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PubMed1981

Adrenergic influence on glucocounterregulation in man.

To investigate the adrenergic role in glucocounterregulatory mechanisms, single-blind randomised studies were performed in 7 normal males during severe insulin-induced hypoglycaemia with or without adrenergic blockade. Intravenous phentolamine administration (5 mg stat and 0.5 mg/min) did not interfere with the restoration of euglycaemia from hypoglycaemia. However, recovery of blood glucose in the presence of propranolol (3 mg/3 min and 0.8 mg/min) was retarded when compared with control studies (mean plasma glucose levels +/- SEM , 50 +/- 6 mg/dl versus 66 +/- 4 mg/dl at 120 min after insulin administration) despite appropriate glucagon, epinephrine, cortisol, and growth hormone responses. Plasma norepinephrine response was unaffected by propranolol but augmented threefold by phentolamine. Increases in plasma lactate, pyruvate and non-esterified fatty acids were blunted with propranolol while rebound non-esterified fatty acid was observed with phentolamine infusion. These data suggest that complete recovery of blood glucose from sever hypoglycaemia requires full sympathetic nervous system activity despite the integrity of other counterregulatory mechanisms.

Adult↗
PubMed1988

Relationship between vascular adrenergic receptors and prostaglandin biosyntheses in canine diabetic coronary arteries.

Before the onset of histologically detectable alterations of diabetic arteries, a considerable decrease of vasodilation ability develops. The role of an altered prostaglandin biosynthesis in this phenomenon was investigated in connection to the altered vascular adrenergic mechanisms. The effect of phenylephrine on prostacyclin production of isolated coronary arterial rings (100 mumol/l) as well as on conductivity of the coronary arterial bed (7.5-15-30-60 pmol. kg-1.min-1) were compared in 12 metabolically healthy and 12 alloxan-diabetic (560 mumol/kg) dogs. Furthermore, the effect of phentolamine (5 mumol/l) on the prostacyclin and thromboxane productions of the isolated vessels (coronary, femoral and basilar arteries) was investigated by radioimmunoassay. Although the basal prostacyclin amounts synthesized by healthy and diabetic coronary vessels were not different (5.1 +/- 1.6 and 4.9 +/- 1.4 pg/mg vessel/30 min), similarly to femoral and basilar arteries, the diabetic arterial rings produced significantly (p less than 0.05) more thromboxane than the control rings. The alpha-adrenergic blockade by phentolamine did not influence the prostacyclin production in the healthy arteries, but considerably (p less than 0.05) increased it in the diabetic coronary arteries. Phentolamine normalised the thromboxane synthesis in the diabetic group (p less than 0.01) and enhanced (p less than 0.05) it in the metabolically healthy group. Phenylephrine was ineffective (98 +/- 6%) on the prostacyclin production in vitro versus the stimulated (150 +/- 22%) prostacyclin synthesis detected in the metabolically healthy group; and in vivo induced a more significant (p less than 0.05) decrease in the coronary conductivity in diabetic than in control groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Evidence for multiple adrenoceptor sites in rainbow trout vasculature.

The importance of neuronal and lumenal vascular adrenoceptors in the regulation of vascular reactivity was examined in rainbow trout (Oncorhynchus mykiss), in vivo and in vitro. In vivo, ganglionic blockade with hexamethonium or alpha-adrenoceptor blockade, with either phentolamine or prazosin, produced similar (7mmHg) decreases in dorsal aortic blood pressure. The drop in dorsal aortic pressure produced by phentolamine or prazosin was due to reduced systemic vascular resistance. Neither the alpha-adrenoceptor antagonist, phenoxybenzamine nor chemical sympathectomy with 6-hydroxy-dopamine affected dorsal aortic pressure. However, after chemical sympathectomy, phenoxybenzamine lowered dorsal aortic pressure to levels similar to that produced by either phentolamine or prazosin. Plasma epinephrine and norepinephrine concentrations increased four- and twofold, respectively, in sympathectomized fish. Sympathectomy also produced a leftward shift in the epinephrine dose/response curve of the in vitro perfused splanchnic vasculature, placing the effective catecholamine concentration well within the in vivo plasma levels. These results indicate that following chemical sympathectomy arterial blood pressure is stabilized by circulating catecholamines through the combined effect of increased plasma catecholamine concentrations and increased sensitivity of vascular adrenoceptors. Phenoxybenzamine is incapable of blocking neuronal vascular adrenoceptors but is a potent antagonist of the up-regulated adrenoceptors, suggesting that the latter are localized on the lumenal side of the vessel.

Animals↗
PubMed1975

Effects of antagonists upon locomotor stimulation induced by injection of dopamine and Noradrenaline into the nucleus accumbens of nialamide-pretreated rats.

The effects of injections of monoamines, alone and in combination with different antagonists, bilaterally into the nucleus accumbens of nialamide-pretreated rats were investigated. Dopamine was found to produce a stronger stimulation of locomotor activity than noradrenaline, whereas serotonin was effective only in a small number of animals, in which the duration of locomotor stimulation was shorter than after dopamine or noradrenaline. The effects of both dopamine and noradrenaline were completely antagonized by administration of a small dose of the dopamine antagonist haloperidol, administered bilaterally 15 min after the catecholamines. The alpha-adrenergic antagonist phentolamine did not inhibit the effect of noradrenaline but, on the contrary potentiated and considerably prolonged the duration of locomotor stimulation. Aslo, the effect of dopamine was potentiated and prolonged by phentolamine. Bilateral injection of phentolamine alone had no influence upon locomotor activity. The effect of noradrenaline was not clearly inhibited nor potentiated by the beta-adrenergic antagonist propranolol. It is suggested that the stimulation of locomotor activity induced by injection of noradrenaline into the uncleus accumbens of nialamide-pretreated rats is brought about via dopaminergic mechanisms.

Animals↗
PubMed1982

alpha-Adrenoceptors mediating the positive inotropic effect of phenylephrine in the right ventricular muscle of the monkey (Macaca fuscata).

The property of adrenoceptors mediating the positive inotropic effect (PIE) in the ventricular muscle of the Japanese monkey (Macaca fuscata) was investigated by the use of phenylephrine (PE) and adrenoceptor antagonists. The intrinsic activity (0.6) and the pD2-value (5.41) for PE were comparable to those in other mammalian species. The beta-adrenoceptor antagonist, pindolol (3 x 10(-8) mol/l) shifted only the upper part of the concentration-response curve (CRC) for PE to the right; the pD2-value for PE was not significantly affected by pindolol. On the other hand, phentolamine (10(-6) mol/l) shifted the lower part of the CRC for PE more than the upper part. In the presence of both pindolol and phentolamine the curve was shifted to the right in a parallel manner. The time required for twitch relaxation was negatively correlated to the degree of PIE of PE in the presence of phentolamine but not pindolol. These results indicate that both beta- and alpha-adrenoceptors mediate the positive inotropic action in the ventricular muscle of the Japanese monkey and that in contrast to the action via beta-adrenoceptors the action via alpha-adrenoceptors is not accompanied by the "relaxant effect".

Animals↗
PubMed1975

Adrenoceptors in cardiac ventricular muscle and changes in duration of action potential caused by noradrenaline and isoprenaline.

1. On guinea-pig papillary muscle we investigated whether a prolonging effect of noradrenaline on the duration of the cardiac ventricular action potential (AP) is attributable to an action on beta-adrenoceptors. 2. Propranolol (5 X 10(-6) M), which itself shortens AP (at 90% repolarization level), inhibits both effects of noradrenaline on the AP, i.e. the sustained prolongation by low concentrations (10(-7)--10(-6)M) and the steady-state shortening which follows an initial prolongation by a high concentration (10(-5)M). In the presence of propranolol, the prlonging effect of noradrenaline is shifted to higher concentrations (10(-6)--10(-5)M). This prolongation of AP duration does not exceed the prior shortening effect by propranolol; it is not prevented by 10(-5)M phentolamine. 3. Phentolamine, which itself prolongs AP duration, inhibits neither the initial prolongation nor the steady-state shortening of the AP by 10(-5)M noradrenaline. Instead, the biphasic change in AP duration as well as the positive inotropic effect of 10(-5)M noradrenaline are enhanced in the presence of 3Z10(-6)M phentolamine. 4. The effect of isoprenaline on the duration of AP qualitatively resembles that of noradrenaline. In a concentration of 10(-8)M, isoprenaline produces a sustained prolongation of the AP; concentrations of 10(-7)M and 10(-6)M cause an initial prolongation which is followed by a steady-state shortening. These effects are inhibited by propranolol. 5. It is concluded that not only the steady-state shortening effect on AP duration by 10(-5)M noradrenaline but also the prolongation of AP, induced by lower noradrenaline concentrations (10(-7)--10(-6)M), are mediated solely by an action on beta-adrenoceptors.

Action Potentials↗
PubMed1975

Studies on the mechanism of the action of morphine on the peristalsis of guinea pig ileum in situ.

The influence of some drugs on the effect of morphine on the threshold pressure required to elicit peristalsis in the guinea pig ileum in situ was studied, in order to test the hypothesis that this effect of morphine is mediated by catecholamine release. Tachyphylaxis to this effect of morphine was confirmed. Pretreatemnt with two 8 mg/kg doses of reserpine, 24 and 48 hrs before the experiment, significantly reduced the effect of morphine on the pressure threshold. The i.v. administration of 10 mg/kg dl-Dopa re-established the effect of morphine in reserpinized animals to the level of the untreated controls. Pretreatment with guanethidine (15 mg/kg) decreased and even prevented this effect of morphine. Phentolamine pretreatment (10 mg/kg) also significantly inhibited the effect of morphine. Neither DCI nor propranolol influenced this morphine effect. Pretreatment with reserpine, guanethidine or phentolamine reduced the basic pressure threshold needed to elicit peristalsis. The possibility that the decrease of local circulation induced by hypotenison would reduce the local concentration of morphine was rejected because the same doses of guanethidine or phentolamine did not modify the effect of hexamethonium given i.v. in this preparation. All these results support the idea that the effect of morphine on intestinal peristalsis is mediated by a catecholamine acting on alpha-receptors, e.g. norepinephrine.

Animals↗
PubMed1983

Involvement of central dopamine receptors in the hypotensive action of pergolide.

The involvement of central dopamine receptors in the hypotensive action of the dopaminergic ergoline, pergolide was determined in anesthetized rats. Intravenous (i.v.) or intracerebroventricular (i.v.t.) administration of pergolide (12.5, 25 and 50 micrograms/kg) produced dose-dependent decreases in blood pressure. The magnitude of hypotension seen following either i.v. or i.v.t. administration of pergolide was similar. However, while both sulpiride (1 mg/kg, i.v.) as well as phentolamine (1 mg/kg, i.v.) antagonized the hypotensive action of i.v. pergolide, only sulpiride (1 mg/kg, i.v.t.) was able to antagonize the hypotension seen following i.v.t. administration of pergolide. Phentolamine (1 mg/kg, i.v.t.) did not alter the central hypotensive action of pergolide. In a separate group of rats, clonidine (25 micrograms/kg, i.v.t.) also produced a decrease in blood pressure. While phentolamine (i.v.t.) antagonized the central hypotensive action of clonidine, sulpiride (i.v.t.) did not have any effect on the action of clonidine. These results show that selective activation of central dopamine receptors was responsible for the hypotensive action of centrally-administered pergolide. In a separate group of rats greater splanchnic sympathetic nerve activity was measured. Intravenous pergolide produced similar hypotensive response as seen in previous groups, and this was accompanied by a concomitant decrease in the sympathetic nerve activity. The maximum fall in blood pressure (26 +/- 6 mm Hg) was correlated with a 40% reduction in sympathetic nerve activity. The return of blood pressure to control levels occurred after 60-70 min and was also associated with the return of sympathetic nerve activity to control levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Effects of renal nerve stimulation on vascular resistance in the toad kidney.

Stimulation of the renal nerves to the perfused toad kidney produced an increase in intravascular pressure. This response was always abolished by bretylium, indicating that it was mediated by adrenergic nerves. The response was usually reduced by tubocurarine, indicating that some of the fibres in the renal nerve trunks were preganglionic. The vasoconstrictor response was abolished by treatment with yohimbine or phenoxybenzamine, but was only partially reduced by phentolamine. It is postulated that adrenaline released from nerve terminals acts primarily on "junctional" adrenoceptors which are not antagonised by phentolamine. However, part of the vasoconstrictor response appears to be due to occupation of nearby "extra-junctional" receptors by neurally-released adrenaline: only this part of the response can be antagonised by phentolamine. The vasoconstrictor response was enhanced by propranolol in both summer and winter. This indicates that neurally-released adrenaline can occupy beta-adrenoceptors, to antagonise the effects of alpha-receptor occupation, at both times of the year. In this respect, the beta-receptors mediating the effects of renal nerve stimulation are different from those acted upon by perfused adrenaline. A non-adrenergic vasodilatation was sometimes revealed after abolition of the vasoconstrictor response, but the nature of the nerve fibres mediating this response could not be determined.

Action Potentials↗
PubMed1976

Alteration of shivering threshold in cold- and warm-adapted guinea pigs following intrahypothalamic injections of noradrenaline and of an adrenergic alpha-receptor blocking agent.

The role of adrenergic receptors in the central thermoregulatory pathways controlling the shivering activity has been studied in groups of cold-adapted (CA), warm-adapted (WA) and newborn (NB) guinea pigs, which show quantitative differences in shivering threshold. In the CA and NB animals, which normally start to shiver at lower mean body temperature levels than the WA controls, microinjection of noradrenaline (1 mug in 1 mul) into the noradrenaline-sensitive area of the anterior hypothalamus elicited shivering at higher body temperatures at which normally only WA animals start to shiver. Similar injections into the hypothalamus of WA animals did not induce any further shift of the shivering threshold. Microinjections of the alpha-receptor blocking agent phentolamine into the same brain area shifted the shivering threshold in all groups of animals to lower body temperatures, the shift being proportional to the injected dose of phentolamine. The CA and NB animals required higher doses of phentolamine to produce a change in shivering threshold. It is concluded that adrenergic alpha receptors are involved in the central thermoregulatory mechanisms which adjust the thresholds for the thermoregulatory reactions.

Adaptation, Physiological↗
PubMed1989

Inhibition of noradrenaline release in the rat brain cortex via presynaptic H3 receptors.

The effects of histamine and related drugs on the evoked tritium overflow from superfused rat brain cortex slices preincubated with 3H-noradrenaline were determined. Tritium overflow was stimulated electrically (3 Hz; slices superfused with normal physiological salt solution) or by introduction of CaCl2 1.3 mmol/l (slices superfused with Ca2(+)-free medium containing K+ 20 mmol/l). Histamine slightly decreased the electrically evoked 3H overflow in slices superfused in the presence of desipramine. The degree of inhibition obtained with histamine was doubled when both desipramine and phentolamine were present in the superfusion medium (pIC15 6.46). Under the latter condition, the evoked overflow was inhibited by the H3 receptor agonist R-(-)-alpha-methylhistamine and its S-(+) enantiomer (pIC15 7.36 and 5.09, respectively), but was not affected by the H2 receptor agonist dimaprit and the H1 receptor agonist 2-thiazolylethylamine (both at up to 32 mumols/l). The concentration-response curve of histamine was shifted to the right by the H3 receptor antagonists thioperamide, impromidine and burimamide (apparent pA2 8.37, 6.86 and 7.05, respectively), by the H2 receptor antagonist ranitidine (apparent pA2 4.27) and was not affected by the H1 receptor antagonist dimetindene (32 mumols/l). The inhibitory effect of R-(-)-alpha-methylhistamine on the evoked overflow was also counteracted by thioperamide. Given alone, none of the five histamine receptor antagonists affected the evoked overflow. In the absence of desipramine plus phentolamine, impromidine and burimamide facilitated the electrically evoked 3H overflow whereas thioperamide had no effect. The facilitatory effects of impromidine and burimamide were abolished by phentolamine, but not affected by desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Abnormalities of innervation of internal anal sphincter in fecal incontinence.

Physiological and histological studies have shown that the internal and sphincter is abnormal in idiopathic fecal incontinence. We have recently demonstrated that the in vitro contractile response of the internal anal sphincter to the sympathetic neurotransmitter noradrenaline is decreased in incontinence. In this study we have further defined this reduced sensitivity and provided more information about the intrinsic innervation in both the normal and the incontinent sphincter muscle. Muscle strips from 12 incontinent patients undergoing post and repair and from 11 controls undergoing rectal excision for low rectal carcinoma were studied. Responses to noradrenaline were recorded initially alone and then in the presence of phentolamine, an alpha-adrenoceptor blocker. In the presence of phentolamine, noradrenaline caused relaxation: there was no significant difference in the relaxation-response curves and the EC50 was the same in the two groups. These results demonstrate that the previously documented reduced sensitivity to noradrenaline is due to an altered sensitivity of the alpha-adrenoceptors. Electrical field stimulation produced relaxations in all muscle strips, but only in the controls was the magnitude of the relaxation significantly increased in the presence of phentolamine. This indicates that there is an alpha-adrenergic excitatory component of the response to electrical field stimulation of the intramural nerves, which was present in tissues from control patients but which was absent in tissues from patients with idiopathic fecal incontinence.

Anal Canal↗
PubMed1993

Dopamine receptor modulation of noradrenaline release by carmoxirole in human cortical kidney slices.

The effect of the dopamine D2-receptor agonist carmoxirole on noradrenaline release was investigated in human and rat cortical kidney slices. After preincubation with 3H-noradrenaline, the slices were electrically stimulated at 5 Hz in superfusion chambers, and the stimulation-induced (S-I) outflow of radioactivity was taken as the index of noradrenaline release. In human but not in rat cortical kidney slices, carmoxirole (0.03 microM) inhibited the S-I outflow of radioactivity. Carmoxirole (0.3 microM) also failed to inhibit the S-I outflow of radioactivity from human kidney slices. When alpha-adrenoceptors were blocked by the non-selective alpha-adrenoceptor antagonist phentolamine (1 microM), carmoxirole (0.03 microM, 0.3 microM) inhibited S-I outflow to a similar extent. The inhibitory effect of carmoxirole (0.03 microM) was prevented by the D2-receptor antagonist (-)-sulpiride (10 microM) but not by the D1-receptor antagonist SCH 23390 (1 microM) in human kidney slices. Phentolamine (1 microM) by itself induced a five-fold greater enhancement of the S-I outflow of radioactivity in rat than in human cortical kidney slices. The data suggest that activation of prejunctional D2-receptors by carmoxirole inhibits noradrenaline release from human renal sympathetic nerves. Carmoxirole in higher concentrations (0.3 microM) blocks inhibitory prejunctional alpha-autoreceptors, which seems to mask the inhibitory D2-receptor mediated effect. The different effects of phentolamine and carmoxirole in human and rat kidney may indicate a difference of the prejunctional alpha-autoreceptor mechanism in the two species.

Animals↗
PubMed1986

Ethanol influence on insulin secretion from isolated rat islets.

This study was done to delineate the role of alpha- and beta-adrenergic receptors and cyclic AMP in the mechanism of ethanol effects on insulin release from isolated islets. Rats were given an alpha-adrenergic blocker, phentolamine, or a beta-adrenergic blocker, propranolol. In addition, ethanol 1 g/kg was given intragastrically 1 h prior to sacrifice. Glucose mediated insulin release from isolated islets was enhanced by phentolamine and decreased by propranolol. Ethanol treatment inhibited glucose-induced insulin release from isolated islets of control rats as well as those given phentolamine and/or propranolol. Insulin release from isolated islets in response to dibutyryl-cyclic AMP was attenuated by ethanol. Theophylline enhanced glucose mediated insulin release from control islets but ethanol treatment produced a significant inhibition of insulin response. The data suggest that the site of action of the deleterious effects of ethanol on insulin release from isolated islets in rat does not involve adrenergic system and cyclic AMP.

Animals↗
PubMed2000

Mechanisms of blood pressure alterations in response to the Valsalva maneuver in postural tachycardia syndrome.

The postural tachycardia syndrome (POTS) is characterized clinically by orthostatic lightheadedness and tachycardia. When these patients perform a Valsalva maneuver, there is an excessive blood pressure increment after cessation of the maneuver (phase IV) that is sometimes associated with headaches. It is not known whether excessive phase IV is due to excessive peripheral vascular tone (an alpha-adrenergic mechanism) or is a manifestation of increased beta-adrenergic tone (hyperadrenergic state). The authors undertook a pharmacologic study evaluating the effect of intravenous phentolamine (alpha-adrenergic antagonist) and propranolol (beta-adrenergic antagonist) on the different phases of the Valsalva maneuver in a group of patients with POTS and age-matched normal control subjects. Patients with POTS had mean phases, when compared with controls, that were characterized by more negative II_E (p = 0.07), smaller II_L (p = 0.04), and significantly larger phase IV (p = 0.001). The effect of phentolamine was qualitatively and quantitatively different in POTS when compared with controls. Ten mg phentolamine in controls resulted in a significant accentuation of phase II_E (p = 0.001), attenuation of phase II_L (p = 0.002), and increase of phase IV (57.6 vs 30.7 mm Hg; p = 0.025). These changes resembled those of patients with POTS at baseline. In patients with POTS, the phase II abnormalities, already present, were further accentuated (p <0.001), and phase IV became smaller (50.6 vs 73.8 mm Hg; p = 0.09). Propranolol had no significant effect on phases II_E and II_L, but significantly reduced phase IV in both controls (p <0.05) and in patients with POTS (p <0.001) and improved the headache symptoms, when present, during and after phase IV. The authors conclude that phase IV is mainly under beta-adrenergic regulation and that the exaggerated phase IV in POTS is a result of a hyperadrenergic state.

Adrenergic alpha-Antagonists↗
PubMed1992

Spinal cord alpha-2 noradrenergic receptors mediate conditioned analgesia.

The present experiment investigated the effects of direct spinal administration of the monoaminergic receptor blockers yohimbine, phentolamine and methysergide on the expression of conditioned analgesia. Animals in the Paired group received classical conditioning trials in which one context was paired with footshock administration (1 mA shock for 15 s). Animals in the Unpaired control group were administered shock in a second, different, context. On the test day animals within each condition were administered saline (20 microliters), yohimbine (30 micrograms), phentolamine (30 micrograms), or methysergide (30 micrograms) prior to receiving a hot plate test (50 degrees C) in the context previously used to shock the Paired group. These ligands were administered into the spinal fluid through a chronic, indwelling spinal catheter. Animals in the Paired group which received saline displayed longer paw lick latencies than saline-treated animals in the Unpaired group. Yohimbine, but not phentolamine or methysergide, attenuated this conditioned analgesia. These results suggest that spinal cord noradrenergic substrates mediate conditioned analgesia, and that this mediation occurs specifically through the alpha-2 noradrenergic receptor.

Analgesia↗
PubMed1998

Age-related changes in sympathetic modulation of sensory nerve activity in rat skin.

OBJECTIVES: Sensory nerves play an important role in mediating neurogenic inflammation and subsequent tissue healing. A decrease in sensory nerve function with increasing age has been reported to correlate with poor tissue healing. Sympathetic nerves are known to modulate sensory nerve function, and changes in this modulation could also have important implications with ageing. The aims of this study were to examine the effect of different frequency electrical stimulation (ES) on the microvascular responses obtained to sensory nerve activation in young, aged and capsaicin-pretreated rats and modulation of these responses by sympathetic efferents. METHODS: Using laser Doppler flowmetry, vascular responses to antidromic ES of the sciatic nerve were monitored in the base of vacuum-induced blisters in the hind footpad. The non-selective alpha-adrenoceptor antagonist phentolamine (3 mg/kg, i.v.) was administered 20 min prior to ES. RESULTS: At high frequency ES (20V, 2ms, 15Hz for 1 min), the vascular response in old rats was significantly reduced (46 percent decrease, p < 0.05) compared to young control. At low frequency ES (20 V, 2 ms, 5 Hz for 1 min) however, older rats produced similar vascular responses to the young. Capsaicin-pretreated rats showed significantly reduced vascular responses to both high and low frequency ES, regardless of age. Pretreatment with phentolamine significantly increased the microvascular response in young rats at high (87 percent) and low (36 percent) frequency ES. In contrast, phentolamine significantly increased the ES-induced response in old rats at high frequency only (147 percent increase). CONCLUSIONS: The results suggest that the aged sensory nerve responds preferentially to low frequency ES and that sympathetic efferents exert an inhibitory modulatory effect on the vascular response evoked by sensory nerve stimulation. There are age-related changes in sympathetic modulation of sensory nerve-mediated responses which is dependent on stimulation frequency.

Adrenergic alpha-Antagonists↗
PubMed1999

Related changes in sympathetic activity, cerebral blood flow and intracranial pressure, and effect of an alpha-blocker in experimental subarachnoid haemorrhage.

We investigated the changes in sympathetic nerve activity (SNA) and cerebral blood flow (CBF) with or without increase in intracranial pressure (ICP) in the acute stage of experimental subarachnoid haemorrhage (SAH). ICP was increased or controlled by rapid or slow injection of blood and saline, and the effect of an alpha-blocker, phentolamine, was also investigated in each condition. Following marked increase in ICP induced by rapid injection of blood or saline, increase in intracranial and general SNA and decrease in CBF were observed. Both changes were significantly decreased in magnitude by prior administration of phentolamine. When increase in ICP was not induced, by slow injection of blood, both SNA and CBF decreased, and these changes were alleviated by phentolamine. However, when increase in ICP was not induced by saline, neither SNA nor CBF significantly changed. These findings suggest that marked increase in ICP is the primary cause of the pathological changes occurring immediately after SAH, and that the decrease in CBF in mild SAH without increase in ICP is caused by blood itself. Administration of an alpha-blocker may be effective in improving the abnormal sympathetic nervous system induced by marked increase in ICP.

Adrenergic alpha-Antagonists↗