Search PubMed⌕ Search

Biomedical subjects

S Mellander

Publications and source records attributed to S Mellander.

At least 19 recordsLinked to original sources
PubMed1992

Myogenic vascular regulation in skeletal muscle in vivo is not dependent of endothelium-derived nitric oxide.

The hypothesis, based on in vitro experiments on large conduit arteries, that endothelium-derived nitric oxide is a mediator of vascular myogenic reactivity was tested in cat gastrocnemius muscle in vivo. This was done by comparing, in the absence and presence of effective endothelium-derived nitric oxide blockade by the specific inhibitors NG-monomethyl-L-arginine or NG-nitro-L-arginine methyl ester, myogenic responses in defined consecutive vascular sections to dynamic vascular transmural pressure stimuli, to arterial occlusion (reactive hyperaemia), and to arterial pressure changes (autoregulation of blood flow and capillary pressure). The results demonstrated that the myogenic vascular reactivity to quick ramp transmural pressure stimuli was not attenuated by endothelium-derived nitric oxide blockade, but rather reinforced. The amplitude of the reactive hyperaemia response was unaffected by endothelium-derived nitric oxide blockade, but its duration was shortened because of faster myogenic constriction, especially of large-bore arterial resistance vessels greater than 25 microns, in the recovery phase. Both the improved myogenic responsiveness to transmural pressure stimuli and the shortening of the reactive hyperaemia by endothelium-derived nitric oxide blockade suggested that endothelium-derived nitric oxide released in vivo acts as a 'metabolic' factor which certainly does not improve, but rather depresses myogenic vascular reactivity. Autoregulation of blood flow and capillary pressure were well preserved in the presence of endothelium-derived nitric oxide blockade. It was concluded from the results of these multifaceted tests that myogenic vascular regulation in skeletal muscle in vivo seems independent of endothelium-derived nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Protective role of sympathetic nerve activity to exercising skeletal muscle in the regulation of capillary pressure and fluid filtration.

This study describes the integrated sympathetic/metabolic control of capillary pressure (Pc) and filtration in cat skeletal muscle as studied during graded exercise and superimposed graded (2, 6 and 16 Hz) vasoconstrictor nerve excitation. The applied technique permitted simultaneous analysis of the underlying changes of resistance in the whole vascular bed (RT) and in its large-bore arterial resistance vessels (greater than 25 microns), small arterioles (less than 25 microns) and veins. Graded exercise per se caused graded increases in capillary pressure, which at heavy work exceeded the resting control value by 12.2 mmHg, in turn leading to marked loss of plasma fluid by filtration. Sympathetic nerve stimulation was much more efficient in lowering capillary pressure during exercise than at rest, in spite of an exercise-induced marked attenuation of the vasoconstrictor response (RT). The sympathetically evoked capillary pressure fall per unit resistance increase was larger the greater the degree of exercise vasodilation, implying a highly nonlinear relation between capillary pressure and RT and also between the more direct determinant of capillary pressure the post- to precapillary resistance ratio, and RT. Strenuous exercise in vivo is known to be associated with a markedly increased reflex sympathetic discharge to exercising muscle which has been a puzzling feature in view of its untoward restriction of the exercise hyperaemia response. To the extent the present results are representative for this in vivo situation, they suggest that sympathetic discharge to exercising muscle, in spite of some flow restricting effect, might serve a highly beneficial function, causing effective protection against excessive work-induced rise of capillary pressure and harmful plasma fluid loss into the extravascular space of working muscle.

Animals↗
PubMed1990

Sympathetic alpha-adrenergic control of large-bore arterial vessels, arterioles and veins, and of capillary pressure and fluid exchange in whole-organ cat skeletal muscle.

The sympathetic nervous control of the vascular bed of cat gastrocnemius muscle was studied with a new whole-organ technique which permits simultaneous, continuous and quantitative measurements of capillary pressure (Pc), capillary fluid exchange and resistance reactions in the whole vascular bed and in its three consecutive sections: large-bore arterial vessels (greater than 25 microns), arterioles (less than 25 microns) and veins. The results demonstrated a distinct neural control of all three consecutive vascular sections, graded in relation to the rate of nerve excitation up to maximum at 16 Hz. Stimulation at high rates, which in the steady state caused an average rise of overall regional resistance from 15.3 to 120 PRU (7.8-fold increase), thus raised large-bore arterial vessel resistance from 8.8 to 64 PRU (7.3-fold increase), arteriolar resistance from 4.5 to 49 PRU (10.9-fold increase) and venous resistance from 2.0 to 7 PRU (3.5-fold increase). The rate of resistance development (PRUs-1) of the sympathetic constrictor response was much higher in the arteriolar than in the other sections, which indicates that the neural control is especially prompt and efficient in the arterioles. A passive component was shown to contribute to the described responses only on the venous side, but in no case by more than 10% of the total sympathetic venous resistance response, which thus is mainly active. Of special functional importance was that the new technique provided information about the adrenergic control of Pc in absolute figures. From the control value of 19 mmHg, graded sympathetic stimulation caused a graded decline in Pc, at maximum constriction by about 7 mmHg. This resulted in marked net transcapillary fluid absorption, in turn increasing plasma volume.

Animals↗
PubMed1990

Resistance responses in proximal arterial vessels, arterioles and veins during reactive hyperaemia in skeletal muscle and their underlying regulatory mechanisms.

The reactive hyperaemia response cat skeletal muscle to 2-120 s arterial occlusions was analysed with regard to amplitude, duration, 'excess blood flow' and site of dilator action along the vascular bed. The last-mentioned was assessed with a new whole-organ technique permitting continuous segmental resistance recordings in arterial vessels greater than 25 microns, arterioles less than 25 microns and veins. Peak amplitude, duration and excess flow all increased with increasing occlusion length, of which excess flow was linearly related to occlusion length. The site of active dilatation was preferentially confined to arterioles less than 25 microns in which complete relaxation was observed after only 20 s occlusion, although the duration of the response continued to increase with more prolonged occlusions. A graded, but less pronounced, dilatation occurred in the arterial vessels greater than 25 microns and in the veins, the former exhibiting a 63% inhibition of tone as a maximum response at 120 s occlusion. The recovery phase was characterized by a vivid active constrictor component apparently protecting the capillaries from excessive pressure load upon arterial occlusion release, but this constriction became attenuated at long occlusions, thereby prolonging the hyperaemia response. The role of myogenic regulatory mechanisms in the responses was assessed from observed segmental resistance reactions to selectively applied transmural pressure stimuli similar to those elicited by arterial occlusion/release. It was concluded that myogenic mechanisms alone could explain the amplitude of the reactive hyperaemia response at short (up to 30 s) occlusions. Metabolic mechanisms seemed to be responsible for further relaxation of the proximal arterial vessels at longer occlusions, and also for the increased duration of the hyperaemia response at occlusions exceeding 10 s. Blockade of nitric oxide formation (endothelium-derived relaxing factor) did not seem to affect the reactive hyperaemia response.

Animals↗
PubMed1990

Relation between capillary pressure and vascular tone over the range from maximum dilatation to maximum constriction in cat skeletal muscle.

An attempt was made to assess, from a large sample (n = 567), the normal level of hydrostatic capillary pressure (Pc) in resting skeletal muscle and the extent of Pc regulation as effected by strictly graded activation of metabolic and adrenergic control mechanisms over the entire physiological range of vascular tone. With the use of a new whole-organ technique, Pc towards the venous end of the capillary was continuously recorded at constant arterial pressure (100 mmHg) and under simultaneous observations of total regional vascular resistance (RT), precapillary resistance (Ra) and post-capillary resistance (RV). In the control state with a Starling fluid equilibrium, a venous pressure of 7 mmHg and normal vascular tone (RT = 19.1 +/- 0.3 PRU), Pc averaged 16.7 +/- 0.3 mmHg. Graded metabolic dilatation (muscle exercise), decreasing RT to a minimum value of 1.7 PRU, caused progressive increase in Pc up to 32 mmHg and consequent fluid filtration. Conversely, graded adrenergic constriction, increasing RT to a maximum of 100 PRU, caused a progressive decrease in Pc down to 10 mmHg and consequent fluid absorption. The relation between Pc and RT was highly non-linear, Pc increasing more steeply the more RT approached low values, and was described by the power function: Pc = 36.43 x RT-0.27 (r = -0.79, P less than 0.001). The resistance ratio, Rv/Ra (the main determinant of Pc), and vascular tone (RT) showed a similar non-linear relation. Regulatory change of Rv/Ra was mainly accomplished by active change of Ra, but a pronounced Rv decrease (venodilatation) occurred in the lowest RT range, exerting a protective function against excessive increase in Pc and detrimental plasma fluid loss.

Animals↗
PubMed1990

Effects of hypertonic NaCl solution on microvascular haemodynamics in normo- and hypovolaemia.

The aims of this study were to investigate possible resuscitation effects of a single, 10-min, 350-microliters intravenous infusion of 7.5% NaCl in hamsters in hemorrhagic shock and to compare the effects of such infusion with an identical one of 0.9% NaCl on the hamster cheek pouch microcirculation during normovolaemia and after acute bleeding to a hypotension level of about 40 mmHg. No significant differences could be detected between the effects of either infusion given to normovolaemic normotensive hamsters. In the animals subjected to haemorrhage, upon bleeding, arterioles larger than 40 microns constricted, arterioles smaller than 40 microns dilated and venular diameter did not change, while blood flow decreased in all vessels. The main differences between the infusions after haemorrhage were a significant increase in mean arterial pressure and arteriolar blood flow, venoconstriction and a tendency for the smaller arterioles to remain more dilated and the larger ones more constricted after the hypertonic infusion. Central nervous and/or reflex excitation of the sympathetic nervous system could account for the constriction of venules and larger arterioles, while a direct effect of hyperosmolarity could explain the dilatation of the smaller arterioles. The study can therefore help to explain some of the mechanisms underlying the reported resuscitation effect of 7.5% NaCl infusion in animals during severe haemorrhagic hypovolaemia.

Animals↗
PubMed1990

Role of endothelium-derived nitric oxide in the regulation of tonus in large-bore arterial resistance vessels, arterioles and veins in cat skeletal muscle.

The role of endothelium-derived nitric oxide in the regulation of vascular resistance (tonus) in cat skeletal muscle was studied with the use of NG-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide formation from L-arginine. The study was performed with a whole-organ technique which permits simultaneous, continuous and quantitative recordings of resistance reactions in the whole vascular bed (RT) and in its three consecutive sections: large-bore arterial resistance vessels (greater than 25 microns; Ra,prox), small arterioles (less than 25 microns; Ra,micro) and veins (Rv). NG-monomethyl-L-arginine (3-100 mg kg-1 tissue, i.a.) induced a dose-dependent increase in resistance that was preferentially, but not selectively, confined to the large-bore arterial resistance vessels. At a maximally effective dose (100 mg kg-1), the nitric oxide inhibitor caused a marked constriction, within 5 min, on average increasing RT by 99%, Ra,prox by 138%, Ra,micro by 18% and Rv by 23%. The constrictor response to NG-monomethyl-L-arginine was long-lasting but disappeared gradually over a period of about 1 h. However, it could be abruptly abolished by excess L-arginine (300 mg kg-1, i.a.). The vasodilator response (RT) to acetylcholine was significantly attenuated in the presence of NG-monomethyl-L-arginine compared with the control response. The results suggested that nitric oxide formation from L-arginine by the vascular endothelium plays a fundamental role in the regulation of vascular resistance (tone) in vivo, with its main site of action located in the large-bore arterial resistance vessels.

Animals↗
PubMed1989

Metabolic control of large-bore arterial resistance vessels, arterioles, and veins in cat skeletal muscle during exercise.

The metabolic control of the vascular bed in cat gastrocnemius muscle during exercise was studied with a new technique (Björnberg et al. 1988) permitting continuous and simultaneous recordings of arteriolar and capillary pressures, and of resistances in the following consecutive vascular section: proximal arterial resistance vessels greater than 25 microns, arterioles less than 25 microns, and on the venous side. The study thereby provided quantitative data for resistance and active intrinsic tone in these vascular segments at rest, during graded exercise vasodilatation, and in the post-exercise period. Slight activation of the metabolic control system by low-frequency somatomotor nerve stimulation ('light exercise') caused inhibition of intrinsic tone and decreased vascular resistance selectively in the arteriolar section. At increasing workloads, arteriolar resistance was further decreased, but resistance and tone in the proximal arterial resistance vessels and the veins then became clearly reduced as well. This difference in effectiveness of the metabolic control system on the different segments of the vascular bed was expressed quantitatively in terms of a 'metabolic vasodilator index'. Graded activation of the metabolic control system led to a marked segmental redistribution of intrinsic vascular tone, in turn resulting in an increased pressure drop across the proximal arterial vessels in the veins and a decreased pressure drop over the arterioles. The observed decrease in the pre- to post-capillary resistance ratio caused, at a constant arterial pressure of 100 mmHg, a graded increase in capillary pressure with increasing workloads, at maximum vasodilatation by an average value of 14 mmHg above the resting control value of 15.4 +/- 0.6 mmHg. In the post-exercise period, recovery of vascular tone to control was more rapid in the proximal arterial resistance vessels and the veins than in the arteriolar segment.

Animals↗
PubMed1989

Functional aspects of myogenic vascular control.

Recent in vivo observations, especially in skeletal muscle, of macro- and microvascular myogenic reactivity and its functional consequences suggest that myogenic regulatory mechanisms contribute directly or indirectly to circulatory homeostasis by exerting the following main functions: (1) A blood pressure-induced tonic excitatory function of the vasculature, thereby initiating a pronounced intrinsic myogenic basal tone in the arterial microvessels; (2) a homeostatic resistance function (high total peripheral resistance), mainly exerted by the myogenic tone and serving to maintain normal arterial pressure at rest; (3) functions serving to improve nutritional flow and exchange, exemplified by blood flow recruitment, capillary recruitment, adjustments to the capillary perfusion:diffusion ratio for optimum exchange in the heterogeneous capillary network, and reactive hyperaemia; and (4) protective functions directed against harmful circulatory effects of changes in blood pressure, exemplified by autoregulation of blood flow and autoregulation of capillary hydrostatic pressure during changes in arterial pressure, and by autoregulation of transcapillary filtration during a hydrostatic load on the vascular bed.

Animals↗
PubMed1989

Effects of hypertonic NaCl solution on the hamster cheek pouch microcirculation in normo- and hypovolemia.

The aim of this study was to evaluate the effects of a single, 10 min, intravenous infusion of a hypertonic NaCl solution [2400 mOsm/l; infused volume 0.35 +/- 0.03 ml (SEM)] on the hamster cheek pouch microcirculation during normovolemia and after acute bleeding to a hypotension level of about 40 mmHg. Upon bleeding, the arterial pressure dropped to 39 mu 1 mmHg, arterioles greater than 40 microns constricted 12 +/- 3% (from their control value), arterioles less than 40 microns dilated 6 +/- 2%, venules stayed largely unchanged, while RBC velocity and volume flow decreased 57 +/- 7% in all vessels. During the subsequent hypertonic NaCl infusion, the arterial pressure increased rapidly to a new steady state level of 66 +/- 3 mmHg. After the infusion, the large arterioles stayed constricted 11 +/- 1% and the small arterioles dilated 7 +/- 1% for a 1-h observation period. The venules constricted initially by 6 +/- 2% and returned to control diameter in 30-40 min. RBC velocity and calculated volume flow returned to the pre-hemorrhage control values in about 10 min for the arterioles and in 40 min for the venules. An identical hypertonic infusion given to normovolemic hamsters caused no significant alterations of the measured variables.

Animals↗
PubMed1988

Site of autoregulatory reactions in the vascular bed of cat skeletal muscle as determined with a new technique for segmental vascular resistance recordings.

An arterial and venous microcannulation technique was developed for circulatory studies in the cat gastrocnemius muscle which, based on detailed morphological and functional observations of the microvascular arrangement, seems to permit continuous recordings of pressure in arterioles (diameter approximately 25 microns) and capillary pressure. These variables in combination with measurements of arterial and venous pressure and blood flow provided a means of continuous simultaneous recordings of total as well as segmental resistances in defined sections of the vascular bed, viz. in large arterial vessels (diameter greater than 25 microns), arterioles (less than 25 microns), and on the venous side. This new technique was applied to a study of the site(s) of autoregulatory reactions along the vascular bed evoked by changes of arterial pressure over the range 50-150 mmHg. The results indicated that active autoregulation mainly occurred within arterioles smaller than about 25 microns. In larger arterial vessels concomitant moderate active smooth muscle adjustments barely balanced out the pressure-induced passive calibre changes, and the venous vessels did not seem to contribute actively to autoregulation, but exhibited a passive change in postcapillary resistance (Rven). The described pattern of response results in quite effective autoregulation of blood flow and capillary pressure (PC). The observed passive Rven change, via its effect on the pre- to postcapillary resistance ratio, seems to explain the fact that autoregulation of PC can be more efficient than flow autoregulation. The study also provided quantitative data for the level of active intrinsic vascular tone in defined consecutive sections of the muscle vascular bed at normal arterial pressure and for segmental redistributions of tone evoked by pressure alterations.

Animals↗
PubMed1987

Vasoactive intestinal polypeptide in relation to penile erection in the cat evoked by pelvic and hypogastric nerve stimulation.

The hemodynamics of penile erection were elucidated in the anesthetized cat by studying volumetrically determined erectile responses of the penis and penile blood flow during frequency-graded bilateral stimulation of the pelvic and the hypogastric nerves, selectively or in combination. The study also provided information on possible neurotransmitter mechanisms. The results indicated that the erectile response is mediated by both the pelvic and hypogastric nerves, operating synergistically to evoke a seemingly maximum erection. Optimum erectile responses for either nerve system were obtained at 16 Hz and threshold responses at 0.5 to one Hz. In the presence of atropine, the erectile response to selective stimulation of the pelvic and the hypogastric nerves, respectively, were clearly curtailed, suggesting a cholinergic mechanism to be partly responsible for the diversion of blood from the penile "resistance vessels" to the cavernous bodies, possibly accomplished via the opening of vessels with a shunt-like function. However, the magnitude of the erectile response to combined pelvic and hypogastric nerve stimulation seemed to be surprisingly little affected by muscarinic blockade. Selective stimulations of the pelvic and the hypogastric nerves, respectively, were both found to cause about a five-fold increase in VIP output from the penis, coordinated in time with the local blood flow increase during erection. These data suggest a VIP-ergic neurotransmitter mechanism to be involved in penile erection in the cat, possibly controlling the dilation of the penile arterial "resistance vessels."

Animals↗
PubMed1987

Method for continuous recording of hydrostatic exchange vessel pressure in cat skeletal muscle.

A venous microcannulation technique applied to the cat gastrocnemius muscle was developed which, based on morphological and functional demonstrations of anastomotic connections between two supplying segmental vascular circuits at the level of capillaries and/or post-capillary venules, seems to permit continuous recordings of hydrostatic pressure (denoted Pcvenule) transmitted from such anastomoses, that is, from a site close to the main fluid exchange vessels. For validity tests, such Pcvenule recordings were compared with simultaneous estimates of capillary pressure (Pc) with the isogravimetric technique (Pciso) and, further, with data for experimentally evoked changes of Pc derived from volumetric recordings of net transvascular fluid flux divided by the capillary filtration coefficient (delta Pcvol). Simultaneously obtained data for Pcvenule and Pciso showed close agreement, and the Pcvenule and Pcvol data showed a highly significant linear correlation over a wide range of Pc changes. These results indicate that reliable estimates of Pc can be obtained with the Pcvenule method. It allows for continuous Pc recordings without interfering with normal vascular reactivity and can be applied to non-isogravimetric conditions and combined with simultaneous observations of whole-organ transvascular fluid exchange. At normal arterial and venous pressures and vascular tone, Pcvenule averaged 16.2 +/- 0.2 mm Hg, at which a Starling fluid equilibrium prevailed, and increased with decreasing vascular tone, resulting in net transvascular fluid filtration.

Animals↗
PubMed1987

Autoregulation of capillary pressure and filtration in cat skeletal muscle in states of normal and reduced vascular tone.

The controversial hypothesis that capillary pressure (Pc) is autoregulated in response to arterial pressure (PA) alterations was tested in sympathectomized cat skeletal muscle by studying the relation between Pc and PA under conditions of well preserved vascular tone and reactivity, during papaverine-induced maximal vasodilatation (passive vascular bed), and during impaired vascular reactivity caused by preparatory surgery, or by low dose isoproterenol administration. The latter states resembled such under which Pc autoregulation unintentionally seems to have been studied previously. Capillary pressure was assessed with the Pcvenule method for continuous direct pressure recordings from capillaries/postcapillary venules (Mellander et al. 1987) and simultaneously derived from observed net transvascular fluid flux divided by CFC. Resistances in the whole vascular bed and in its pre- and postcapillary segments (Ra and Rv) were determined from recordings of blood flow, PA, Pc, and PV. During preserved vascular reactivity, Pc was found to be virtually constant, that is, almost perfectly autoregulated, over the PA range from 50 to 180 mmHg, whereas in the passive vascular bed there was a direct linear relation between Pc and PA (y = 0.137x + 11.69; r = 0.97). The delta Pc/delta PA ratio was about 1/70 in the normal reactive, and 1/7 in the passive, vascular bed, implying an increase in Pc by 1 mmHg for every 70 mmHg and every 7 mmHg increase in PA, respectively. Capillary pressure autoregulation was explained by precise adjustments of Ra/Rv in relation to PA elicited by myogenic and metabolic regulatory mechanisms. This protective reaction against plasma loss during increased PA was abolished during maximal vasodilation, and was much impaired by surgical trauma, partly via a beta-adrenergic inhibitory effect, and by isoproterenol, in turn causing gross transcapillary fluid fluxes. The latter findings might explain failing Pc autoregulation in some previous studies undertaken under seemingly similar conditions.

Adrenergic beta-Agonists↗
PubMed1984

An evaluation of the metabolic interaction with myogenic vascular reactivity during blood flow autoregulation.

An attempt was made to evaluate the possible metabolic interaction with myogenic vascular reactivity during autoregulation of blood flow in sympathectomized cat skeletal muscle. This was done by studying the extent to which a purely myogenic response, elicited by a standardized 2 s vascular transmural pressure impulse stimulus was altered when mean arterial inflow pressure was varied in the range from 160 down to 40 mmHg. The observations were made during the steady state blood flows encountered at the different pressure levels. The data were corrected for the effects of physical factors inherent in altered basal vascular tone and intravascular pressure with the aid of a mathematical model for purely myogenic responses. The results demonstrated a flow dependent decline in myogenic vascular reactivity during reduction of arterial pressure, even in the range where blood flow was autoregulated quite effectively. This suggested a significant metabolic interaction with myogenic reactivity, an interpretation corroborated by a similar decline in myogenic reactivity found during more defined activation of the vascular metabolic control system by graded light muscle exercise. The fact that a significant metabolic interaction was revealed even at such minute flow changes that occur in the autoregulatory range indicates a high 'gain' in the metabolic feedback interacting, directly or indirectly, with myogenic mechanisms in local vascular regulation.

Adrenergic alpha-Antagonists↗
PubMed1983

Neural vasodilator control in the rectum of the cat and its possible mediation by vasoactive intestinal polypeptide.

Vascular and motor responses in the rectum to pelvic nerve stimulation are described in the anaesthetized cat and compared with corresponding effects observed in the colon. The responses comprise a cholinergic and a non-cholinergic component, and an attempt has been made to elucidate the latter. Pelvic nerve stimulation evoked a pronounced and well maintained vasodilator response in the rectum whereas that in the colon was transient. Maximal vasodilatation occurred at much lower stimulus frequencies in the rectum (2-4 Hz) than it did in the colon (8-16 Hz) and maximal blood flow under these conditions was also greater in the rectum (greater than 200 ml 100 g-1 min-1) than the colon (less than 150 ml 100 g-1 min-1). Muscarinic blockade further curtailed the colonic vasodilator response to pelvic nerve stimulation, whereas the rectal dilatation was only slightly reduced in the presence of atropine. Pelvic nerve stimulation caused a substantial release of vasoactive intestinal polypeptide (VIP) from the rectum, which was related both in magnitude and duration to the vasodilatation. Intra-arterial infusions of VIP, which reproduced this rise in rectal venous VIP concentration, caused a rectal vasodilator response which closely resembled that during pelvic nerve stimulation after cholinergic blockade. The rectal vasculature was estimated to be 50-100 times more sensitive to VIP than the colonic vasculature. VIP therefore seems to be the most likely putative neurotransmitter responsible for non-cholinergic rectal vasodilatation. Stimulation of the pelvic nerves also caused rapid contractile motor responses before, and more gradual motor responses after, muscarinic blockade in both the colon and rectum, in the latter preceded by a non-cholinergic relaxation. These patterns of motor activity largely confirm previous results. Infusions of substance P effectively mimicked the non-cholinergic contractile motor responses but failed to demonstrate significant release of this peptide during pelvic nerve stimulation in the present experiments. However, substance P is rapidly inactivated and might possibly be involved in these responses. Stimulation of the pelvic nerves in bursts at high frequencies (up to 80 Hz), simulating a discharge pattern observed electrophysiologically in vivo, was effective in eliciting all the above responses, with the exception of the colonic contraction.

Animals↗
PubMed1982

Neural beta-adrenergic dilatation of the facial vein in man. Possible mechanism in emotional blushing.

Ring preparations of the superficial buccal segment of the human facial vein, taken from extirpated tissue in 12 patients during neck surgery, were studied in vitro. The vein developed a maintained intrinsic myogenic tone in response to passive stretch and was supplied with alpha- as well as beta-adrenoceptors, both of which could be influenced by transmural nerve stimulation (TNS) and noradrenaline. These unusual characteristics for a vein are basically similar to the ones described for the rabbit facial vein by Pegram, Bevan & Bevan (1976). In man there seemed to be an inter-individual difference with regard to the abundance of 'innervated' alpha- and beta-adrenoceptors. Facial vein specimens from some subjects thus responded with prompt and pronounced net dilatation to TNS with maximum at 4 Hz and those from others with net constriction with maximum at 16 Hz. The latter showed a reversal into neural beta-adrenergic dilatation after alpha-adrenergic blockade. The human external jugular vein was devoid of intrinsic tone and beta-adrenoceptors. It is tentatively proposed that a beta-adrenergic neuro-effector mechanism in superficial ramifications of the facial vein in man might be involved in the emotional blushing reaction.

Adult↗