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PubMed1987

Comparison of norepinephrine- and veratrine-induced phosphoinositide hydrolysis in rat brain.

Stimulation of phosphoinositide hydrolysis by depolarization with veratrine was compared to that produced by stimulation of alpha-1 adrenoceptors by norepinephrine. The phosphoinositides in rat cerebral cortex were labeled with [myo-3H]inositol and the effects of the drugs on the formation of the following inositol phosphates were determined: inositol 1-phosphate (IP); inositol 1,4-bisphosphate (IP2); mixture of inositol 1,4,5-trisphosphate and inositol 1,3,4-trisphosphate (IP3). Termination of the hydrolysis by trichloroacetic acid resulted in lower basal levels and more reproducible results than termination by water lysis or a chloroform-methanol mixture (CHCl3-MeOH). The amounts of IP and IP2 formed by a maximal concentration of veratrine were about one half of that formed by a maximal concentration of norepinephrine although the amount of IP3 formed after stimulation by veratrine was only about 10% of that produced by norepinephrine. The increase in IP was linear with time (30 min) for both norepinephrine and veratrine. Stimulation of IP2 and IP3 formation by veratrine reached a maximum at 5 min whereas that produced by norepinephrine continued to increase for 30 min. Blockade of voltage-dependent calcium channels with manganese produced nearly complete antagonism of the veratrine response while only partially antagonizing the norepinephrine response. Norepinephrine-induced IP2 formation was less sensitive to manganese than was formation of IP or IP3. These data suggest that either veratrine and norepinephrine cause hydrolysis of different pools of phosphoinositide or that the hydrolysis occurs by different mechanisms. The data also suggest that IP and IP2 may be produced directly from phosphatidylinositol and phosphatidylinositol 4-phosphate rather than solely as a metabolite of IP3.

Animals↗

PubMed1986

Verapamil, diltiazem and nifedipine block the depolarization-induced potentiation of norepinephrine contractions in rabbit aorta and porcine coronary arteries.

The effectiveness of verapamil, diltiazem and nifedipine in reducing potassium-induced enhancement of vascular responses to norepinephrine was studied in rabbit aorta and porcine coronary arteries. At multiple levels of external potassium concentration (4-28 mM), norepinephrine concentration-response curves were performed. Whereas the tissue was only slightly depolarized (about 5 mV) by an increase in external potassium to 20 mM, the norepinephrine response was markedly potentiated. For example, the EC50 of norepinephrine in aortic rings was reduced from 4.7 X 10(-8) M in 4 mM potassium to 4.7 X 10(-9) M in 20 mM potassium. Calcium channel blockers reduced potassium- and calcium-induced contractions, the IC50 being 6 X 10(-8) M for verapamil, 5 X 10(-7) M for diltiazem and 3 X 10(-9) M for nifedipine. These concentrations only minimally reduced norepinephrine contraction in 4 mM potassium but virtually abolished the depolarization-induced potentiation of the norepinephrine contraction. Even short exposures to levels of potassium, which resulted in little or no contraction by themselves, markedly potentiated the norepinephrine contraction. Therefore, the abolition of this potentiation by calcium channel blockers cannot be explained by a reduction of potassium-induced contraction. Similar observations were made in porcine coronary arteries. Thus, the potency of calcium channel blockers against norepinephrine-induced contractions is markedly increased in depolarized vascular smooth muscle. Calcium channel blockers may be especially effective in preventing enhanced vascular contractions resulting from physiological concentrations of catecholamines in partially depolarized vascular smooth muscle.

Animals↗

PubMed1985

Ascorbic acid regulation of norepinephrine biosynthesis in isolated chromaffin granules from bovine adrenal medulla.

The effect of ascorbic acid on the conversion of dopamine to norepinephrine was investigated in isolated chromaffin granules from bovine adrenal medulla. Ascorbic acid was shown to double the rate of [3H]norepinephrine formation from [3H]dopamine, despite no demonstrable accumulation of ascorbic acid into chromaffin granules. The enhancement of norepinephrine biosynthesis by ascorbic acid was dependent on the external concentrations of dopamine and ascorbate. The apparent Km of the dopamine beta-hydroxylation system for external dopamine was approximately 20 microM in the presence or absence of ascorbic acid. However, the apparent maximum velocity of norepinephrine formation was nearly doubled in the presence of ascorbic acid. By contrast, the apparent Km and Vmax of dopamine uptake into chromaffin granules were not affected by ascorbic acid. Norepinephrine formation was increased by ascorbic acid when the concentration of ascorbate was 200 microM or higher; a concentration of 2 mM appeared to induce the maximal effect under the experimental conditions used here. The effect of ascorbic acid on conversion of dopamine to norepinephrine required Mg-ATP-dependent dopamine uptake into chromaffin granules. In contrast to ascorbic acid, other reducing agents such as NADH, glutathione, and homocysteine were unable to enhance norepinephrine biosynthesis. These data suggest that ascorbic acid provides reducing equivalents for hydroxylation of dopamine despite the lack of ascorbate accumulation into chromaffin granules. These findings imply the functional existence of an electron carrier system in the chromaffin granule which transfers electrons from external ascorbic acid for subsequent intragranular norepinephrine biosynthesis.

Adenosine Triphosphate↗

PubMedDate not supplied

Actions and interactions of norepinephrine and acetylcholine on sinus node potassium movements.

The influence of norepinephrine and/or acetylcholine on K uptake of the guinea pig sinus node was investigated. Both "high" (10(-6) M) and "low" (10(-9) M) mediator concentrations were employed. The following results were obtained: 1) high concentration of norepinephrine increased K uptake; 2) high concentration of acetylcholine had a similar effect; 3) simultaneous exposure to both mediators did not lead to summation of the effects; 4) low concentration of norepinephrine depressed K uptake; 5) high concentration of acetylcholine overcame the inhibitory effect of the small concentration of norepinephrine; 6) 2-deoxy-D-glucose did not abolish the stimulating effect of acetylcholine on potassium uptake; and 7) strophanthidin abolished the stimulatory effect of norepinephrine, but not that of acetylcholine. The following conclusions are drawn: 1) both neuromediators in suitable concentrations increase K uptake in the sinus node; 2) the mechanism of such an increase is different, norepinephrine increasing the active and acetylcholine increasing the passive potassium transport; 3) a low concentration of norepinephrine depresses K uptake; and 4) when the two mediators are administered together, acetylcholine suppresses the action of norepinephrine on K transport.

Acetylcholine↗

PubMed1984

Induction of Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels by norepinephrine activation of alpha-1 receptors.

This study was undertaken to determine which alpha adrenoceptor subtype(s) is involved in the activation of isolated rat aorta and mesenteric resistance vessels by norepinephrine and to ascertain whether norepinephrine-induced Ca++ influx into the smooth muscle is activated by one alpha adrenoceptor subtype while intracellular Ca++ release is mediated by the other subtype. The concentration-response curves for prazosin and yohimbine inhibition of norepinephrine-induced 45Ca influx, intracellular Ca++ release (as judged from contractions in Ca++-free solution) and contraction in the rat aorta indicate that the norepinephrine activation of the alpha-1 adrenoceptor was responsible for both Ca++ mobilization processes leading to norepinephrine contraction of this tissue. Contractions induced by norepinephrine in the isolated rat mesenteric resistance vessels demonstrated a phasic component, which was shown to be primarily dependent on intracellular Ca++ release, and a tonic component, which was completely dependent on Ca++ influx. Prazosin was three orders of magnitude more potent than yohimbine in inhibiting both components of the norepinephrine contracture in these vessels. We conclude that norepinephrine activation of alpha-1 adrenoceptors is responsible for both Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels.

Animals↗

PubMed1982

Potentiation of the ganglionic blocking action of norepinephrine by cocaine.

Concentration-response curves for the blocking action of norepinephrine were determined in the isolated stellate ganglion of the hamster. The blocking effect of norepinephrine on the postganglionic compound action potential from preganglionic nerve stimulation at 0.2 Hz was reduced by phentolamine (10(-5) M), but was not altered by propranolol (10(-6) M). Cocaine (10(-6) and 10(-5) M) increased the sensitivity of the ganglion to norepinephrine. These concentrations of cocaine produced less than 25% blockade when applied alone. The local anesthetic, procaine, did not change the sensitivity of the ganglion to norepinephrine. The blockade by norepinephrine in the presence of cocaine was antagonized by phentolamine and unaffected by propranolol. The time course of the blockade by norepinephrine was more rapid in onset and slower in recovery in the presence of cocaine. If it is assumed that cocaine is blocking norepinephrine uptake into cells within the ganglion, these results indicate that the catecholamine uptake mechanism is involved in terminating the blocking action of exogenously applied norepinephrine.

Animals↗

PubMed1982

Prolonged infusion of norepinephrine in the conscious dog: effects on blood pressure, heart rate, renin, angiotensin II, and aldosterone.

Eight conscious beagle dogs were given continuous intravenous infusions for 4 weeks: 0.9% NaCl solution was given for the first week; norepinephrine for the following 2 weeks, (at 125 ng/kg/min or at 250 ng/kg/min each in four dogs), 0.9% NaCl for the final week. Norepinephrine at the lower dose did not raise blood pressure but did reduce heart rate significantly. The higher rate of norepinephrine infusion raised blood pressure, but for the first week of infusion only, and again heart rate was reduced significantly during both weeks. Blood pressure fell on stopping infusion whether or not it had been raised previously. Plasma concentrations of renin, angiotensin II, and aldosterone were reduced, but the changes were of borderline significance only. These changes occurred when plasma concentrations of norepinephrine were increased four-sevenfold. The acute response to high infusion rates of norepinephrine (500, 1,000, and 2,000 ng/kg/min each for 1 h) was tested at weekly intervals in each dog. At each of these high rates of infusion, blood pressure, renin and angiotensin II, and haematocrit increased while plasma potassium concentration and heart rate fell. These changes occurred with increases of plasma norepinephrine greater than 14-fold. Prolonged infusion of norepinephrine did not alter the relation between plasma norepinephrine and arterial pressure as assessed by these dose-response studies.

Aldosterone↗

PubMedDate not supplied

Effects of selective and nonselective beta-agonists on plasma potassium and norepinephrine.

The effects of graded infusions of the beta-agonists isoproterenol (nonselective), l-prenalterol (beta 1-selective), and salbutamol (beta 2-selective) on plasma potassium and norepinephrine were compared in subjects with borderline hypertension. Potassium levels fell with all three agonists, and norepinephrine levels rose with isoproterenol and salbutamol. These effects on potassium and norepinephrine were closely correlated and occurred at the same dose ranges as the cardiovascular responses. The fall in plasma potassium was probably caused by activation of beta-receptors, mainly on skeletal muscle, with subsequent stimulation of active sodium-potassium transport across the cellular membrane. The rise in plasma norepinephrine may have been due to activation of beta-receptors on sympathetic nerve endings. Activation of these presynaptic receptors is known to enhance the release of norepinephrine during nerve stimulation. For a given increase in heart rate and cardiac contractility, as measured by the heart rate-corrected duration of total electromechanical systole, which are mainly beta 1-responses, the effects on potassium and norepinephrine were in the order: salbutamol greater than isoproterenol greater than prenalterol. beta-Blockade with propranolol (nonselective), 80 mg four times a day, or atenolol (beta 1-selective), 100 mg once a day, antagonized the hypokalemic effect of isoproterenol as well as the rise in norepinephrine, but when isoproterenol was infused in doses high enough to overcome the blockade of the heart rate response, the effects on norepinephrine and potassium were abolished by propranolol and not by atenolol. Thus, the receptors in question appear to be of the beta 2-subtype.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗

PubMed1983

Functional evidence for two stereochemically different alpha-2 adrenoceptors regulating central norepinephrine and serotonin release.

The effects of norepinephrine and of various alpha adrenoceptor antagonists on the depolarization-evoked release of norepinephrine and 5-hydroxytryptamine were studied in nerve terminals isolated from rat cerebral cortex, preincubated with the radioactive amines and exposed during superfusion to 15 mM KCI. Exogenous norepinephrine inhibited in a concentration-dependent way both the release of norepinephrine and that of serotonin. The inhibitory effect of norepinephrine was antagonized by yohimbine and mianserin, but not by prazosin, indicating the involvement of alpha-2 adrenoceptors. The two enantiomers of mianserin were examined as alpha-2 adrenoceptor antagonists in the two release systems. Only (+)-mianserin was an effective antagonist at the alpha-2 autoreceptors mediating regulation of norepinephrine release; (-)-mianserin was inactive. In contrast, both enantiomers antagonized exogenous norepinephrine at the alpha-2 adrenoceptors regulating 5-hydroxytryptamine release. It can be concluded that the alpha-2 adrenoceptors which regulate, respectively, norepinephrine and serotonin release in the cerebral cortex are located on presynaptic nerve terminals and represent two stereochemically different subtypes of alpha-2 adrenoceptors.

Animals↗

PubMed1983

Demonstration of an alpha adrenoceptor-mediated inotropic effect of norepinephrine in rabbit papillary muscle.

Other investigators have claimed that norepinephrine does not evoke a significant alpha adrenergic inotropic effect in rabbit ventricular myocardium in contrast to some other mammalian species, indicating an important functional limitation of the cardiac alpha adrenoceptors. We therefore characterized the inotropic effects of norepinephrine in isometrically contracting rabbit papillary muscles. We studied both contraction and relaxation by measuring developed tension and its first and second derivatives. Both the influence of propranolol and prazosin on concentration-effect curves of norepinephrine and the qualitative characteristics of the responses revealed that norepinephrine evoked both alpha and beta adrenergic inotropic effects. The alpha adrenergic response to norepinephrine was qualitatively markedly different from the beta adrenergic effect and qualitatively similar to the alpha adrenergic effect of phenylephrine which was also characterized for comparison. Although the alpha adrenergic response to norepinephrine was marked, the beta adrenergic effect was the dominating one when norepinephrine was administered alone. Thus, the beta adrenergic effect had to be extensively blocked to reveal the prazosin-sensitive alpha-1 adrenergic response. It is concluded that also in rabbit papillary muscles, norepinephrine evokes inotropic effects through both alpha and beta adrenoceptors.

Animals↗

PubMed1982

Specific uptake of norepinephrine and dopamine by homogenates of rat cerebral cortex after locus ceruleus lesion.

Unilateral injection of 6-hydroxydopamine into the locus ceruleus led to long lasting depletion of norepinephrine in the ipsilateral parietal cerebral cortex of the rat up to 8 weeks after injection. The uptake of both norepinephrine and dopamine by homogenates of parietal cortex was decreased markedly on the ipsilateral, but not on the contralateral, side. The uptake of four other neurotransmitter candidates or precursors was unaffected by the lesion. Desipramine (DMI) markedly inhibited the uptake of both norepinephrine and dopamine by cortical preparations from the contralateral side and from control rats, but this effect was not seen in preparations from the norepinephrine-depleted, ipsilateral cortex. The decreases DMI-sensitive uptake of norepinephrine or dopamine was highly correlated with decreased norepinephrine in the ipsilateral cortex. These results suggest that the specific uptake of norepinephrine and dopamine is a valid marker of noradrenergic innervation of the parietal cortex and that dopamine seems to be accumulated primarily by norepinephrine terminals in this region. Two and 8 weeks after locus ceruleus lesion, a DMI-insensitive, benztropine-sensitive dopamine uptake becomes apparent in ipsilateral cortical preparations, This may represent proliferation or increased function of dopaminergic cortical projections, compensating for noradrenergic denervation.

Animals↗

PubMed1994

[Anesthetic management for pheochromocytoma resection: a comparison of epinephrine predominant and norepinephrine predominant pheochromocytoma].

Eleven patients with pheochromocytoma were divided into two groups; epinephrine predominant group (n = 4) and norepinephrine predominant group (n = 7). In each case, anesthesia was given using only inhalational anesthetics and adenosine triphosphate (ATP); and the same strategy was used to control cardiovascular variables. If arterial blood pressure, pulmonary artery pressure, central venous pressure or heart rate failed to be controlled with the strategy before the tumor resection, phentolamine, trinitroglycerine or propranolol was used. After the tumor resection, if decreasing the anesthetic concentration, cessation of ATP infusion and rapid intravenous infusion could not maintain the systolic arterial blood pressure above 80 mmHg, norepinephrine was infused. Maximum heart rate and arterial blood pressure during the tumor exploration were similar in both groups. No ventricular arrhythmias were recognized in any case. The frequency of usage of the cardiovascular depressants was not different between the two groups. In the norepinephrine predominant group, five cases required norepinephrine infusion after the tumor resection, but in the epinephrine predominant group, none required the norepinephrine infusion. Desensitization of alpha 1 adrenergic receptor induced by continuous high plasma norepinephrine concentration, was considered to decrease vascular resistance. In conclusion, except for the hypotension after the tumor resection in the norepinephrine predominant pheochromocytoma, both epinephrine predominant and norepinephrine predominant pheochromocytoma could be managed with similar anesthetic risks.

Adrenal Gland Neoplasms↗

PubMed1993

Augmented coronary blood flow response to intracoronary norepinephrine after ventricular sympathectomy.

BACKGROUND: Ventricular sympathetic denervation may occur as a result of myocardial infarction or heart transplantation. The present study examined the time-dependent effects of surgical ventricular sympathectomy on coronary flow and myocardial contractile responses to intracoronary norepinephrine administration in conscious dogs. METHODS: Adult mongrel dogs (18-26 kg), were either ventricular sympathectomized or served as a sham-operated control. Animals were studied 2, 4, and 8 weeks after surgery. Measurements of left ventricular systolic pressure (LVSP), maximum rate of left ventricular pressure generation (dP/dtmax), maximum negative rate of segmental shortening (-dL/dtmax), heart rate, and mean circumflex flow velocity (CFV) were obtained before and after bolus administration of norepinephrine into the circumflex artery in doses ranging from 0.01 to 0.50 microgram. RESULTS: Intracoronary norepinephrine administration caused significant increases in LVSP, dP/dtmax, -dL/dtmax, heart rate, and CFV. After reaching a peak or maximum response, these variables returned to their respective preinjection values, except for CFV, which exhibited a biphasic response. CFV continued to decline below control levels, indicating a vasoconstrictor response to norepinephrine, before returning back to preinjection levels. With the 0.5-microgram dose of intracoronary norepinephrine, the percent increases in CFV were 124% +/- 25% and 105% +/- 15% (P < 0.05) at 2 and 4 weeks respectively, compared with the sham-operated controls, which only increased 56% +/- 15%. The response to the 0.5-microgram dose of norepinephrine at 8 weeks (61% +/- 6%) was not significantly different from control. Elevated myocardial contractile responses in the sympathectomized hearts were also evident at 2 and 4 weeks, but not at 8 weeks. The vasoconstrictor response to norepinephrine administration was not significantly different between sympathectomized and sham-operated hearts. Finally, there was no difference in the change in LVSP, dP/dtmax, or heart rate between any of the groups at any of the doses. CONCLUSIONS: These results suggest that a supersensitivity to the coronary functional hyperemic response after intracoronary norepinephrine is present in ventricular sympathectomized hearts, but a coronary constrictor supersensitivity does not exist.

Animals↗

PubMed1993

[Effect of elevated plasma norepinephrine on electrocardiographic changes in subarachnoid hemorrhage].

We compared electrocardiographic abnormalities and plasma norepinephrine concentration in 40 patients with subarachnoid hemorrhage within the first 24 hours, at 72 hours, and after 1 week. In the 20 patients with high plasma norepinephrine concentrations within the first 24 hours, sinus tachycardia and negative T waves were more frequently seen than in the 20 patients with normal plasma norepinephrine concentrations. After 72 hours, only sinus tachycardia was found with increased frequency in the 26 patients with high plasma norepinephrine concentrations. Although 24 patients had high plasma norepinephrine concentrations after 1 week, we found no difference in the frequency of electrocardiographic abnormalities as compared with patients with normal plasma norepinephrine. QT prolongation, U waves, ST depression, and arrhythmias were found with similar frequency in patients with high and normal plasma norepinephrine concentrations. We conclude that, with the exception of sinus tachycardia and negative T waves, other electrocardiographic changes in patients with subarachnoid hemorrhage do not depend on elevated plasma norepinephrine concentrations.

Adult↗

PubMed1993

Prejunctional modulation of norepinephrine release in the human iris-ciliary body.

PURPOSE: To characterize the prejunctional mechanisms that control the impulse-evoked release of norepinephrine in the isolated, superfused human iris-ciliary body. METHODS: Human iris-ciliary body tissue segments were preincubated with 3H-norepinephrine, superfused and electrically-stimulated in vitro to evoke the discharge of 3H-norepinephrine. The effects of prejunctional modulators on evoked 3H-norepinephrine overflow were evaluated. RESULTS: Stimulation-evoked (but not spontaneous) 3H-norepinephrine release was inhibited by alpha 2-adrenergic, muscarinic, dopaminergic, neuropeptide Y, and prostaglandin agonists and was enhanced by angiotensin II. Agonist-induced effects on 3H-norepinephrine overflow were blocked by selective antagonists, where available. Yohimbine and atropine alone enhanced 3H-norepinephrine output, suggesting that prejunctional alpha 2-adrenergic and muscarinic receptors undergo tonic activation by endogenously released neurotransmitters. CONCLUSIONS: Human ocular sympathetic nerves express inhibitory alpha 2-adrenergic, muscarinic, dopaminergic, prostaglandin, and neuropeptide Y receptors and facilitatory angiotensin II receptors that control the impulse-evoked release of 3H-norepinephrine. These receptors may be useful targets for pharmacologic manipulation of the adrenergic system in vivo.

Adolescent↗

PubMed1977

Inhibition of norepinephrine uptake by phenoxybenzamine and desmethylimipramine in the isolated guinea-pig atrium.

The effects of phenoxybenzamine (PBZ) and desmethylimipramine (DMI) on 3H-norepinephrine uptake by sympathetic nerve terminals of isolated guinea-pig left atrium has been investigated in the absence and in the presence of norepinephrine, tyramine, cocaine and isoproterenol, used as protecting agents. PBZ blocked the uptake of 3H-norepinephrine by 50% at a concentration of 3 micronM. For DMI the ID50 was approximately 0.33 micronM. These doses were used for all subsequent protection experiments. When incubation with PBZ was carried out in the presence of tyramine (574 micronM) the blocking effects of PBZ were completely reversed. In contrast, tyramine was unable to protect against 3H-norepinephrine uptake blockade elicited by DMI. Norepinephrine (20 micronM) or cocaine (29 micronM) afforded no protection against DMI-induced 3H-norepinephrine uptake blockade, but both agents significantly protected against blockade of PBZ. Isoproterenol (40 micronM) was unable to protect against 3H-norepinephrine uptake blockade evoked either by PBZ or DMI. The results provide strong evidence for a different site and/or mechanism of action of PBZ and DMI on the norepinephrine uptake system at adrenergic nerve terminals.

Animals↗

PubMed2002

Castration increases nisoxetine-evoked norepinephrine levels in vivo within the olfactory bulb of male rats.

In the present experiment we compared differences in extracellular norepinephrine levels in vivo within the olfactory bulb of intact and castrated male rats following infusion of the norepinephrine transport inhibitors, nisoxetine and tomoxetine. With this approach it was possible to assess whether dynamic changes in in vivo norepinephrine transporter function occur as a function of the gonadal state of the animal. Norepinephrine levels following infusion of nisoxetine were significantly increased in castrated compared with intact male rats. While a similar trend was present in response to tomoxetine infusion, these differences failed to achieve a statistically significant difference. These results demonstrate that castration of male rats alters norepinephrine transporter function within the olfactory bulbs. The increased extracellular levels of norepinephrine in response to agents which inhibit transporter function suggest that castration reduces transporter activity. Such effects have important implications not only with regard to processes involving the norepinephrine system in the olfactory bulb but also to the generalized sites and mechanisms by which gonadal steroid hormones modulate central nervous system functions.

Animals↗

PubMed1975

Norepinephrine in treatment of ocular hypertension and glaucoma.

Norepinephrine (4%) as free base produced a significant fall in intraocular pressure and resistance to outflow. This effect was sustained for up to 20 weeks. No significant difference could be shown between the effect of 2%, 3%, and 4% norepinephrine on the aquious humor dynamics. The effect on pressure and facility was shown in eyes with ocular hypertension and with glaucoma. An additive effect was observed after use of norepinephrine with pilocarpine in the treatment of glaucoma. Crossover studies between epinephrine borate 1% and norepinephrine borate 4% revealed no significant difference. Like epinephrine, norepinephrine produces a conjunctival hyperemia in many patients. However, there is an absence of tachycardia after use of norepinephrine, and one person in this study showed an allergic reaction to epinephrine that cleared promptly and completely when norepinephrine was substituted.

Aged↗