level but the arterial changes previously established persist. The sequence of pathological events responsible for these changes could be: increment of blood pressure; increase in wall stress; proliferation of smooth muscle cells; thickening of arterial wall; correction of the wall stress; end of proliferation. The consequence of this early proliferation of aortic smooth muscle cells is not clear but it is probably one of the mechanisms through which high blood pressure is sustained. It can also participate in atherogenesis, being in this way one of the bases of the well-known relationship between hypertension and atherosclerosis.

Animals↗