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Biomedical subjects

R H Verhaeghe

Publications and source records attributed to R H Verhaeghe.

12 recordsLinked to original sources
PubMed1991

Renal artery stent placement with use of the Wallstent endoprosthesis.

The Wallstent endoprosthesis was placed in 12 renal arteries of 11 patients; a total of 15 stents were placed. Indications for placement were restenosis after dilation and insufficient result after dilation. In two patients, malpositioning of the stent required placement of a second stent. Complications included a case of massive cholesterol embolization and a case of unexplained transient hematuria, proteinuria, and deterioration of renal function. At repeat angiography of seven renal arteries after stent placement, one was occluded and required thrombolysis and dilation. Another showed restenosis due to shortening of the stent and required redilation and, later, placement of another stent. This stent became occluded after 1 month. In this patient and in three other cases, angiography disclosed tissue buildup in the stent but without significant stenosis after this short-term follow-up. After a clinical follow-up of 6.7 months +/- 3.4 in 10 patients treated for hypertension, three were cured, four were improved, and three were unchanged when blood pressure levels before stent placement were compared with those obtained after stent placement.

Adult↗
PubMed1987

Local thrombolysis in femoropopliteal occlusion: early and late results.

The early and late results of local thrombolysis with low-dose streptokinase followed by balloon dilatation in 64 patients with an occluded femoropopliteal artery are reviewed. The primary success rate was 77% for the native arteries; it was higher (80%) for short (less than 10 cm) as compared with long occlusion (40%) and for patients with claudication as compared with those with advanced ischemia (89% versus 48%). Eleven complications were observed in 10 patients, most frequently a local hematoma at the puncture site. Ascending thrombosis and absence of lysis or incomplete lysis were the main reasons for failure. The cumulative patency rate after 1 and 2 years follow-up was 87% and 82%, respectively.

Angioplasty, Balloon↗
PubMed1982

Effect of thrombin on isolated canine blood vessels.

The aim of the present study was to assess whether or not thrombin affects vascular smooth muscle activity by a direct action on the blood vessel wall. In isolated saphenous veins and femoral and pulmonary arteries thrombin did not affect basal tension, but in pulmonary and portal mesenteric veins it caused contraction. In saphenous and femoral veins and in femoral and pulmonary arteries the enzyme depressed contractions evoked by alpha-adrenergic stimulation. In the saphenous vein thrombin also depressed contractions induced with acetylcholine or potassium ions. In this blood vessel the relaxation caused by thrombin was abolished by antithrombin III and the tripeptide D-phenylalanine-proline-arginine-CH2Cl, a specific inhibitor of the enzyme center of thrombin. In pulmonary and portal mesenteric veins, thrombin potentiated the contractile response to norepinephrine. These contractile effects of thrombin were also abolished by D-phenylalanine-proline-arginine-CH2Cl. Thus, thrombin causes relaxation or contraction of blood vessels through a direct action on the blood vessel wall. These effects are due to its proteolytic activity.

Acetylcholine↗
PubMed1978

Metabolic modulation of neurotransmitter release--adenosine, adenine nucleotides, potassium, hyperosmolarity, and hydrogen ion.

Evidence has accumulated that several factors, which have been proposed as mediators of exercise hyperemia, can modulate adrenergic neurotransmission in blood vessels. Adenosine and the adenine nucleotides depress the response of isolated blood vessels of the dog to nerve stimulation more than that to exogenous norepinephrine; this difference is explained by a decreased release of the neurotransmitter. Potassium, hyperosmolarity, and acidosis also depress adrenergic neurotransmission in isolated veins. These results are consistent with the hypothesis that metabolic changes in the vicinity of the adrenergic neuroeffector junction are capable of decreasing the output of neurotransmitter to the blood vessels in the exercising muscle.

Adenine Nucleotides↗
PubMed1977

Action of adenosine and adenine nucleotides on dogs' isolated veins.

Adenosine depressed norepinephrine contractions of dogs' saphenous vein strips in both the presence and the absence of Ca2+ and after inhibition of calcium influx by verapamil. It antagonized noncompetitively contractions induced by Ca2+ in depolarized strips after alpha-adrenergic blockade. Contractions obtained with acetylcholine were also depressed by adenosine. This depression was not accompanied by an increase in cAMP or a decrease in the elevated cGMP level. Thus the depression of the smooth muscle cell reactivity still occurs in the absence of calcium influx and is not mediated by the cyclic 3',5'-nucleotide system. Adenosine diphosphate and triphosphate, but not adenosine (10(-6) to 10(-4) M), increased the basal tension of resting saphenous strips. This was prevented by removal of calcium from the bath. In contracted strips, lower concentrations of both nucleotides (10(-6) to 10(-5) M) caused relaxation whereas with high concentrations (10(-4) to 10(-3) M) further contraction occurred. Thus, unlike adenosine, the adenine nucleotides facilitate calcium influx.

Acetylcholine↗
PubMed1977

Inhibition of sympathetic neurotransmission in canine blood vessels by adenosine and adenine nucleotides.

Adenosine and the adenine nucleotides caused a greater relaxation of strips of canine saphenous vein and tibial artery when they had been contracted by nerve stimulation than by exogenous norepinephrine. An infusion of adenosine into the dogs' lateral saphenous vein, perfused at constant flow, caused a greater relaxation of this vein when constricted by electrical stimulation of the lumbar sympathetic chain than by exogenous norepinephrine. That this difference was due to inhibition by these compounds of the output of neurotransmitter from the sympathetic nerve endings was demonstrated by column chromatographic analysis of the radioactivity in the superfusion fluid of vein strips, previously incubated with tritiated norepinephrine. Both adenosine and adenosine triphosphate (10(-5) M) reduced the efflux of 3H-norepinephrine during nerve stimulation with electrical impulses. Adenosine also reduced the efflux caused by potassium (30 mM), but not that caused by tyramine (6 X 10(-6) M). Theophylline antagonized the inhibitory effect of adenosine on the sympathetic neurotransmission. We found that at 4 X 10(-4) M adenosine triphosphate still caused a decreased efflux of neurotransmitter during electrical stimulation, but with adenosine the 3H-norepinephrine efflux no longer decreased and the overflow of deaminated compounds increased. Furthermore, the same concentration of adenosine increased the efflux of 3H-norepinephrine and deaminated compounds in unstimulated strips, and the increase of 3H-norepinephrine was enhanced after monoamine oxidase inhibition. Thus, we conclude that at higher concentrations adenosine increases the intraneuronal leakage of norepinephrine out of the storage vesicles.

Adenine Nucleotides↗
PubMed1976

Effect of nitroprusside on smooth muscle and adrenergic nerve terminals in isolated blood vessels.

Experiments were designed to assess the mode of action of nitroprusside on isolated blood vessels and its relative potency on venous and arterial smooth muscle. Strips from dog blood vessels were mounted in an organ bath for isometric tension recording. Sodium nitroprusside (10(-5) M) depressed the contraction of saphenous vein strips caused by electric stimulation, tyramine, K+, Ba++, norepinephrine and acetylcholine. The depression of the norepinephrine-induced contractions also occurred in a Ca++- free medium and when Ca++ influx was inhibited by verapamil. Nitroprusside reduced the frequency of the spontaneous contractions of strips of portal-mesenteric veins. It depressed the contraction caused by norepinephrine in tibial artery strips more than in saphenous vein strips. Saphenous vein strips were incubated with (3H)norepinephrine and mounted for superfusion and isometric tension recording. Sodium nitroprusside (10(-5) M) had no effect on the basal efflux of 3H compounds. During electric stimulation, it did not change the output of (3H)norepinephrine but increased the outflow of deaminated and O-methylated metabolites. Thus sodium nitroprusside 1) has a direct effect on the smooth muscle cells which is independent of Ca++ influx, 2) depresses contractions of different types of vascular smooth muscle and 3) does not inhibit the release of norepinephrine from the nerve endings.

Animals↗