[Biophysics of the rapid measurement of local blood irrigation].
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Biomedical subjects
Publications and source records attributed to J Seylaz.
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The effects of removing the endothelium of the rabbit central ear artery on the response to noradrenaline have been examined in vitro. A 10 mm segment of this artery was cannulated and connected to a constant flow perfusion circuit; the endothelium of some arteries was first removed mechanically. Vasomotor activity was determined by measuring the pressure at the input to the artery. Scanning electron microscopy, light microscopy and functional test with acetylcholine on intact and rubbed arteries showed that the endothelium had been effectively removed in lesioned arteries and remained intact in control arteries throughout the experiment. Internal or external noradrenaline-induced a concentration-dependent constriction which was significantly greater in the rubbed arteries. In contrast, there was no significant difference in the pressure/flow curves of control and rubbed arteries whether preconstricted with K+ or not. We conclude that the endothelium in the rabbit isolated ear artery greatly influences the response to internal or external noradrenaline, and that this effect cannot be explained by changes in the physical characteristics of de-endothelialized arteries. The endothelium thus may play an inhibitory role in noradrenaline-induced vasoconstrictions.
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In segments of rabbit basilar artery (BA) platelet-activating factor (PAF) initiated a concentration-dependent transitory contraction which was unaffected by indomethacin or nordihydroguaiaretic acid (NDGA). N omega-nitro-L-arginine (NLA) did not change the magnitude of PAF-induced contraction, but in the presence of NLA the contraction tended to be more prolonged. In precontracted BA segments, PAF caused a concentration-dependent relaxation which was unaffected by NDGA. Indomethacin and NLA decreased PAF-induced relaxation by 10-30 and 70-90%, respectively; in combination these agents totally eliminated PAF-induced vessel reactions. Treatment of BA segments by rabbit peritoneal polymorphonuclear leukocytes (PMNLs) activated with N-formyl-methionyl-leucyl-phenylalanine (fMLP) for 20 min led to PMNL adhesion to the vascular endothelium and a significant decrease (60-100%) in acetylcholine-induced endothelium-dependent vessel relaxation. After the treatment of BA segments, PAF induced strong, slow, tonic contraction of either non-precontracted or precontracted vessels which was unaffected by indomethacin or NLA. NDGA decreased this contraction by 30-60%. These results indicate that PAF is an endothelium-dependent vasodilator that can also produce an insignificant constrictor effect. However, when the vessels are affected by activated PMNLs, PAF is transformed to a strong vasoconstrictor, presumably due to the generation of as yet unknown vasoconstrictor stimuli resulting from PMNL-endothelium interactions. Under these conditions the PAF-induced contraction is partly mediated by 5-lipoxygenase metabolites.
Simultaneous measurements were made of spike activity and perfusion pressure (PA) in intact segments of rabbit middle cerebral artery in vitro. The segments were mounted on a Teflon tube designed so that the perfusing solution flowed in the annular space between the tube and the artery wall, thus magnifying the PA changes occurring when the artery constricted or dilated. A widened portion of the Teflon tube immobilized 1--2 mm of the artery segment for electrical recording with fine glass microelectrodes. Spontaneous spike activity (extra- and intracellular) was regularly observed. When a steady PA and spike discharge was obtained, tests were performed by substituting for the normal perfusion liquid, solutions containing 5 microgram/ml norepinephrine, 5 microgram/ml angiotensin II or 7.5 microgram/ml isoproterenol. Norepinephrine and angiotensin each increased spike frequency (+ 293 and + 126%) and PA (+ 6.6 and + 7.9 mm Hg) whereas isoproterenol decreased spike frequency (-89%) and PA (-22.9 mm Hg). These results a) confirm the presence of receptors to these agents in pial arteries, and b) demonstrate a high degree of correlation between membrane electrical events and mechanical activity of these spontaneously-active myovascular cells.
We tested the reproducibility of consecutive measurements of regional cerebral blood flow (rCBF) made in 13 areas of each hemisphere in patients with cerebrovascular diseases by the atraumatic 133Xe intravenous injection method. The data were analysed by a two-compartment model similar to that used in the Obrist inhalation method. Four parameters derived from the model were tested: Fg (flow of the fast-clearing compartment), FF and W (respectively fractional flow and relative tissue weight of the same compartment), ISI (initial slope index as defined by Risberg et al.). No significant variation was found in these four parameters between two consecutive rest measurements for all the areas studied and whatever the time interval between the measurements. The variances of the differences of Fg and ISI between the two measurements were found to be similar to those found in normal healthy subjects. The variances of FF and, consequently, W were greater than the values determined in healthy volunteers. An attempt to improve the quality of the results, by correcting them for the effects of PaCO2 changes between the measurements, resulted on the contrary in a general increase of the variances of the differences, showing the inadequacy of the correction coefficients used for healthy subjects at least for a proportion of the patients with cerebrovascular diseases. Sensitivity, tested by activation (hand work), shows a positive answer for FG but no significant change in ISI in any area. These findings demonstrate that in cases of cerebrovascular diseases the raw data (uncorrected for the changes in PaCO2) are the most reliable data but the meaning of the values found for FF and W must be regarded with caution since they may be affected by the "slippage" phenomenon. It is suggested that the ISI should only be used when there is evidence of a failure of the compartmental model, but only as a rough estimation of the flow level because of its lack of sensitivity.
The inactivation of the norepinephrine transmitter in the region of the adrenergic receptor is one important function of the sympathetic nerve terminals innervating blood vessels. This capacity was tested on isolated cat's middle cerebral artery (MCA) by recordings of the contractile response induced by norepinephrine at various stages after sympathectomy (excision of the superior cervical ganglion). Within three days after denervation, when fluorescence microscopy revealed a disappearance of neuronal norepinephrine in the vessel wall, there was a threefold increase in sensitivity of the test system which was not further enhanced at two weeks. This, and the finding of a similar amount of sensitization (of non-denervated vessels) to norepinephrine or tyramine after cocaine treatment, showed that a prejunctional type of sensitivity had developed. The sympathetic denervation did not influence the dose-response curve obtained with acetylcholine, supporting the specific nature of the supersensitivity reaction only to the sympathetic transmitter. Half a year after sympathectomy the sensitivity of the pial arteries to norepinephrine returned to control levels despite the absence of reinnervation, indicating that postjunctional changes also occurred. The findings offer further evidence for a functional role of the sympathetic nerves supplying intracranial arteries and show that the mode of innervation resembles that found in peripheral vessels.
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