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Biomedical subjects

E Bassenge

Publications and source records attributed to E Bassenge.

At least 73 records · Page 4Linked to original sources
PubMed1991

[CO2-induced acral blood flow and the oxygen partial pressure in arterial occlusive disease].

The effect of CO2-containing water on foot skin blood flow (laser-Doppler flux) and transcutaneous oxygen partial pressure (tcpO2) was measured in 16 patients (15 men and 1 woman; mean age 58 [49-71] years) with peripheral arterial occlusive disease (stage II of Fontaine: bilateral occlusions of the superficial femoral arteries). After 30 minutes lying down and 10 minutes sitting up, one lower leg was immersed in fresh water, the other in CO2-containing water (1400 mg CO2/kg H2O), both at 34 degrees C for 20 minutes. On the next day the measurements were repeated changing sides. Skin blood flow of the dorsum of the foot and rhythmic flow oscillations (flux motion) increased threefold in the CO2 water-bath, after a latency period averaging 2 minutes, within 3 minutes from 1.1 to 3.9 relative units (P less than 0.005). Average tcpO2 increased during the bath in CO2 water by 9 mm Hg (P less than 0.005). There was no change in fresh water. The increase in cutaneous blood flow and oxygen partial pressure, which persisted throughout the period in CO2 water, is interpreted as an increase in microcirculation and can explain part of the effectiveness of this largely empirical treatment.

Aged↗
PubMed1991

Effects of native and oxidized low-density lipoproteins on endothelium-dependent and endothelium-independent vasomotion.

Native and oxidized low-density lipoproteins (LDL) were investigated for their direct influence on EDRF-formation, EDRF-activity, and vascular smooth muscle tone. Native (n) LDL, isolated from fresh human plasma, was oxidized by Cu(2+)-incubation. EDRF released from cultured endothelial cells was inactivated by both n-LDL and ox-LDL (1 mg/ml) as detected in a bioassay system. n-LDL reduced the EDRF-mediated vasodilations of the detector segments by 38.5 +/- 5.3%, and ox-LDL by 55.5 +/- 4.6%. The effects of lipoproteins on EDRF-formation were studied on cultured endothelial cells, preincubated with either n-LDL or ox-LDL (1 mg/ml, 1 h) and stimulated for EDRF-release with bradykinin after washout of the lipoproteins. EDRF was assessed by measuring its stimulatory effect on the activity of a purified soluble guanylate cyclase. Preincubation with both n-LDL and ox-LDL did not reduce the bradykinin-induced EDRF-formation. Accordingly, acetylcholine-induced, EDRF-mediated dilations of intact rabbit femoral artery segments were not impaired by luminal exposure to n-LDL or ox-LDL (1 h, 1mg/ml). Effects of n-LDL and ox-LDL on vascular smooth muscle tone were investigated in isolated perfused rabbit femoral arteries. Perfusion of endothelium-intact and -denuded segments with ox-LDL (80-500 micrograms protein/ml) caused no or only weak vasoconstrictions in the absence of contractile agonists. However, in the presence of ox-LDL, vasoconstrictions to threshold concentrations of norepinephrine (NE), serotonin (5-HT), phenylephrine (PE) or potassium were significantly enhanced. Native LDL (80-1000 micrograms/ml) had no effect on vascular tone, neither in presence nor in absence of contractile agonists. Preincubation with verapamil, diltiazem, and nitrendipine inhibited vasoconstrictions evoked by ox-LDL. The contractile responses to ox-LDL were significantly greater in endothelium-denuded segments than in endothelium-intact segments. In conclusion, neither n-LDL nor ox-LDL acutely impair the formation of EDRF, but do inactivate EDRF after its release from endothelial cells. n-LDL has no direct influence on vascular smooth muscle tone, but ox-LDL greatly enhances vasoconstrictions to various contractile agonists by direct interaction with vascular smooth muscle. Thus, in regions of lipoprotein-accumulation in the arterial wall, both n-LDL and ox-LDL may favor inappropriate vasoconstrictions.

Animals↗
PubMed1991

Endothelium-mediated regulation of coronary tone.

To what extent endothelial autacoids like endothelium-derived relaxant factor/nitric oxide (EDRF/NO), in addition to neural-humoral factors, are involved in the regulation of myocardial perfusion, is presently not known. Therefore, we investigated in conscious, chronically instrumented dogs the effect of stereospecific inhibitors (NG-monomethyl-L-arginine (L-NMMA), NG-nitro-L-arginine (L-NNA), NG-monomethylester-L-arginine (L-NAME] of nitric oxide-synthesis and -release on epicardial coronary tone (and coronary diameter) and myocardial perfusion. A hydraulic coronary cuff was used, to produce reactive hyperemia and to keep the myocardial perfusion constant over short periods. 40 mg/kg L-NNA i.v. caused a long-lasting increase in mean arterial blood pressure from 94 +/- 8 to 129 +/- 11 mmHg and a simultaneous decrease in coronary diameter by 2.8 +/- 0.3%. Heart rate dropped from 87 to 58 min-1, but the double product of heart rate and blood pressure dropped by only 8 +/- 2% (p = 0.05). The maximal coronary conductance during peak reactive hyperemia (after 20 s ischemia) indicating complete coronary dilation was diminished by 48% after L-NNA. The severe drop in resting myocardial perfusion and O2-supply, and nearly unchanged rate pressure product and thus myocardial metabolic rate following the inhibition of nitric oxide formation demonstrate a substantial contribution of EDRF/NO to the regulation of myocardial perfusion.

Acetylcholine↗
PubMed1991

Antiplatelet effects of endothelium-derived relaxing factor and nitric oxide donors.

Several circulating agonists and hydromechanical factors, such as the viscous drag-induced shear forces of the blood stream, stimulate the release of endothelium-derived relaxing factor (EDRF) or nitric oxide (NO) from endothelial cells. Abluminally released EDRF controls vascular tone, while luminally released EDRF diffuses into the platelets, especially when they come into close contact with the endothelial cell lining. Stimulation of soluble guanylyl cyclase in platelets causes a rise in cyclic 3',5'-guanosine monophosphate (cGMP) and a reduction in intracellular Ca(2+)-concentrations. This suppresses platelet adhesion and aggregation and potentiate similar prostacylin-induced rises in cyclic 3',5'-adenosine monophosphate. Nitrovasodilators, which spontaneously release NO, such as molsidomine and sodium nitroprusside, can act as a substitute for diminished EDRF release from deficient endothelium and similarly suppress platelet aggregation in vitro and in vivo.

Cyclic GMP↗
PubMed1991

EDRF-mediated shear-induced dilation opposes myogenic vasoconstriction in small rabbit arteries.

In small saline-perfused rabbit mesenteric arteries (diam 221 +/- 4 microns, means +/- SE; n = 48) in situ, the interactions of endothelium-derived relaxing factor (EDRF)-mediated flow-dependent dilation and myogenic constriction were studied. When pump flow was increased two- to fivefold (2.8 +/- 0.1-fold), input perfusion pressure rose by 133 +/- 17%. Vessel diameter first increased passively by 9 +/- 1% and then decreased to or below control values reflecting the vascular myogenic activity. This was followed by a 16 +/- 3% increase in diameter, which was flow dependent, because nonperfused vessels exposed to the same intravascular pressures did not dilate. When the perfusate viscosity was increased with dextran solutions, both the basal diameters and the flow-induced dilator responses were significantly augmented, indicating that the increase in shear stress was the stimulus. The flow-dependent dilation was abolished by inhibition of EDRF with either hemoglobin (10 microM) or NG-nitro-L-arginine (0.3 mM) and also after preincubation with neuraminidase (0.2 U/ml, 30 min), which removes part of the membrane glycocalyx. Thus, myogenic responses in small mesenteric arteries can be effectively opposed by shear-induced release of EDRF. This might be a major mechanism for maintaining adequate tissue perfusion when pressure and shear stress increase simultaneously (e.g., exercise hyperemia, autoregulation) and otherwise myogenic activity would reduce vascular conductivity.

Acetylcholine↗
PubMed1991

[Inhibition of platelet activation by endothelium-derived relaxing factor EDRF/NO and NO releasing dilator substances].

Several circulating agonists and hydromechanic factors such as the viscous drag-induced shear forces of the bloodstream stimulate the release of EDRF/NO from endothelial cells. Abluminally released EDRF controls vascular tone, luminally released EDRF diffuses into the platelets, especially when they come into contact with the endothelial cell lining. Stimulating soluble guanylate cyclase in the platelets causes a rise in cGMP and a reduction in intracellular Ca(2+)-concentrations which suppresses platelet adhesion and aggregation, and potentiates the effects of PGI2-induced cAMP-increases. Nitrovasodilators which spontaneously release NO, such as molsidomine and sodium nitroprusside, can substitute for diminished EDRF-release from deficient endothelial cells and, likewise, suppress platelet aggregation in vitro and in vivo.

Animals↗
PubMed1991

[Increase in skin blood circulation and transcutaneous oxygen partial pressure of the top of the foot in lower leg immersion in water containing carbon dioxide in patients with arterial occlusive disease. Results of a controlled study compared with fresh water].

Semi-quantitative Doppler laser flowmetry and measurement of transcutaneous oxygen partial pressure (TCPO2 in mmHg) are reliable, non-invasive methods of continuous measurement suitable for underwater use. We measured the effect of aqueous CO2 (succinate + sodium bicarbonate = Kao Bub; 1400 mg CO2 per kg water) compared with fresh water (both at 34 degrees C, depth of leg immersion 35 cm, immersion time 20 min) on circulation and TCPO2 in the feet of 15 patients with bilateral stage-II occlusion of the Aa. fem. superf. intraindividually in a randomised, crossover trial. Measurements were made at the same time of day on two consecutive days. No change in either cutaneous microcirculation or TCPO2 was observed during immersion in fresh water. During immersion in a CO2 bath both culaneous blood flow (as expressed by Doppler laser flux) and the amplitude of the Doppler laser vasomotion flux increased more than threefold (p less than 0.001, Wilcoxon), while sitting TCPO2 increased by over 10% (from 63 to 71 mmHg; p less than 0.001). The observed changes in oxygen dissociation and cutaneous microcirculation may help to provide an explanation for the well-known therapeutic effect of CO2 baths in all stages of occlusive arterial disease.

Adult↗
PubMed1991

[Effect of low density lipoproteins on vascular reactivity].

Investigations of circulation in humans and various animal models demonstrate changes in the reactivity of atherosclerotic arteries. Both attenuation of endothelium-dependent vasodilations and enhancement of contractile responses to different contractile agonists have been described. Recent in vitro studies provide evidence that low-density lipoproteins (LDL) accumulating in atherosclerotic arteries are involved in the mechanisms responsible for these changes. Perfusion of isolated arteries with native and oxidatively modified LDL results in attenuation of endothelium-dependent dilations. Furthermore, oxidized LDL impairs dilations to endothelium-independent agonists, and potentiates agonist-induced contractile responses. These in vitro observations are in accordance with alterations of the reactivity of arteries obtained from cholesterol fed rabbits. In these atherosclerotic arteries, contractile responses to the same agonists as used in the in vitro studies were enhanced, and endothelium-dependent dilations were attenuated. The extent of these changes was positively correlated with the degree of intimal atherosclerotic plaques, thus, with the regions containing oxidized LDL. Therefore, accumulation of oxidized LDL in atherosclerotic arteries may lead to an imbalance of vascular tonus regulation which favors inadequate vasoconstriction.

Animals↗
PubMed1990

Converting enzyme inhibition by enalapril in experimental heart failure.

We analyzed the effect of enalapril (0.1 mg/kg p.o. twice daily) on plasma electrolytes, urea, and creatinine in low cardiac output failure. In 14 male dogs implanted with chronic instrumentation, tachycardia was induced by ventricular pacing (265 impulses/min., 10-14 days). In 7 untreated dogs, pacing progressively lowered aortic flow by 44% and induced hyponatremia and elevations of plasma urea, creatinine, and potassium. Treatment with enalapril (n = 7) during pacing reduced the decrease in aortic flow by 33% and prevented changes in plasma urea, potassium, and sodium. We conclude that this is due to enalapril-induced retardation of heart failure progression.

Administration, Oral↗