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PubMed1987

Hemodynamic and clinical evaluation of piroximone, a new inotrope-vasodilator agent, in severe congestive heart failure.

To assess the potential utility of piroximone (MDL-19,205), an investigational inotrope-vasodilator agent, in severe heart failure, 15 patients with severe left ventricular failure refractory to conventional agents were enrolled in an acute hemodynamic study. After incremental intravenous dosing (mean total dose 1.8 +/- 0.4 mg/kg body weight), cardiac index increased (1.7 +/- 0.3 to 2.6 +/- 0.6 liters/min per m2; p less than 0.001) and left ventricular filling pressure decreased (25 +/- 7 to 19 +/- 7 mm Hg; p less than 0.001). Also decreasing significantly were right atrial pressure (13 +/- 6 to 7 +/- 5 mm Hg; p less than 0.005) and systemic vascular resistance (1,633 +/- 394 to 1,183 +/- 278 dynes.s.cm-5; p less than 0.001). Heart rate and mean arterial pressure did not change, whereas stroke work index increased significantly (13.3 +/- 4.3 to 21.6 +/- 7.3 g.m/m2; p less than 0.005). The increase in stroke work index with a concomitant decrease in left ventricular filling pressure indicates an improvement in systolic performance after treatment with piroximone. Similar responses were obtained after incremental doses of piroximone in oral solution. After oral doses of piroximone tablets, cardiac index also increased significantly (2.1 +/- 0.6 to 2.4 +/- 0.5 liters/min per m2; p less than 0.05), although this magnitude of increase was comparatively low. In a subgroup of 10 patients who underwent equilibrium gated radionuclide blood pool scintigraphy before and after intravenous piroximone, end-diastolic volume index tended to increase (106 +/- 42 to 132 +/- 60 ml/m2; p = 0.07), whereas left ventricular filling pressure decreased significantly (26 +/- 8 to 19 +/- 9 mm Hg; p less than 0.01).

Aged↗
PubMed1977

2,6-dialkylpiperazines. VIII (1)-N1-arylalkyl-N4-(2'-pyridyl)-2,6-dimethylpiperazines as adrenolytic and vasodilator agents.

A series of cis and trans N1-arylalkyl-N4-(2'-pyridyl)-2'6-dimethylpiperazines were synthetized and tested as adrenolytic and vasodilator agents. The N1-substitution with the 3,4-dimethoxyphenethyl group seems the most promising with regard to pharmacological activity, which was found to reside mainly in the trans isomer (3-II b). The adrenolytic activity of (3-II b) is comparable with that of the related 2-methyl derivative (1-III), while it is higher than that of (IV) in which the piperazine nucleus is C-unsubstituted.

Animals↗
PubMed1989

Comparative evaluation of the Ca2+-antagonistic activity of some Bulgarian vasodilating agents and of known Ca2+-antagonists on K+-depolarized smooth muscle from guinea-pig taenia coli.

The informative value of the experimental model for inhibition of the effect of the Ca2+-induced contraction in 40 mM K+-depolarized smooth muscle from guinea-pig taenia coli, is investigated in order to determine the intensity of the Ca2+-antagonistic activity of different agents on the voltage-dependent calcium channels. The Ca2+-antagonistic activity of two original Bulgarian vasodilating agents - piperazine derivatives (aligeron and P-11) possessing potential Ca2+-blocking properties, is compared with the activity of known Ca2+-antagonists which are widely used in clinical practice (verapamil, nitrendipine, cinnarizine and flunarizine). Cumulative dose-response curves of CaCl2 (0.1-3.0 mM) in Ca2+ free K+-depolarizing solution are recorded in advance and 30 min after the administration of the test-substances. On the basis of the intensity of the Ca2+-antagonistic activity, determined by their pA2 values, the substances investigated are ordered as follows: nitrendipine greater than verapamil greater than cinnarizine greater than or equal to flunarizine greater than aligeron greater than P-11. On the background of the CaCl2-induced (1 mM) long-lasting contraction, the substances tested manifest qualitatively different relaxing effects, which suggest different mechanisms of action of the Ca2+ antagonists studied, as well as the significance of the experimental protocol in evaluating the intensity of the Ca2+ antagonistic activity.

Animals↗
PubMed1993

The effect of topical application of vasodilating agents on cochlear electrophysiology.

The aim of this investigation was to study whether increased blood flow has beneficial effects on the ear or whether it is damaging to the auditory function, expressed as the auditory gross neural response. Four vasodilating agents were examined after topical application with respect to their influence on cochlear blood flow (CBF), blood pressure, and auditory function in the normal guinea pig. CBF was recorded with laser-Doppler. The drugs used were sodium nitroprusside, hydralazine, nicotinic acid and histamine. Sodium nitroprusside and hydralazine increased CBF and induced concentration dependent loss of auditory function. Neither nicotinic acid nor histamine had any effect on CBF. Nicotinic acid had varying effects: in some cases a negative influence on threshold shifts was seen, and in others a positive one. In most cases histamine caused improvement of the auditory function. The data indicate that topical administration of drugs to the inner ear is effective to influence both CBF and auditory function.

Administration, Topical↗
PubMed1994

Effects of vasodilating agents on cochlear blood flow in mice.

The mouse has several distinct advantages as an experimental model for study of the cochlear blood flow (CBF) in the mammal, particularly for studies involving genetic manipulation, development and aging factors. In this investigation we evaluated the effects of selected vasodilating agents on CBF using laser-Doppler flowmetry. Sodium nitroprusside, hydralazine and pentoxifylline were applied topically on the round window (RW) or systemically by a subcutaneous injection. Topical application of sodium nitroprusside and hydralazine elevated CBF significantly, while systemic administrations of these two drugs failed to elevate CBF consistently. Pentoxifylline did not change CBF following topical application but increased CBF slightly following systemic administration. Age and gender did not influence the CBF response to topical application of sodium nitroprusside.

Administration, Topical↗
PubMed1992

Unmasking the vasoconstrictor response to neuropeptide Y and its interaction with vasodilating agents in vitro.

Neuropeptide Y (NPY) is a powerful vasoconstrictor in vivo but is usually much less active on isolated blood vessels. The contractile effect of NPY was examined in the isolated rat femoral artery exposed to various degrees of vasoconstriction. The effects of NPY on the relaxation induced by vasodilator agents was also studied. NPY (< or = 1 microM) had no contractile effect. In vessels pretreated with a low concentration of phenylephrine (0.3-1.0 microM), NPY evoked a concentration-dependent contraction, which was similar in intact and in endothelium-deprived vessels. Other vessels were contracted with phenylephrine (3-10 microM) and relaxed with histamine (0.1 mM). Subsequent addition of NPY elicited a contraction which was much greater than that observed in vessels pretreated with phenylephrine only. The Y1 receptor agonist, [Pro34]NPY, but not the Y2 receptor agonist, NPY 13-36, evoked a concentration-dependent contraction in phenylephrine-pretreated vessels. Acetylcholine (ACh) induced endothelium-dependent relaxation in vessels contracted with phenylephrine. NPY (0.1 microM) induced a rightward shift of the concentration-response curve and a lower maximum relaxation in response to ACh. NPY was without effect on the dilatation evoked by nitroprusside, histamine or forskolin. In conclusion, under appropriate vasoconstrictor and vasodilator influence, NPY can act at Y1 receptors to evoke vasoconstriction in the femoral artery via endothelium-independent mechanisms. In addition, NPY seems to attenuate the endothelium-dependent relaxation induced by ACh. These actions of NPY may contribute to explain the strong vascular effects of the peptide in vivo.

Acetylcholine↗
PubMed1985

Alterations in left ventricular function, coronary hemodynamics and myocardial catecholamine balance with MDL 17043, a new inotropic vasodilator agent, in patients with severe heart failure.

To evaluate changes in myocardial energetics and systemic and cardiac sympathetic activity associated with improved left ventricular function after MDL 17043, a new inotropic vasodilator agent, systemic and coronary hemodynamics and myocardial catecholamine balance were determined in 17 patients with severe heart failure. After the administration of MDL 17043, cardiac index increased by 67% and pulmonary capillary wedge pressure decreased (25 +/- 5 to 14 +/- 7 mm Hg, p less than 0.01), indicating improved left ventricular function. Coronary sinus blood flow (75 +/- 29 to 111 +/- 51 ml/min, p less than 0.01) and myocardial oxygen consumption (9.9 +/- 3.3 to 11.8 +/- 5.4 ml/min, p less than 0.05) increased despite decreased myocardial oxygen extraction (11.7 +/- 2 to 10.1 +/- 3.3 vol%, p less than 0.05) and a higher coronary sinus oxygen content. Although transmyocardial lactate extraction remained unchanged, increased myocardial oxygen consumption has potential deleterious effects on myocardial metabolic function. Arterial norepinephrine concentrations and transmyocardial norepinephrine release also remained unchanged. These findings suggest that MDL 17043 improves left ventricular pump function, but produces no detectable change in systemic and cardiac sympathetic activity. Improved left ventricular function is associated with increased myocardial oxygen consumption despite primary coronary vasodilation.

Adult↗
PubMed1980

Cutaneous microcirculatory effects of various vasodilator agents on the conscious rabbit, with special regard to changes in the rhythmic property of vasomotion.

Microcirculatory effects of intravenous administrations in the appropriate doses of phenoxybenzamine (POBA), phentolamine (PTA), nicotinic acid (NAc), trimetazidine (TMZ), dilazep (DZ), cepharanthine (CT), alpha-tocopheryl acetate (TP-A), and alpha-tocopheryl nicotinate (TP-N) as vasodilator agents were investigated in the subcutaneous tissue within a transparent ear chamber of the normal conscious rabbit. The intra-vital microscopic findings obtained following administration of the drugs were as follows: POBA, a marked and long-lasting vasodilatation without vasomotion (more than 1 hour); PTA, a quite brief vasodilatation followed by a marked and long-lasting vasoconstriction without vasomotion (more than 1 hour); NAc, a short-lasting vasodilatation with slightly blunted vasomotion (less than 10 minutes); TMZ, DZ, CT, TP-A, and TP-N, a similar notable and transient vasodilatation with vasomotion (about 1 hour or more). Some physiological implications on the microcirculatory changes induced by administrations of the drugs were discussed especially in relation to the significance of sustaining the rhythmic fluctuations of blood flow due to vasomotion.

Animals↗
PubMed2003

Vasodilator agents protect against indinavir nephrotoxicity.

Indinavir (IDV) is a protease inhibitor widely used in AIDS treatment. A sustained elevation of creatinine was identified in IDV-treated patients. We have previously demonstrated that IDV causes renal vasoconstriction in rats. The objective of this study was to investigate the mechanism of IDV-induced vasoconstriction and the effect that the vasodilator agents L-arginine (LA), nifedipine (NF), as well as magnesium supplementation (Mg), have on IDV-induced nephrotoxicity. Male Wistar rats were kept on fast overnight and given free access to water. IDV (80 mg/kg BW) and NF (3 mg/kg BW) were given by gavage for 15 days. LA (1.5%) and MgCl2 x 6H2O (1%) were added to drinking water. Six groups were studied: Control (n=6): normal rats treated with vehicle, a 0.05 M citric acid solution; IDV (n=7): IDV-treated rats; IDV+LA (n=6): IDV- and LA-treated rats; IDV+NF (n=7): IDV- and NF-treated rats; IDV+Mg (n=7): IDV- and MgCl2-treated rats; IDV+Mg+L-NAME (n=9): IDV- and MgCl2-treated rats, supplemented with L-NAME (2.5 mg/l in drinking water). Clearance studies and evaluations of urinary nitrite (NO2) excretion were performed on day 16. No changes in blood pressure were observed. NO2 excretion decreased in IDV-treated rats. LA and NF protected against IDV effects, improving GFR (IDV+LA, 1.95 +/- 0.10; IDV+NF, 1.94 +/- 0.07 vs IDV, 1.15 +/- 0.07 ml/min, P<0.001) and RBF (IDV+LA, 7.83 +/- 0.09; IDV+NF, 7.63 +/- 0.14 vs IDV, 6.17 +/- 0.25 ml/min, P<0.001). These results suggest that IDV-induced vasoconstriction is mediated by NO and Ca2+ channels. Magnesium also ameliorated GFR and RBF in IDV-treated rats (GFR IDV+Mg, 1.77 +/- 0.08 ml/min, P<0.001; RBF IDV+Mg, 7.35 +/- 0.158 ml/min, P<0.001). Magnesium protection is not NO-mediated since it was not blocked by L-NAME. In conclusion, LA, NF and Mg protect against IDV-induced nephrotoxicity in rats. This study may have potential clinical implications for prevention of IDV-induced nephrotoxicity.

Animals↗
PubMed1988

Use of the novel cardiotonic and vasodilator agent pimobendan in traumatic shock.

The effect of 4,5-dihydro-6-[2-(4-methoxyphenyl)-1H-benzimidazol-5-yl]-5-methyl- 3(2H)- pyridazinone (pimobendan, UD-CG 115 BS), a novel positive inotropic and vasodilator agent, was studied in a severe model of murine traumatic shock. Noble-Collip drum trauma produced a shock state characterized by a significantly reduced mean arterial blood pressure (MABP), a 5-fold increase in plasma cathepsin D and myocardial depressant factor (MDF) activities, and a survival time of 80 +/- 12 min. Administration of pimobendan (100 micrograms/kg, i.v. bolus) significantly prolonged the survival time to 175 +/- 24 min (p less than 0.01). Although plasma cathepsin D was not affected by pimobendan, this agent significantly attenuated the accumulation of MDF activity in the plasma when compared to animals receiving only its vehicle (37 +/- 6 vs 61 +/- 9 U/ml, p less than 0.05). Additionally, pimobendan inhibited platelet aggregation in cat platelet rich plasma, but failed to have an antiproteolytic effect in cat pancreatic homogenates. These results suggest that cardiotonic and vasodilator activities combined with inhibition of platelet aggregation could mediate the beneficial effects of pimobendan in traumatic shock.

Animals↗