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PubMed1984

Effects of uptake and surface of entry on the responses of the rat caudal artery to noradrenaline, adrenaline and methoxamine.

The action of adrenaline on the rat tail artery was similar to that of noradrenaline in that (i) adrenaline was more potent by the intraluminal than the extraluminal route of application, and (ii) cocaine eliminated the difference in potency by selectively enhancing the response to extraluminal adrenaline. In the absence of cocaine, extraluminal adrenaline was more potent than extraluminal noradrenaline; in the presence of cocaine, the two amines were equipotent, irrespective of the route of application. The intraluminal and extraluminal potencies of methoxamine did not differ, either in the absence or presence of cocaine. It is concluded that neuronal uptake is responsible for differences between the potencies of noradrenaline and adrenaline and for the effect of the route of applications on these potencies. Potentiation of responses to both noradrenaline and adrenaline by 27 microM deoxycorticosterone acetate was minor compared with that by cocaine. The results provide further evidence that in the rat tail artery the extraneuronal uptake system is poorly developed compared with the neuronal uptake system.

Animals↗
PubMed1975

Effects of nitroglycerin and nitroglycerin-methoxamine during acute myocardial ischemia in dogs with pre-existing multivessel coronary occlusive disease.

Nitroglycerin (TNG) reduces ischemic injury during acute coronary occlusion in dogs with otherwise normal coronary arteries, but its effect in the presence of pre-existing multivessel coronary disease is unknown. We therefore examined the influence of TNG on acute ischemia in dogs with chronic multivessel coronary occlusions. The left anterior descending (LAD) coronary artery was acutely occluded by a balloon cuff in conscious dogs two weeks after placement of ameroid constrictors to produce gradual occlusion of the obtuse marginal and posterior descending coronary arteries. Adequacy of balloon and ameroid coronary occlusion and degree of collateralization were assessed by coronary angiography. Nitroglycerin decreased arterial pressure and increased heart rate. Myocardial ischemia, determined after LAD occlusion by summing ST-segment elevation (sigmaST) from eight intramyocardial electrodes, lessened with TNG in those six dogs whose heart rate increased less than 50 per cent, but increased in those four whose heart rate increased greater than 50 per cent. When TNG-induced change in either heart rate or arterial pressure was prevented by adding methoxamine, sigma ST was diminished even more (avg decrease 25 per cent; P smaller than 0.05). We conclude that, in the presence of pre-existing multivessel coronary occlusions, 1) TNG reduces ischemic injury during experimental acute coronary occlusion provided arterial pressure and heart rate responses are not excessive and 2) uniform improvement occurs when pressure and rate responses are abolished by an alpha-adrenergic agonist. Although results in animal studies must be extrapolated to the clinical situation with caution, these findings suggest that a similar pharmacologic approach might be applicable to the treatment of acute myocardial infarction in man, even in the presence of multivessel disease.

Animals↗
PubMed1978

Role of the peripheral vasculature in changes in venous return caused by isoproterenol, norepinephrine, and methoxamine in anesthetized dogs.

We studied effects on venous return of alpha- and beta-adrenergic agonists in anesthetized dogs. Blood from the superior and inferior venae cavae (venous return) was drained at the level of the tricuspid valve into a reservoir, from which blood was pumped into the right atrium at a constant rate. Isoproterenol infused into the ascending aorta or the right atrium increased the venous return and heart rate and decreased systemic blood pressure. The increase in venous return produced by isoproterenol given into the right atrium was not significantly different from that produced by isoproterenol administered into the ascending aorta, although the increase in heart rate was more marked with the latter route of administration. Norepinephrine infused into the ascending aorta increased the systemic blood pressure, venous return, and heart rate. Methoxamine infused into the ascending aorta increased the systemic blood pressure and decreased the venous return but produced no change in heart rate. Isoproterenol increased the venous return even when the sinoaortic baroreceptor reflex was eliminated. Propranolol abolished the increase in venous return caused by isoproterenol and reversed the increase in venous return caused by norepinephrine. The results suggest that a decrease in venous resistance mediated through a beta-adrenergic mechanism is important in increasing venous return, whereas an increase in venous resistance mediated through an alpha-adrenergic mechanism is responsible for a decrease in venous return.

Animals↗
PubMed1991

Synthesis and adrenergic properties of new duplicated analogs of methoxamine.

New duplicated analogs of the alpha 1-selective agonist methoxamine and of its cyclic derivative 5,8-dimethoxy-1,2,3,4-tetrahydro-2-naphthylamine have been synthesized and tested for their adrenergic properties. All the compounds prepared, presenting a polymethylene spacer of varying length between two units of the active structure, turned out to be completely devoid of any alpha-stimulating activity. Surprisingly, some of them showed a marked beta-adrenergic agonistic effect, being the most interesting compound active at nanomolar concentration.

Adrenergic alpha-Agonists↗
PubMed1990

Influence of preinduction methoxamine, lactated Ringer solution, or hypertonic saline solution infusion or postinduction dobutamine infusion on anesthetic-induced hypotension in horses.

A controlled study of the cardiovascular responses in horses anesthetized with acepromazine (0.05 mg/kg of body weight, IV), guaifenesin (100 mg/kg, IV), thiamylal (5.0 mg/kg, IV), and halothane in O2 (1.2 to 1.4% end-expired concentration) was performed to determine whether hypotension could be prevented by use of various treatments. Six horses were given 5 treatments in a randomized sequence: no treatment (control), methoxamine (0.04 mg/kg, IV), lactated Ringer solution (20.0 ml/kg, IV), 7.5% hypertonic saline solution (4.0 ml/kg, IV), or constant infusion of dobutamine (5.0 mg/kg/min, IV) during anesthesia. Heart rate, ECG, blood pressure, central venous pressure, cardiac output, blood gas analysis, PVC, and plasma total protein concentration were measured during the study. Compared with the control value, an increase in blood pressure during halothane administration was observed after administration of lactated Ringer solution, hypertonic saline solution, or dobutamine (P less than 0.05). The improved blood pressure response to hypertonic saline solution and dobutamine was related to an increase in cardiac output, which was statistically significant (P less than 0.05). Other statistically significant differences in cardiopulmonary responses among treatments were not observed during anesthesia. The PCV was increased in response to dobutamine infusion, and plasma total protein concentration was reduced in response to administration of hypertonic saline or lactated Ringer solution.

Acepromazine↗
PubMed1989

[Hemodynamic effects of dobutamine, dopamine and methoxamine during thoracic epidural anesthesia in dogs with coronary stenosis].

Dobutamine (DOB), dopamine (DOP) and methoxamine (MEX) were compared as to their effectiveness in controlling circulatory depression caused by thoracic epidural anesthesia in dogs with instituted coronary stenosis. DOB appeared to best serve the purpose of reestablishing systemic circulation, notably with an elevation of blood pressure. DOP achieved the best restoration of the absolute value of regional myocardial blood flow (RMBF), but DOB and DOP both caused RMBF in stenosed and non-stenosed areas to increase to virtually the same extent, and furthermore, worsened the intramyocardial distribution of RMBF in stenosed area. With MEX, an alpha-stimulant, there was noted a significant increase in blood flow through a stenosed area and, moreover, the increment tended to be greater than in a non-stenosed area, a fact suggesting involvement of such a mechanism as reverse coronary steal.

Anesthesia, Epidural↗
PubMed1989

Pretreatment with an inhaled alpha 1-adrenergic agonist, methoxamine, reduces exercise-induced asthma.

In order to assess the role of the bronchial circulation in the pathogenesis of exercise-induced asthma (EIA), we conducted a double-blind, randomized study of the effects of pretreatment with an inhaled alpha 1-adrenergic agonist, methoxamine (Mx), in nine asthmatic teenagers with known EIA. Exercise consisted of 5 min cycle ergometry at a submaximal, constant work-load, while the subjects breathed dry air at ambient temperature. Forced expiratory volume in one second (FEV1) was measured at baseline, 15 min after pretreatment of either Mx or saline, and serially after exercise. Mx significantly reduced the exercise-induced fall of FEV1 without modifying baseline FEV1 in five of the eight subjects, had little or no effect in three and caused an acute asthmatic attack in the remaining subject. Mx has potent constrictor effects on both bronchial and vascular smooth muscles through stimulation of postjunctional alpha 1-adrenoceptors. Therefore, the protective effect of Mx on EIA may be attributed to vasoconstriction of tracheobronchial vessels opposing the hyperaemia and mucosal airway oedema that may cause, at least in part, the exercise-induced acute bronchial obstruction in EIA. Alternatively, Mx stimulates mucus, water and electrolyte secretion by airway epithelium and may, therefore, oppose the dehydration of airway surface that could be a causative factor of EIA.

Administration, Inhalation↗
PubMed1985

Inhibitory effects of norepinephrine, methoxamine and phenylephrine on renin release from rat kidney cortical slices.

We attempted to determine whether the inhibition of renin release from rat kidney cortical slices by alpha adrenoceptor agonists is mediated by activation of alpha-1 and/or alpha-2 adrenoceptors, and to investigate the role of calcium in the mechanisms of this inhibition. Norepinephrine (NE), methoxamine (ME) and phenylephrine (PE) produced a concentration-dependent inhibition of renin release from rat kidney cortical slices, whereas clonidine was without effect. NE-, ME- and PE-induced inhibition of renin release was blocked by prazosin, which was 2 or 3 orders of magnitude more potent than yohimbine. The inhibitory effects of NE, ME and PE on renin release from the slices were abolished by removal of calcium from the incubation medium. Calcium antagonists, verapamil and nifedipine, attenuated the responses of renin release to NE, ME and PE, in a concentration-dependent manner. The inhibitory effects of NE, ME and PE on renin release were blocked significantly by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide, a calmodulin antagonist, but not by N-(6-aminohexyl)-1-naphthalenesulfonamide, which has virtually no calmodulin antagonistic activity. These findings suggest that alpha adrenoceptor agonists inhibit renin release from rat kidney cortical slices mainly via alpha-1 adrenoceptors and that calcium influx followed by the activation of the calcium-calmodulin system is involved in the above inhibition.

Animals↗
PubMed1985

Effects of isoproterenol and methoxamine on the electrocardiogram.

The effects of isoproterenal (ISP) and methoxamine (MTX) infusion in 20 asymptomatic subjects with labile T wave were studied. In those treated with ISP the T wave showed an early negative trend and later became clearly positive in 5 subjects. In the majority of the subjects treated with MTX the T wave became positive. T wave changes match variations of both the ventricular gradient and, to a lesser degree, the QRS area. These changes were not related to heart rate or, in the subjects treated with MTX, to the baroreceptorial sensitivity deduced from the slope of the regression equation between R-R internal and systolic arterial pressure. The results of this study confirm the existence of a neurogenic mechanism affecting the electrocardiographic changes in T wave.

Adult↗
PubMed1982

Effects of semirigid methoxamine analogs on vascular smooth muscle: studies of methoxy-2-aminotetralin and 2-aminoindane derivatives.

The effects of semirigid methoxy analogs of 2-aminotetralin (2-AT) and 2-aminoindane (2-AI) were studied on superfused dog metatarsal veins to investigate postjunctional interactions produced by these agents on sympathetically innervated vascular smooth muscle. The following compounds were tested: norepinephrine (NE); serotonin (5-HT); amphetamine (AMP); methoxamine (MTH); 2-di-n-propylamino-4,7-dimethoxyindane (RDS-127); 2-di-n-propylamino-5,6,-dimethoxyindane (JPC-211); 2-di-n-propylaminoindane (JPC-6036); 2-methylamino-5,8-dimethoxytetralin (DR-31); 2-methylamino-4,7-dimethoxyindane (RDS-31). The results of this study indicate that contractions produced by these compounds have the following ranked ordered potencies: 5-HT greater than NE much greater than MTH greater than or equal to RDS-127 = DR-31; JPC-6036, RDS-31, JPC-211 and AMP were inactive. The contractions produced by NE, MTH, RDS-127 or DR-31, but not 5-HT, probably occur through alpha1-adrenergic receptors since these contractions were blocked with prazosin. 5-HT and RDS-127, but not NE, MTH or DR-31 activate serotonin receptors since methysergide blocked the response produced by 5-HT or RDS-127. NE-induced contractions were augmented and tyramine-induced contractions were attenuated with cocaine. The responses of MTH, RDS-127 or DR-31 probably do not displace NE through a tyramine-like action since cocaine had no effect on contractions induced by these compounds. These data suggest that semirigid paramethoxylated derivatives of 2-AT and 2-AI are potent postjunctional receptor agonists which probably initiate venoconstriction via direct receptor interactions. The structure-activity relationships of these compounds are discussed.

Animals↗
PubMed1976

[Study of systolic times by external phonomechanocardiography in myocardial infarction. 2. Results of sensitizing tests: methoxamine, venous tourniquets, isomeric contration].

In an attempt to improve the quality of information provided by measuring the systolic times, the effect of three thpes of sensitising test was studied: the test with venous tourniquets on the lower limbs, the test with methoxamine, and the test under isometric exercise. In none of these tests was there found to be a statistically significant difference between the controls and the patients with myocardial infarction, with or without left ventricular failure. Taken as a whole, however, the sensitising tests studied tended to accentuate the abnormalities in the systolic times established under basal conditions in patients with myocardial infarction more grossly than in controls.

Exercise Test↗