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At least 19 recordsLinked to original sources
PubMed1979

Effect of the addition of a vasoconstrictor to local anesthetic solution on operative and postoperative bleeding, analgesia and wound healing.

A clinical study of local anesthetic solutions with and without epinephrine was conducted involving 32 healthy adults requiring removal of bony impacted mandibular third molars. The time elapsing from the administration of the anesthetic solution until analgesia was obtained was significantly shorter in the vasoconstrictor group (P less than 0.001). Additional anesthetic was necessary in 44% of the patients in the control group. The blood loss in the vasoconstrictor group was significantly lower (P less than 0.001) than in the group receiving anesthetic solution without the vasoconstrictor. No statistically significant difference in operation time between the groups was found, although the profuse bleeding in the control group impeded to some extent the surgical procedure. A positive correlation coefficient between operation time and blood loss of r = 0.65 in the vasoconstrictor group (P less than 0.006) and r = 0.77 in the control group (P less than 0.001) was found. Hemorrhage occurring 24 h postoperatively was recorded in 37% of the subjects in the vasoconstrictor group, and of these 83% revealed a healing of the socket by second intention.

Adolescent↗
PubMed1976

Vasoconstrictor actions of delta8- and delta9-tetrahydrocannabinol in the rat.

Cardiovascular effects of delta8- and delta9-tetrahydrocannabinol (THC) were studied after systemic intravenous administration and intra-arterial administration into a perfused vascular bed in the urethane-anesthetized rat. Intravenous administration of delta8- and delta9-THC produced dose-related transient increases in blood pressure followed by more prolonged hypotensive responses and bradycardia. Intra-arterial administration of delta8- and delta9-THC into the perfused hindquarters of the rat produced an increase in perfusion pressure indicative of vasoconstriction. The vasoconstrictor response to the cannabinoids corresponded temporally to a similar response produced by i.a. norepinephrine and was in contrast to the more prolonged vasoconstrictor responses produced by vasopressin. Phentolamine, in a dose which reduced the vasoconstrictor effect of norepinephrine by 90%, significantly reduced the response to i.a. delta9-THC while having no effect on the actions of i.a. vasopressin. It was demonstrated that reserpine pretreatment significantly reduced vasoconstrictor actions of i.a. tyramine and delta9-THC but did not alter the responses to norepinephrine. These data suggest that delta8- and delta9-THC have peripheral vasoconstrictor activity in the rat which may be mediated, in part, through a tyramine-like action on adrenergic nerve terminals.

Adrenergic alpha-Antagonists↗
PubMed1976

Modification by prostaglandins E1 and E2, indomethacin, and arachidonic acid of the vasoconstrictor responses of the isolated perfused rabbit and rat mesenteric arteries to adrenergic stimuli.

In isolated perfused rabbit mesenteric arteries, prostaglandin (PG) E1 and E2, 1-5NG/ML, did not alter the basal perfusion pressure, but reduced the vasoconstrictor responses to sympathetic nerve stimulation; the responses to injected norepinephrine were reduced by PGE1 and variably affected by PGE2. In contrast, in rat mesenteric arteries PGE1 and PGE2, 1-5 ng/ml, potentiated the vasoconstrictor responses to nerve stimulation and to injected norepinephrine. In rabbit mesenteric arteries, the inhibitor of PG synthesis, indomethacin, augmented the responses to sympathetic nerve stimulation and to injected norepinephrine, whereas in rat mesenteric arteries indomethacin inhibited the responses to both adrenergic stimuli. Arachidonic acid, a PG precursor, reduced the vasoconstrictor responses to sympathetic nerve stimulation and to injected norepinephrine in rabbit, whereas in rat, potentiation of the responses to adrenergic stimuli occurred. Since these effects of arachidonic acid were abolished by the simultaneous infusion of indomethacin, they appear to be mediated through conversion of arachidonic acid to PG. We conclude that prostaglandins modulate adrenergic transmission in mesenteric arteries and this effect is species dependent.

Animals↗
PubMed1978

Inhibitory effect of hypertonic mannitol on vasoconstrictor and vasodilator responses of isolated coronary arteries.

The effect of hypertonic mannitol on pressor responses to vasoactive agents was studied in isolated canine coronary arteries perfused with physiologic salt solution at a constant flow. When perfusion pressure was increased with 60 mM KCl, mannitol (50 mosM) consistently caused a decrease in perfusion pressure that lasted for at least 1 h. Withdrawal of mannitol from the perfusion media was associated with a vasoconstrictor response that was not prevented by alpha- or beta-adrenoceptor blockade or by the presence of either nitroglycerin or norepinephrine. Hypertonic mannitol also reduced the responsiveness of the isolated smooth muscle preparations to several different mechanistically unrelated vasodilator agents. The mechanism(s) responsible for the paradoxical ability of hypertonic mannitol to reduce vascular responsiveness to both vasoconstrictor and vasodilator interventions in isolated canine coronary arteries is not known, but future studies should be directed at elucidating it as well as determining whether similar phenomena occur in vivo.

Animals↗
PubMedDate not supplied

Selective arterial infusion of vasoconstrictors for control of traumatic splenic hemorrhage.

The spleen of each of 20 mongrel dogs was traumatized by creating a wedge laceration, and selective arterial infusion was then performed with vasopressin in four dogs, pituitrin in eight, and epinephrine in eight. Infusion therapy with vasoconstrictors controlled the splenic hemorrhage in 19 of 20 dogs. The 15 dogs surviving the experimental period of four to eight weeks showed well-healed scars at the sites of lacerations. Three dogs had small contracted spleens as a result of massive infarction. The results of this experiment indicate that splenic hemorrhage in the experimental dogs can be controlled by selective infusion of pituitrin or vasopressin, but is more effectively controlled with epinephrine.

Animals↗
PubMed1976

Beta2-adrenoceptors facilitating noradrenaline secretion from human vasoconstrictor nerves.

Isolated biopsy specimens of human peripheral arteries and veins, preincubated with 3H-(-)- noradrenaline (NA) to label the neural stores of NA, were used to study the Beta-adrenoceptors previously found to increase the secretion of 3H-NA evoked by electrical field stimulation of the adrenergic nerves of this tissue. The increase in nerve stimulation induced secretion of 3H-NA caused by 0.04 muM isoprenaline was prevented by 1 muM propranolol. This beta-blocking drug by itself slightly but significantly depressed the secretion of 3H-NA caused by nerve stimulation in the absence of isoprenaline. While the secretion of 3H-NA was not affected by known beta1-agonists, it was dose-dependently and reversibly increased by two different beta2-agonists. The effect of isoprenaline on 3H-NA secretion was not altered by a selective beta1-antagonist, but strongly reduced or abolished by a beta2-blocking drug. The results indicate that the beta-adrenoceptors involved in the control of NA secretion from the vasoconstrictor nerves of human omental blood vessels are only to a minimal extent stimulated by NA secreted from the nerves, and therefore do probably not mainly serve to mediate local positive feedback control of transmitter secretion; the receptors appear to be beta2 in nature.

Adrenergic beta-Antagonists↗
PubMed1976

A proposed mechanism for the biphasic vasoconstrictor responses to 5-hydroxytryptamine and methysergide in the rabbit ear artery.

Rabbit ear arteries were isolated and perfused at a constant flow rate so that the perfusate flowed into the fluid bathing the adventitial surface of the artery. Submaximal doses of intraluminally applied noradrenaline injected as a bolus into the perfusion fluid produced transient monophasic vascoconstrictor responses. In contrast, similarly administered 5-hydroxytryptamine (5-HT) or methysergide caused prolonged biphasic vascoconstrictor responses. The extraluminal/intraluminal potency ratios for noradrenaline, 5-HT and methysergide were 230, 15 and 6 respectively, which indicates that 5-HT methysergide are relatively more potent when administered extraluminally than noradrenaline. Cocaine (3-0 X 10(-5) mol litre-1) markedly increased the potency of extraluminally administered noradrenaline and converted the monophasic responses produced by noradrenaline to biphasic responses. It is concluded that under the experimental conditions used 5-HT and methysergide produced biphasic responses by an action on the medial smooth muscle firstly via the intraluminal surface and secondly an additional direct action via the adventitial surface. Noradrenaline's extraluminal potency is low because of its neuronal uptake and hence the responses are normally monophasic.

Animals↗
PubMed1976

Valsalva vasoconstrictor reflex in human hypertension in after beta-adrenoreceptor blockade in conscious rabbits.

1. A Valsalva-like manoeuvre was used to elicit graded rises in total peripheral resistance (TPR) in conscious rabbits. The rises were reflex and mediated through sympathetic constrictors. Propranolol infused at different rates reaching plasma concentrations up to 240 (SEM 33) ng/ml had no effect on this reflex but reduced mean arterial pressure. However, the response was attenuated by clonidine in a dose-dependent manner. 2. Valsalva manoeuvres were used to elicit graded sympathetically mediated rises in TPR index in twenty-nine subjects with mean arterial pressure ranging from 75 to 165 mmHg. Absolute sensitivity of the constrictor response increased with rising resting TPR index, resulting in some enhancement of constrictor responses in the hypertensive subjects. It seems likely that non-autonomic factors (e.g. vessel structure) rather than hyperactive neural constrictor effects are involved in the enhanced constrictor responses in essential hypertension.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Effects of some catecholamines on noradrenergic transmission in the rabbit ear artery.

1. The effects of noradrenaline, adrenaline, isoprenaline, dopamine and the N-methyl and alpha-methyl homologoues of dopamine were studied on tritium release and on vasoconstrictor responses to sympathetic nerve stimulation in isolated arteries of the rabbit ear after labelling noradrenergic transmitter stores with 3H-noradrenaline. These observations were made in the presence of cocaine (100 muM). 2. Noradrenaline (0-5 and 5 muM) inhibited transmitter release and abolished vasoconstrictor responses. A concentration of 0-05 muM had no effect on transmitter release, although the vasoconstrictor response was reduced and there was sometimes a vasodilator response. 3. Adrenaline in concentrations of 0-05, 0-5 and 5 muM decreased transmitter release and vasoconstrictor responses; sometimes there was a vasodilator response. 4. Isoprenaline in concentrations of 0-05, 0-5 and 5 muM did not affect transmitter release. Vasoconstrictor responses were either unaffected or enhanced by all concentrations of isoprenaline when infusions had been in progress for 15 min; but immediately after beginning the infusion of 5 muM isoprenaline, the response was reduced. 5. Dopamine (0-05, 0-5 and 5 muM) produced a concentration-dependent decrease in transmitter release, but vasoconstrictor responses were not reduced with infusions of 0-05 or 0-5 muM; during infusions of 5 muM, stimulation produced a vasodilator response.

Animals↗
PubMed1977

Prostaglandins in adrenergic transmission of isolated perfused rat pancreas.

In the isolated, perfused rat pancreas, prostaglandins (PGs) E1 and E2 1-5 ng/ml, reduced the vasoconstrictor responses to periarterial nerve stimulation and variably affected those to injected norepinephrine. Prostaglandin F2alpha had no consistent effect on the vasoconstrictor responses to both adrenergic stimuli. Stimulation of adrenergic nerves or administration of norepinephrine released a PGE-like substance from the perfused pancreas which was abolished by inhibitors of PG synthesis, acetylsalicylic acid, indomethacin, meclofenamate, and eicosa-5,8,11,14-tetraynoic acid. The latter three agents did not potentiate, but rather reduced the vasoconstrictor responses to both adrenergic stimuli. Arachidonic acid that was converted by the pancreas into PGE2 and PGF2alpha inhibited the vasoconstrictor responses to adrenergic stimuli. The latter effect of arachidonic acid was not altered by the simultaneous infusion of PG synthetase inhibitors. Although these results, which could be attributed to a direct effect of inhibitors of PG synthesis and arachidonic acid on adrenergic neuroeffector junction, fail to establish the role of endogenous PGs in modulating adrenergic responses in rat pancreatic vessels, they emphasize the differences in the effect of PGE1 and PGE2 on adrenergic responses in various vascular beds of the rat.

5,8,11,14-Eicosatetraynoic Acid↗