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M Verbeke

Publications and source records attributed to M Verbeke.

9 recordsLinked to original sources
PubMed1999

Beneficial effect of serotonin 5-HT2-receptor antagonism on renal blood flow autoregulation in cyclosporin-treated rats.

Renal blood flow (RBF) autoregulation reappears in postischemic rat kidneys during serotonin (5-HT2) antagonism. The aim of the present study was to analyze whether 5-HT2 antagonism can ameliorate impaired RBF autoregulation in rats treated with 20 mg/kg per d cyclosporin A during 10 d. Autoregulation of RBF was assessed during stepwise lowering of renal perfusion pressure from 110 to 70 mmHg by gradual compression of the aorta. Autoregulation was lost in the cyclosporin A-treated rats. During administration of the 5-HT2 antagonist ritanserin (0.6 mg/kg intravenous bolus, followed by 1.2 mg/kg per h intravenous infusion during 1 h), autoregulation acutely reappeared. Intrarenal bolus injections of a selective 5-HT2-agonist, 2,5 dimethoxy-4-iodoamphetamine hydrochloride, elicited a significantly stronger renal vasocontraction in cyclosporin A-treated rats than in control rats. This finding was also observed with serotonin after nitric oxide-synthase blockade. These results (1) show the importance of 5-HT2-receptor-mediated vasoconstriction in the suppression of vasodilatory autoregulation of RBF in experimental cyclosporin A-induced renal dysfunction and (2) demonstrate that the complete loss of RBF autoregulation is not due to damage of the vascular smooth muscle cells.

Animals↗
PubMed1998

Influence of ketanserin on experimental loss of renal blood flow autoregulation.

Serotonin is important for effective renal blood flow (RBF) autoregulation in the normal rat and at two or seven days of reperfusion following renal ischemia. It has been suggested that after these reperfusion periods and during renal perfusion pressure (RPP) lowering, the vasodilatory autoregulation mechanism is not damaged but overwhelmed by increased 5-HT2-mediated vasoconstriction, resulting in complete loss of autoregulation. This study analyzes the influence of the 5-HT2-antagonist ketanserin on RBF autoregulation after two hours or one day of renal reperfusion following ischemia and in a model of cyclosporine (20 mg/kg.day for 10 days)-induced nephrotoxicity. Autoregulation was lost both after brief reperfusion periods and after cyclosporine. Similar to the two or seven days of reperfusion experiments, ketanserin in the cyclosporine model led to reappearance of autoregulation down to RPP 95 mm Hg. Despite an increased response to intrarenal serotonin after two hours of reperfusion, autoregulation was not restored by ketanserin. At one day of reperfusion and with ketanserin, autoregulation was present down to 105 mm Hg. Thus, during the early reflow period, other factors (of decreasing importance) most likely add to autoregulation loss.

Animals↗
PubMed1996

Beneficial influence of ketanserin on autoregulation of blood flow in post-ischemic kidneys.

The influence of ketanserin, a S2-serotonergic receptor blocker, on the impaired renal hemodynamics in a clamp model of renal ischemia in rats was investigated in this study. Serotonin-induced vasoconstriction of the renal vascular bed was augmented after ischemia. This constriction is blocked by ketanserin (0.05 mg/kg i.v. bolus, followed by 0.1 mg/kg per h infusion). The influence of the same ketanserin treatment on the response of RBF versus a stepwise lowering of the renal perfusion pressure was studied in post-ischemic kidneys with an established loss of autoregulation of RBF. An almost perfect restoration of the autoregulatory response was apparent after the S2-serotonergic antagonism. Despite this beneficial effect on renal hemodynamics, renal function, judged by measurement of GFR and urinary sodium excretion rate, was not influenced by an acute infusion of ketanserin in post-ischemic kidneys. It is suggested that serotonin plays a pivotal role in the suppression of autoregulation of RBF by a S2-serotonergic receptor-mediated vasoconstrictor effect in the post-ischemic kidney. It most likely masks the potential myogenic dilatory response of the smooth muscle cells in renal preglomerular microvasculature. Restoration of the renal autoregulatory capacity by S2-serotonergic receptor antagonism could be of clinical relevance in human post-ischemic acute renal failure.

Animals↗
PubMed1995

Regional differences in vasculotoxic effects of cyclosporin in rats.

Studies on cyclosporin-induced vasculotoxicity often yielded discrepant results, possibly as a result of differences in study protocols. The aim of the present study was to analyse cyclosporin-induced vasculotoxicity in arteries of different size and origin. Therefore, rats were treated with cyclosporin, 20 mg.kg-1.day-1, by gastric gavage for 10 days. In our previous studies, this treatment schedule induced renal functional impairment in vivo and an impaired relaxation response of thoracic aortic rings in vitro. Relaxation of various arteries (thoracic and abdominal aorta and carotid, renal, and interlobar arteries) from cyclosporin-treated and control rats in response to endothelium-dependent and -independent vasodilators was analysed. The thoracic aorta showed diminished endothelium-dependent and -independent relaxations; in the abdominal aorta no impairment was observed. Moreover, the dysfunction of the thoracic aorta seemed to be homogeneous along its length and showed an abrupt termination at the level of the diaphragm. In all other segments studied, no impairment of the relaxation responses was found. A similar pattern of vascular damage was found in rats treated with a very toxic cyclosporin treatment (50 mg.Kg-1.day-1 s.c. x 7 days). The results indicate regional differences in cyclosporin-induced vasculotoxicity. The thoracic aorta, and in view of the fall of the renal blood flow, most likely also the renal resistance vessels, could be more susceptible than other vessels to cyclosporin-induced vascular dysfunction.

Acetylcholine↗
PubMed1994

Manual or automatic nulling DC offset for physiological DC amplifier.

An inexpensive circuit to compensate for DC offset is presented. The circuit may be connected in a straightforward manner to any currently existing DC isolation amplifier and causes no deterioration in the performance of the system. The offset voltage is measured at discrete time intervals and then subtracted from the input signal. A switch is provided to bypass the offset compensation when the latter is not required.

Biomedical Engineering↗
PubMed1994

Functional analysis of vascular dysfunction in cyclosporin treated rats.

OBJECTIVE: The aim was to analyse vascular damage after chronic cyclosporin treatment (20 mg.kg-1 during 10 d) in rats. METHODS: The reactivity to different vasoactive agents was studied on thoracic aortic rings from control rats, and from rats subjected to renal ablation or cyclosporin treatment. RESULTS: After cyclosporin treatment the endothelium dependent vasodilator responses to acetylcholine and to the endothelium independent NO donors were suppressed. These defects were restored after a 7 d recovery period. The contractile response after inhibition of basal endothelial NO synthesis was unaffected. Further analysis of the blunted vasodilatations not only points to impairments of cGMP mediated mechanisms but shows that other pathways are possibly involved as well. Renal insufficiency induced by renal mass reduction did not influence the aortic reactivity. CONCLUSIONS: Cyclosporin induced vasculotoxicity is a reversible phenomenon, and is not due to renal dysfunction as such. It seems to provoke a defect in the vasodilator mechanisms at the level of the vascular smooth muscle cells and most likely no impairment of endothelial nitric oxide production.

Acetylcholine↗
PubMed1993

Computer-controlled portable stimulator for paraplegic patients.

A six-channel lightweight, portable and computer-controlled stimulator for the functional activation of paraplegic patients is described. To enable programming of the various functions, the stimulator was designed to work in a remote-control mode hosted by an IBM PC or compatible computer, in addition to its normally used local mode. The stimulus parameters, including current intensity, stimulus frequency and pulse width, are individually adjustable and programmable for each channel. The power source is 12 V 500 m Ah-1, from 10 rechargeable nickel cadmium batteries, with a run time of 1.5 h for a load of 200 mA in four channels. Various training programmes for the activation of paraplegics in the sitting, standing and walking positions are described. The final design of the stimulator is based on experience gained from 25 patients, treated and evaluated during the course of development. Ongoing work including clinical, biomechanical and physiological studies is carried out to evaluate performance of the activated patients and to optimize stimulation.

Humans↗