Intra-arterial Infusion Of Epinephrine Research Articles

Forearm vasodilator mechanisms during mental stress: possible roles for epinephrine and ANP

The contribution of epinephrine (Epi) to forearm vasodilator responses to mental stress was evaluated in 12 healthy men by comparing hemodynamic and plasma catecholamine responses to mental stress and to intravenous and intra-arterial infusions of epinephrine. Mental stress decreased forearm vascular resistance (FVR) by 45%, increased arterial Epi from 0.23 to 0.44 nmol/l in arterial plasma, and increased forearm norepinephrine overflow. Intra-arterial Epi infusion decreased FVR concentration dependently by up to 43%. Intravenous Epi infusion decreased diastolic arterial pressure and increased heart rate and systolic blood pressure dose dependently. FVR decreased by up to 39% at 4.60 nmol/l Epi in arterial plasma. The average Epi contribution to forearm vasodilation during mental stress was calculated to be between 9 and 30%, depending on if responses to stress were compared with intravenous or intra-arterial Epi infusion. Arterial atrial natriuretic peptide immunoreactivity increased by 23% during stress, supporting a vasodilator influence, whereas vasopressin immunoreactivity was unaffected. Thus secretion of Epi explains only part of the stress-induced forearm vasodilation. Intravenous infusion of Epi appears to activate sympathetic counterregulation.

Stimulation of Norepinephrine Release By Peripheral Presynaptic β-Adrenoceptors

Increases in plasma norepinephrine (NE) concentration induced by beta-agonist infusion have been taken as evidence for the existence of peripheral presynaptic beta-adrenoceptors, facilitating NE release. Concomitant hemodynamic changes, however, could invoke reflex mechanisms and thus hamper the interpretation of the results. We studied the presence of peripheral presynaptic beta-adrenoceptors by giving intra-arterial infusions of EPI in the forearm before and during uptake inhibition, and the effects of systemic infusions of very low-dose epinephrine (EPI) and isoproterenol (ISO) on hemodynamics and arterial and venous plasma NE concentrations. An i.a. infusion of EPI, 0.1 ng.kg-1.min-1, increased the net overflow of NE from 0.3 +/- 1.0 to 5.4 +/- 1.8 pmol.min-1 (M +/- SEM, p less than 0.05) and raised the calculated arterial plasma EPI concentration to 0.92 +/- 0.22 nmol.l-1. The uptake inhibition increased the net overflow of NE to 15.4 +/- 2.4 pmol.min-1 and during addition of EPI, 0.1 ng.kg-1.min-1, it further increased to 23.0 +/- 4.1 pmol.min-1 (p less than 0.05), while it decreased during addition of an effective beta-blocking dose of propranolol, 50 ng.kg-1.min-1 i.a., to 18.2 +/- 4.1 pmol.min-1 (n.s.). Systemic infusions of EPI and ISO increased blood pressure, heart rate, and forearm blood flow before significant changes in arterial or venous plasma NE concentrations were found. It is concluded that the increases in net NE overflow from the forearm during local EPI infusions indicate the presence of peripheral presynaptic beta-adrenoceptors which are responsive to physiologic concentrations of EPI. Systemic infusions of EPI or ISO elicit hemodynamic effects, and thus may invoke reflex mechanisms, before an influence on arterial or venous plasma NE concentration is found.

Role of the sympathetic nervous system in blood pressure maintenance and in the antihypertensive effects of calcium antagonists in spontaneously hypertensive rats.

In conscious spontaneously hypertensive rats (SHR), 2, 3, 6, 9, 12, and 16 months of age, the blockade of autonomic ganglia (with chlorisondamine) or postjunctional alpha 1-adrenergic receptors (with prazosin) or the depletion of peripheral norepinephrine stores (with syrosingopine), in contrast to the blockade of alpha 2-adrenergic receptors (with yohimbine, rauwolscine), produced a sustained decrease in the directly measured mean tail artery blood pressure. In 3- to 9-month-old SHR, the fall in blood pressure after prazosin pretreatment was significantly smaller than that after chlorisondamine or syrosingopine pretreatment. In ganglion-blocked SHR, prazosin decreased blood pressure only when this parameter had been elevated by an intra-arterial infusion of epinephrine or norepinephrine. In contrast, under the same experimental conditions, yohimbine or rauwolscine administration failed to modify the pressor effects of either phenylephrine or epinephrine but partially reduced those of norepinephrine and, unlike prazosin, strongly antagonized those of B-HT 920. In either intact or ganglion-blocked SHR, a 30-minute intra-arterial infusion of diltiazem at 100.0, but not 25.0, micrograms/kg/min significantly decreased baseline mean tail artery blood pressure. In ganglion-blocked SHR, the smaller dose of diltiazem antagonized by 40 and 80% the pressor effects of norepinephrine and B-HT 920, respectively, but failed to change the vasoconstrictor responses of phenylephrine, epinephrine, or vasopressin, which were, however, reduced by the higher dose of diltiazem. These results indicate that, in conscious adult SHR, norepinephrine released by peripheral sympathetic nervous terminals and humorally borne epinephrine stimulate almost exclusively post-junctional alpha 1-adrenergic receptors. The latter findings may account for the lack of blood pressure-lowering effects of the studied calcium antagonists at doses that effectively antagonize alpha 2-adrenergic receptor-mediated vasoconstriction in conscious SHR.

Effects of epinephrine on branchial and renal calcium handling in the rainbow trout.

Acute exposure of rainbow trout (Salmo gairdneri) to low external calcium (25 microM) caused an immediate but transient increase in plasma epinephrine concentration that may have been related to a concomitant depression of blood pH. Intra-arterial infusion of epinephrine at normal ambient calcium levels (0.35 mM) for 4 h caused circulating levels of epinephrine to rise from 2.9 X 10(-9) to 8.0 X 10(-8) M but did not affect norepinephrine levels, or branchial unidirectional calcium fluxes. Active (ATP-dependent) calcium transport across basolateral plasma membranes prepared from gill epithelial cells was not affected by pretreatment of fish with epinephrine or by direct application of epinephrine or cAMP, in vitro. Epinephrine infusion elevated urine flow rate, decreased urine pH, and increased urine phosphate levels significantly. Net renal calcium efflux increased significantly as a result of the increased urine flow rate. It is concluded that epinephrine does not stimulate branchial calcium uptake or renal conservation of calcium in rainbow trout at normal external calcium levels and therefore we cautiously suggest that epinephrine is unlikely to be involved in calcium balance during periods of exposure to low external calcium. Instead, epinephrine may play a role in compensating the acid-base disturbances and the increased branchial water influx that are associated with exposure to low ambient calcium.

Evaluation of presynaptic alpha-receptor function in the canine renal vascular bed.

The functional significance of presynaptic alpha-receptor modulation of sympathetic nerves was examined in vivo in the canine renal vascular bed. In pentobarbital-anesthetized dogs, the vasoconstrictor response to renal nerve stimulation and exogenous norepinephrine was compared before and during intra-arterial infusions of epinephrine, oxymetazoline, clonidine, and norepinephrine. Only epinephrine produced a modest decrease in stimulation-induced vasoconstriction at 1 Hz. After pretreatment with desipramine, intra-arterial infusions of epinephrine or norepinephrine did not alter stimulation-induced vasoconstrictor responses relative to exogenous norepinephrine. Further, neither yohimbine nor phentolamine (10(-9) to 10(-3) g, intra-arterial) produced a distinctly increased vasoconstrictor response to nerve stimulation relative to exogenous norepinephrine. Thus, studies using alpha-receptor agonists, antagonists, and inhibition of neuronal uptake failed to reveal a physiologically significant alpha-receptor-mediated negative feedback mechanism for stimulation-induced vasoconstriction in the canine renal vascular bed.

Hypotension and thirst in rats after isoproterenol treatment

Drinking induced in rats by systemic isoproterenol treatment is markedly attenuated after bilateral nephrectomy. The present experiments demonstrate that the hypotension produced by iso-proterenol treatment was more profound, and lasted much longer, in nephrectomized rats than in intact animals. When arterial blood pressure was partially elevated by central administration of angiotensin II or carbachol (Experiment 1) or by intraarterial infusion of epinephrine (Experiment 2), drinking behavior was restored in the nephrectomized animals and their water intakes approximated the amounts consumed by intact rats given isoproterenol. In general, an inverted U-shaped curve was found to define the relation between blood pressure and water intake in rats after isoproterenol treatment. Drinking was most probable when mean arterial blood pressures were in the range of 70–85 mm Hg, whereas rats were unlikely to drink when blood pressures were much below or above this range. These findings indicate that isoproterenol-induced thirst is not dependent on a renal dipsogen, and suggest instead that the hypersecretion of renin that occurs in intact rats is simply permissive of drinking behavior by modulating the hypotensive effects of the drug treatment.

Traumatic Hemobilia: A Complication of Percutaneous Liver Biopsy

Two patients with hemobilia are presented. The first patient, with alcoholic liver disease, had a percutaneous liver biopsy. Subsequently he developed jaundice, with an enlarged tender gallbladder, biliary colic, and gastrointestinal bleeding. Hemobilia was demonstrated by superselective hepatic angiography and bleeding was stopped by intraarterial infusion of epinephrine and propranolol. The second patient, with primary biliary cirrhosis at an advanced stage, had a percutaneous liver biopsy followed by gastrointestinal bleeding, severe abdominal pain, and finally death. In both cases hemobilia was suggested by gastroduodenoscopy.

Primate gastric circulation: effects of catecholamines and adrenergic blockade.

The effects of intra-arterial injections and infusions of epinephrine, norepinephrine, and isoproterenol on gastric blood flow were studied in anesthetized baboons. Blood flow was measured electromagnetically before and after adrenergic blockade. The results for injected epinephrine and norepinephrine indicate these agents to be pure vasoconstrictors in the primate gastric circulation, and this response is attenuated by alpha-adrenergic blockade with phenoxybenzamine. Isoproterenol is a pure vasodilator, and its response is attenuated following beta-adrenergic blockade with propranolol. Intra-arterial infusions of epinephrine and norepinephrine (.05 mug kg-1 min-1) resulted in sustained vasoconstriction with no evidence of autoregulatory escape and no postinfusion "over-shoot." This study suggests that epinephrine and norepinephrine might provide alternatives to vasopressin as a vasoconstrictor for the control of upper gastrointestinal bleeding.

Congenital renal arteriovenous malformation: Angiography in its diagnosis

Two patients with renal arteriovenous malformations are presented along with the distinct changes shown by urography, arteriography, and pharmacoangiography. The relevant roentgen signs in such patients include multiple small cobblestone-like indentations caused by well-formed vascular channels projecting into the collecting structures, no angiographic or urographic evidence of a mass displacing the intrarenal vessels or collecting structures, normal sized arteries and veins leading to and from the malformation, and a decrease in size of the malformation after intra-arterial infusion of epinephrine. These patients may have flank pain or hematuria later in life or may remain asymptomatic. A complete urographic and angiographic examination will help to determine the appropriate therapy. Corrective surgery is usually reserved for symptomatic patients and, when indicated, require only surgical ligation of the vessels feeding and draining the malformation.

Blood flow in the testis of the conscious ram measured with krypton85.

Krypton 85 in saline was injected through a catheter into the testicular artery or directly into the testis, and the radioactivity in the testis measured by external monitoring with a scintillation detector. The disappearance of Kr 85 from the testis followed a single exponential curve during a fiftyfold decrease in radioactivity and showed no delay before beginning to fall. The partition coefficient for Kr 85 between testis and blood was 0.85. The mean nutrient blood flow through the testes of 11 conscious rams was 8.4 ml/100 g/min (66 observations; standard deviation between rams 2.4; standard deviation of estimates on individual rams 2.1). Testicular blood flow was reduced by intraarterial infusions of epinephrine or norepinephrine, practically unaffected by acetylcholine, and increased by isoproterenol. Testicular blood flow was not changed by raising deep testicular temperature from the normal range (32 to 34°C) to body temperature (39 to 40°C). These results are discussed with a view to explaining, in vascular terms, the damage to spermatogenesis caused by elevation of environmental temperature.