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PubMed1987

Non-invasive assessment of end-systolic pressure-length and stress-shortening relationships in normal individuals: significance of different loading conditions induced by methoxamine and angiotensin II.

To evaluate whether the end-systolic pressure-dimension and stress-shortening relations are influenced by the drugs used for their assessment, we analysed the effects of angiotensin II (N = 30) and methoxamine (N = 10) in normal individuals. Serial measurements of left ventricular dimensions and wall thickness were performed by M-mode echocardiography; the end-systolic pressure was assessed by indirect, calibrated carotid pulse tracings. The end-diastolic dimension, which reflects preload, remained unchanged during the afterload challenge using angiotensin II, but increased significantly using methoxamine (P less than 0.001). Significant differences due to the agent used were observed for the end-systolic pressure-dimension relationship (P less than 0.002), the relation between end-systolic wall stress and fractional shortening (P less than 0.0002), and the relation between end-systolic wall stress and mean fibre shortening velocity (P less than 0.02). The extrapolated end-systolic dimension D0 at zero end-systolic pressure was significantly shifted to the left when using angiotensin II (P less than 0.02); this is considered to be due to its negligible effect on preload. Our data suggest that the assessment of the end-systolic pressure-dimension and stress-shortening relationships depends significantly on drug specific effects and the variation of preload during the afterload challenge. Based on these results, the use of angiotensin II is emphasized for the assessment of the end-systolic pressure-dimension and stress-shortening relationships.

Adult↗
PubMed2000

Methoxamine inhibits transient outward potassium current through alpha1A-adrenoceptors in rat ventricular myocytes.

alpha1-Adrenoceptor agonists are known to reduce transient outward potassium current (I(to)) in the heart. The aim of this study was to analyze the effect of methoxamine (mtx) on I(to) and to elucidate which adrenoceptor subtype was involved in this effect. We used the whole-cell configuration of the patch-clamp technique to record I(to). Our experiments confirm that mtx induces a dose-dependent decrease of I(to) that is characterized by an acceleration of time to peak (3.5 +/- 0.2 and 2.3 +/- 0.3 ms for control and mtx, respectively), and a decrease in both inactivation time constants (T(fast) was reduced from 20.8 +/-2.6 to 14.9 +/- 1.1 ms, and tau(slow) was reduced from 138 +/- 32.1 to 114 +/- 28.7 ms; n = 7). All these effects were antagonized by prazosin and the alpha1A-antagonist 5-methylurapidil but not by the irreversible alpha1B-antagonist chloroethylclonidine. These data indicate that stimulation of alpha1A-adrenoceptor subtype is involved in the methoxamine-induced reduction of I(to) in rat ventricular myocytes.

Adrenergic alpha-Agonists↗
PubMed1993

Changes in blood flow and vascular resistance in the arm and leg during spinal anaesthesia and vasopressor therapy with methoxamine.

The effects of subarachnoid block with hyperbaric bupivacaine 0.5% on forearm and calf blood flow and vascular resistance were examined using venous occlusion plethysmography in 10 fit patients. Following blockade there was an increase in mean (SD) calf blood flow from 2.0 (0.4) to 2.6 (1.2) ml.100 ml-1.min-1 (p = 0.057), a decrease in mean (SD) calf vascular resistance from 55 (15) to 38 (14) R units (p < 0.01), a decrease in mean (SD) forearm blood flow from 3.1 (1.2) to 1.8 (0.9) ml.100 ml-1.min-1 (p < 0.01) and an increase in mean forearm vascular resistance from 38 (16) to 62 (24) R units (p < 0.01). Methoxamine 2 mg was administered intravenously when the mean arterial blood pressure decreased by 15%. There was a resultant marked increase in mean (SD) forearm blood flow from 1.8 (0.9) to 3.0 (0.8) ml.100 ml-1.min-1 (p < 0.001) but a decrease in mean (SD) calf blood flow from 2.6 (1.2) to 2.1 (1.4) ml.100 ml-1.min-1 (p = 0.11). Correspondingly, the mean (SD) forearm vascular resistance decreased from 62 (24) to 46 (17) R units (p < 0.01) with an increase in mean (SD) calf vascular resistance from 38 (14) to 56 (22) R units (p < 0.01). These findings indicate that whereas methoxamine produces the anticipated constrictor response in the calf vessels it causes a simultaneous reduction in vascular resistance in the forearm.

Adult↗
PubMed1986

The effects of noradrenaline, B-HT 920, methoxamine, angiotensin II and vasopressin on mean circulatory filling pressure in conscious rats.

The effects of vasoactive substances on mean circulatory filling pressure (MCFP), an index of total body venous tone, were determined in conscious rats. Cumulative doses of saline (0.9% w/v NaCl solution), methoxamine (alpha 1-adrenoceptor agonist), B-HT920 (alpha 2-adrenoceptor agonist) noradrenaline and vasopressin, and individual doses of angiotensin II (AII), were infused into the rats. Mean arterial pressure (MAP), MCFP and heart rate (HR) were determined before and during the plateau responses to infusions of the vasoactive substances. The infusions of all the agonists caused a dose-dependent increase in MAP and a decrease in HR. The infusion of saline affected neither MAP nor HR. The infusions of saline and methoxamine did not affect MCFP while the infusions of B-HT 920, noradrenaline and AII increased MCFP. MCFP was slightly increased during the infusion of high doses of vasopressin. It was concluded that receptors for the alpha 2-adrenoceptor agonist and AII are involved in the control of venous tone. Receptors for the alpha 1-adrenoceptor agonist and vasopressin are not important for the control of venous tone.

Adrenergic alpha-Agonists↗
PubMed1989

Prevention of ischemic neuronal damage by alpha 1-adrenoceptor agonist (methoxamine).

The effect of methoxamine, an alpha 1-adrenoceptor agonist, on ischemic neuronal damage was studied in the gerbil. The animals were subjected to 5 min of ischemia by bilateral common carotid arteries occlusion. Morphological changes and calcium accumulation were evaluated in the CA1 sector of the hippocampus after 7 days of survival. The degree of ischemic neuronal damage and calcium accumulation in the methoxamine-treated groups were significantly attenuated compared with the saline-treated ischemic group. The results suggest that alpha 1-adrenoceptor stimulation prevents ischemic neuronal damage.

Adrenergic alpha-Agonists↗
PubMed2006

Both Ca2+ -dependent and -independent pathways are involved in rat hepatic stellate cell contraction and intrahepatic hyperresponsiveness to methoxamine.

In chronic liver injury, hepatic stellate cells (HSCs) have been implicated as regulators of sinusoidal vascular tone. We studied the relative role of Ca(2+)-dependent and Ca(2+)-independent contraction pathways in rat HSCs and correlated these findings to in situ perfused cirrhotic rat livers. Contraction of primary rat HSCs was studied by a stress-relaxed collagen lattice model. Dose-response curves to the Ca(2+) ionophore A-23187 and to the calmodulin/myosin light chain kinase inhibitor W-7 served to study Ca(2+)-dependent pathways. Y-27632, staurosporin, and calyculin (inhibitors of Rho kinase, protein kinase C, and myosin light chain phosphatase, respectively) were used to investigate Ca(2+)-independent pathways. The actomyosin interaction, the common end target, was inhibited by 2,3-butanedione monoxime. Additionally, the effects of W-7, Y-27632, and staurosporin on intrahepatic vascular resistance were evaluated by in situ perfusion of normal and thioacetamide-treated cirrhotic rat livers stimulated with methoxamine (n = 25 each). In vitro, HSC contraction was shown to be actomyosin based with a regulating role for both Ca(2+)-dependent and -independent pathways. Although the former seem important, an important auxiliary role for the latter was illustrated through their involvement in the phenomenon of "Ca(2+) sensitization." In vivo, preincubation of cirrhotic livers with Y-27632 (10(-4) M) and staurosporin (25 nM), more than with W-7 (10(-4) M), significantly reduced the hyperresponsiveness to methoxamine (10(-4) M) by -66.8 +/- 1.3%, -52.4 +/- 2.7%, and -28.7 +/- 2.8%, respectively, whereas in normal livers this was significantly less: -43.1 +/- 4.2%, -40.2 +/- 4.2%, and -3.8 +/- 6.3%, respectively. Taken together, these results suggest that HSC contraction is based on both Ca(2+)-dependent and -independent pathways, which were shown to be upregulated in the perfused cirrhotic liver, with a predominance of Ca(2+)-independent pathways.

Actomyosin↗
PubMed1990

Hemodynamic actions of intravenous endothelin in rats: comparison with sodium nitroprusside and methoxamine.

We investigated hemodynamic actions of endothelin (ET) in conscious rats. Intravenous injections of ET produced dose-dependent biphasic blood pressure (MAP) responses: initial decreases of up to 84 +/- 11 s were followed by increases of up to 1-h duration. Corresponding responses in cardiac output (CO), heart rate, and efferent splanchnic nerve activity were reciprocal to changes in MAP. Mesenteric blood flow showed an immediate and sustained decrease. Compared with equidepressor doses of sodium nitroprusside (NNP), ET produced a markedly different regional hemodynamic response pattern during the initial depressor phase. Compared with equipressor doses of the alpha-adrenoceptor agonist methoxamine, ET produced significantly greater vasoconstriction in hindlimb and renal vascular bed during pressor phase. ET-induced changes in CO were significantly greater than the respective CO responses to NNP and methoxamine in intact animals and following cardiac autonomic blockade with atenolol and methscopolamine. ET has vasodilator and vasoconstrictor properties that induce a unique hemodynamic response pattern on intravenous injection. Persistence of ET-induced changes in CO following cardiac autonomic blockade suggests direct cardiostimulatory actions of the peptide during depressor phase as well as direct cardiodepressant actions during pressor phase.

Animals↗
PubMed1987

Pressor sensitivities to vasopressin, angiotensin II, or methoxamine in diabetic rats.

We investigated the pressor sensitivities to vasopressin, angiotensin II, and methoxamine of intact and ganglion-blocked rats that had been treated 21 days earlier with streptozotocin or saline. No differences in blood pressure or heart rate responses to vasopressin or angiotensin II were found between the intact groups when these peptides were administered intravenously in equimolar doses. After ganglion blockade a significant enhancement in pressor responsiveness to both vasopressin and angiotensin II was observed in the control groups, but in the streptozotocin-treated animals no enhancement in pressor sensitivity to vasopressin was found. Furthermore, although a significant augmentation of the responses to angiotensin II was observed, it was smaller than that seen in the ganglion-blocked control group. Neither group showed enhanced pressor responsiveness to methoxamine. These results indicate that the previously observed diminished contributions from endogenous vasopressin and the renin-angiotensin system to blood pressure recovery following ganglion blockade in streptozotocin-treated rats may have been due, at least in part, to diminished pressor responsiveness.

Angiotensin II↗
PubMed1992

Effects of anoxia on the biphasic response of isolated strips of rabbit bladder to field stimulation, bethanechol, methoxamine and KCl.

The contractile response of the bladder can be divided into two phases: an initial rapid increase in tension and a prolonged period of sustained tension (plateau phase). The bladder empties primarily during the plateau phase of the contractile response. These two phases can be differentiated using both pharmacologic and metabolic agents, indicating that the two phases have independent energy requirements. The present study compares the phasic (peak) and tonic (plateau) components of the responses of isolated strips of bladder body and base to field stimulation, bethanechol, methoxamine and KCl administration. New Zealand White rabbits were anesthetized with pentobarbital, and the bladder was removed. The bladder was divided between body and base at the level of the ureteral orifices. Three strips of bladder body and three strips of bladder base were mounted in separate baths containing Tyrode's solution at 37 degrees C and equilibrated with 95% O2, 5% CO2. Anoxia was produced by changing the gas mixture to 95% nitrogen, 5% CO2. The effects of anoxia on the responses to field stimulation, bethanechol, methoxamine and KCl were determined at different times after the initiation of anoxia. The results of these studies can be summarized as follows: (1) Anoxia induced time-dependent plateau phases of the response to field stimulation (2 and 32 Hz). (2) The rate of inhibition of the plateau phase was significantly and substantially greater than that of the peak phase in both the bladder body and base. (3) Similarly, anoxia inhibited the plateau phase of the bladder body's response to bethanechol to a significantly and substantially greater degree than anoxia inhibited the peak contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Developmental changes in the volumes, protein, and some electrolyte concentrations of male and female rat submandibular saliva secreted in response to methoxamine and pilocarpine.

Saliva secreted in response to methoxamine and pilocarpine was collected from the cannulated ducts of the submandibular glands of male and female rats at weekly intervals from two to 10 weeks of age. It was analyzed for volume and for concentrations of protein, potassium, calcium, and inorganic phosphate. Following the collection of saliva, the submandibular glands were removed and weighted. The wet weights of the glands increased substantially up to seven weeks of age and then reached almost plateau values in both sexes. The salivary volumes secreted in response to both agents in both sexes were positively correlated with the gland weights, except that after five to six weeks of age there was no correlation between gland weight and methoxamine-stimulated salivary volume. The concentrations of protein, potassium, and inorganic phosphate were inversely related to the flow rates only at relatively low rates of flow. The concentration of calcium was positively correlated with the protein concentration and was independent of the nature of the stimulus and of sex differences during postnatal development.

Animals↗
PubMed1987

Effects of the rise in aortic pressure on coronary flow reserve in dogs. Comparison between constriction of the descending thoracic aorta and injection of methoxamine.

In order to investigate the effect of a rise in aortic pressure on coronary flow reserve and also on the difference of its effect according to the methods used to raise aortic pressure, this experiment was performed. Using 7 anesthetized dogs with heart rate held constant by a pacemaker, both the resting and the peak reactive hyperemic left circumflex coronary flow were measured following raising of the aortic pressure by either descending thoracic aorta constriction or methoxamine injection. The resting and peak reactive hyperemic coronary flows both increased linearly following the rise in aortic pressure. The magnitude of the resting flow increment and the resting coronary vascular resistance following raising aortic pressure did not differ significantly between the two different methods. However, the magnitude of the peak hyperemic flow increment and the peak hyperemic coronary vascular resistance following raising aortic pressure were significantly smaller with methoxamine injection than with aortic constriction. These data indicate that coronary flow reserve increases proportionally with a rise in aortic pressure. However, the magnitude of the increment of coronary flow reserve is smaller following an alpha-adrenoceptor-mediated rise in aortic pressure, because the maximal coronary vasodilation was reduced by alpha-stimulated coronary vasoconstriction.

Animals↗
PubMed1978

[Study of hemodynamic effects of the methoxamine in 8 cases of obstructive cardiomyopathy with mitral valve insufficiency].

The haemodynamic effects of intravenous Methoxamine were studied in 8 patients with hypertrophic obstructive cardiomyopathy (HOCM) with mitral incompetence (group I) and 8 patients with mitral incompetence due to valvular, subvalvular or other causes (group II). In both groups the left ventricular end-diastolic pressure rose significantly without any great change in the end diastolic surface area: the ventricular distensibility is reduced in both cases. The mean capillary pressure, the V wave/mean capillary pressure ratio, and the degree of regurgitation of the two groups changed in opposite ways : in mitral incompetence due to varying causes (group II) the regurgitation increased, but in mitral incompetence due to HOCM (group I), it decreased. The left ventricular intracavitary gradient in HOCM tended to disappear under the effect of Methoxamine as the systolic aortic pressure approached the basal values recorded in the apical area.

Adult↗
PubMed2002

[Priapism secondary to chronic myeloid leukemia: value of initial treatment with cavernous lavage plus adjuvant methoxamine].

OBJECTIVE: To report a case of priapism secondary to leukemia, with special reference to the initial treatment in the emergency services. METHODS: A 53-year-old male with chronic myeloid leukemia presented with prolonged involuntary painful erection of 12 hours' duration. The physical examination and particularly the cavernosal blood gas study, indicated low flow priapism. Punction-lavage of the corpora cavernosa was performed. Because complete response was not achieved with this procedure, adjuvant intracavernous methoxamine was administered. RESULTS: Complete detumescence was achieved after the third dose of methoxamine. There was no recurrence and erectile function was preserved. CONCLUSIONS: We underscore the utility of combined cavernous lavage + adjuvant alpha-1 adrenergic agonist as initial therapy in priapism with this special etiology.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

Inhibition by intraventricular microinfusion of ketanserin of the cardiovascular responses to peripheral administration of methoxamine in rats.

The cardiovascular responses induced by intracerebroventricular or intravenous administration of ketanserin in normotensive rats were evaluated. Ketanserin, which is an antagonist at 5-HT2 receptors, when microinfused into the third cerebral ventricle, did not induce significant cardiovascular effects, except for a slight and transitory hypotensive response after the microinfusion of the highest dose (200 micrograms). However, at doses which were unable to affect directly blood pressure or heart rate, ketanserin, microinfused into the same site, antagonized the pressor response induced by peripheral administration of methoxamine, an alpha 1-adrenoceptor agonist. Furthermore, peripheral administration of ketanserin produced dose-dependent hypotension and bradycardia and antagonized the pressor effect of an intravenous bolus injection of methoxamine. In conclusion, the present experiments confirmed the ability of ketanserin to produce cardiovascular effects when administered peripherally and provides evidence for an involvement of ketanserin-sensitive receptors in the brain in the regulation of phasic responses during experimentally induced hypertension.

Animals↗
PubMed1988

Contractile reactivity of the perfused mesenteric vascular bed from sinoaortic denervated rats to norepinephrine, methoxamine and verapamil.

The contractile reactivity to norepinephrine, methoxamine, and verapamil of the perfused mesenteric vascular bed from sinoaortic denervated (SAD) and sham-operated (SO) rats was studied 3 to 30 days after surgery. A gradual but incomplete reduction of arterial hypertension was observed in SAD rats throughout the study. The norepinephrine- and methoxamine-induced dose-response curves were similar in both SAD and SO groups on day 3, but shifted to the left on days 7 and 15 and demonstrated a tendency to shift to the right at 30 days. Verapamil-induced vasodilation was similar in both groups. Enhanced mesenteric vascular responsiveness to endogenous catecholamines could contribute to the increased vascular resistance.

Animals↗
PubMed1978

Aminotetralin analogs of methoxamine as potential hypertensive agents.

Cardiovascular effects of methoxamine and some aminotetralin derivatives (5,8-ADT, DR-31 and DR-17) were studied after systemic intravenous or intraarterial injection into different perfused vascular beds in anesthetized dogs. Intravenous administration of the compounds produced dose-related prolonged increases in blood pressure, which were antagonized by phentolamine. After intro-arterial injection into the perfused hindlimb, mesenteric artery or the saphenous vein, all compounds produced dose-dependent increases in perfusion pressure indicative of vasoconstriction. Phentolamine antagonized these effects. It was demonstrated that desipramine significantly reduced the vasoconstricting actions of intra-arterially injected tyramine in the hindlimb, but did not alter the responses induced by methoxamine and the aminotetralin derivatives. The data indicate that these compounds elicit peripheral vasoconstriction in the dog, through a direct action on the alpha adrenergic receptors.

Animals↗
PubMed1993

Microvascular mechanisms of change in tumor blood flow due to angiotensin II, epinephrine, and methoxamine: a functional morphometric study.

To elucidate the microvascular mechanisms of change in tumor blood flow elicited by vasopressors, a functional morphometric study of the s.c. microcirculation within a rat transparent chamber was performed. Arteriolar vessels were classified centripetally (a2-a5) according to Strahler's method. Arteriolar pressure in each segment both under normotension and under hypertension induced by angiotensin II, epinephrine, or methoxamine was measured using a microocclusion technique. Vasoconstriction was estimated by changes in vessel diameters. In addition, tissue blood flow of the subcutis and s.c. tumor (LY80, a variant of Yoshida sarcoma) under the same conditions was measured with the hydrogen clearance method. By comparing the sites of the greatest pressure drop and the vasoconstriction induced by each vasopressor, we assessed the sites of vascular resistance (VR) which showed increases due to these vasopressors. The greatest VR increase elicited by angiotensin II occurred across a2 vessels. On the other hand, the sites of VR increase due to epinephrine were in a3 vessels and larger vessels upstream from a3 arterioles. The VR increase induced by methoxamine was much smaller than that induced by epinephrine. We conclude that the fact that the sites of increased VR differ with each vasopressor is the primary reason that various vasopressors have been found to produce different changes in tumor blood flow.

Angiotensin II↗
PubMed2001

Termination of ventricular tachycardia after methoxamine.

A case of ventricular tachycardia which reverted with intravenous methoxamine is presented. The methoxamine was used to increase blood pressure during anaesthesia for direct current cardioversion. While alpha adrenergic agonists have been used previously to increase vagal tone via a baroreceptor mechanism to revert supraventricular tachycardias, this is the first case where a sustained ventricular tachycardia reverted with an alpha adrenergic agonist. The mechanisms likely to have caused the reversion are discussed.

Journal Article↗