Central and Regional Vascular Hemodynamics Following Intravenous Milrinone in the Conscious Rat

Drexler, Helmut; Höing, S.; Faude, Frank; Wollschläger, H; Just, H

doi:10.1097/00005344-198705000-00010

Cited by 26 publications

(21 citation statements)

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“…Levosimendan increased renal medullary blood flow and reduced vascular resistance in both the medullary and cortical beds, indicating that this new drug produces renal vasodilatation. Reductions in renal medullary and cortical vascular resistances were less pronounced with pimobendan and milrinone, respectively, than those observed with levosimendan, supporting the findings of two previous studies (Verdouw et al, 1986;Drexler et al, 1987). Levosimendan increased small intestinal blood flow and reduced vascular resistance in this organ, in contrast to the findings with pimobendan and milrinone.…”

Section: Discussionsupporting

confidence: 88%

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Pagel

Hettrick

Warltier

1996

British J Pharmacology

109

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1 The distribution of cardiac output during administration of levosimendan, a new myofilament calcium sensitizer, is unknown. We examined and compared the effects of levosimendan, pimobendan, and milrinone on regional tissue perfusion by use of the radioactive microsphere technique in barbiturate-anaesthetized dogs. 2 Haemodynamics and regional blood flow were determined before and during infusions of levosimendan (0.75, 1.5, and 3.0 Mg kg-' min-'), pimobendan (10, 20, and 40 ig kg-' min-'), or milrinone (1.0, 2.0, and 4.0 ,ug kg-' min-'). 3 All three drugs caused similar increases in heart rate, cardiac output, and left ventricular + dP/dt and decreases in end-diastolic pressure and systemic vascular resistance. No changes in subendocardial, midmyocardial, and subepicardial blood flow occurred during administration of levosimendan. However, a redistribution of blood flow from subendocardium to subepicardium was observed. Pimobendan increased midmyocardial and subepicardial blood flow and reduced the endo/epi ratio to a greater degree than levosimendan. Milrinone did not affect myocardial perfusion. 4 Levosimendan increased blood flow to the renal medulla and decreased renal medullary and cortical vascular resistance. Levosimendan increased blood flow to the small intestine and liver and reduced vascular resistance in these organs. Pimobendan increased hepatic blood flow to a greater degree than levosimendan but did not alter small intestinal perfusion. All three drugs decreased splenic blood flow to similar degrees. Levosimendan and pimobendan reduced cerebral vascular resistance. Levosimendan and milrinone reduced skeletal muscle vascular resistance. 5The results indicate that levosimendan, pimobendan, and milrinone cause subtlety different alterations in regional tissue perfusion while producing similar haemodynamic effects.

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Section: Discussionsupporting

confidence: 88%

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Pagel

Hettrick

Warltier

1996

British J Pharmacology

109

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“…Regional blood flows in the liver, heart and skeletal muscles tended to increase, and blood flows to other organs remained unchanged. Baseline blood flows in all organs were in good agreement with those reported else where for the rat (10)(11)(12).…”

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confidence: 87%

“…The vasodilator action of RS-1893 may be caused by a specific inhibition of phos phodiesterase-Ill (PDE-III) (5), because it is well-known that PDE-III inhibitors have both cardiotonic and vasodilator actions (13). Specific increase of renal blood flow, however, seems to be not common to all PDE-III inhibitors: milrinone increases renal blood flow (12), but pimobendan (14) and piroximone (15) do not. The mechanisms underlying the organ selectivity of the vasodilator action of RS-1893 remains to be solved, but the increase in renal blood flow may have beneficial effects on excretory function of the kidney in patients with heart failure.…”

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confidence: 99%

Effects of RS-1893, a novel cardiotonic agent, on central and peripheral hemodynamics in anesthetized rats.

Miyake¹,

Shiga²,

Sada³

et al. 1989

Jpn.J.Pharmacol

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Abstract--After the use of two radionuclides in the tracer microspheres technique in the rat was verified, we examined the central and peripheral hemodynamic effects of RS-1893, an orally active cardiotonic agent.An intravenous infusion of RS-1893 at a dose of 3 ug/kg/min gradually decreased blood pressure and increased heart rate and cardiac output.Blood flows in the kidney and stomach were increased. There was no organ in which blood flow was decreased despite the fall in blood pressure.These data suggest that RS-1893 dilates blood vessels in the whole body, especially in the kidney and stomach.

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“…Under the same conditions, mesenteric and renal vascular conductances were either unchanged or, in the case of the latter during the higher dose infusion, reduced. While a relatively selective hindquarters vasodilator effect of (±)-dobutamine has been described previously (Vatner et al, 1974;Robie & Goldberg, 1975;Liang & Hood, 1979) this has not been observed invariably (Drexler et al, 1987;Biro et al, 1988), even in studies that did demonstrate a cerebral vasodilator response to (± )-dobutamine (Drexler et al, 1987). Although there was a greater hindquarters hyperaemia and a better maintenance of mesenteric blood flow during infusion of (+)-dobutamine than of human a-CGRP at either dose level, carotid hyperaemia was greater during infusion of the latter at the higher dose.…”

Section: Discussionmentioning

confidence: 76%

Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

Gardiner

Compton

Kemp

et al. 1991

British J Pharmacology

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1 Comparisons were made of the full haemodynamic profiles of the known cardiostimulant, (± )-dobutamine, and the putative inotropic peptide, human a-calcitonin gene-related peptide (human a-CGRP), in conscious, chronically-instrumented Long Evans rats. Both substances were administered continuously i.v. for 60min at two doses ((±)-dobutamine, 2 and lOpmolkgr'h-i; human a-CGRP, 0.15 and 1.5 nmol kg1 h 1). 2 In spite of their similar (small) effects on mean arterial blood pressure, the low doses of (±)-dobutamine and human a-CGRP influenced cardiac haemodynamics differently. Thus, (±)-dobutamine caused an increase in cardiac index (due to a tachycardia), accompanied by rises in peak aortic flow, maximum rate of rise of aortic flow (dF/dtmai) and total peripheral conductance. However, the latter waned during the infusion, and after the infusion there was a significant systemic vasoconstriction and reductions in peak aortic flow, dF/dtmax and stroke index. Such 'off' effects following dobutamine infusion have not been described previously. The infusion of the lower dose of human cx-CGRP caused only a transient fall in central venous pressure.3 The rise in total peripheral conductance during infusion of the lower dose of (±)-dobutamine was associated with increases in hindquarters and common and internal carotid vascular conductances. The fall in total peripheral conductance after infusion was associated with renal vasoconstriction. Although there was no significant change in total peripheral conductance during the infusion of the lower dose of human a-CGRP there were hindquarters and carotid vasodilatations together with mesenteric vasoconstriction. 4 Infusion of the higher dose of ( )-dobutamine had greater effects than the lower dose on all cardiac haemodynamic variables and additionally, increased stroke index. However, the negative cardiac haemodynamic effects following the offset of infusion were also enhanced in association with marked renal and mesenteric vasoconstrictions. While infusion of the higher dose of human a-CGRP increased cardiac index, peak aortic flow, dF/dtmax and total peripheral conductance, stroke index fell together with central venous pressure. 5 (±)-Dobutamine caused greater cardiostimulation and increases in hindquarters blood flow than did human a-CGRP. However, the latter at the higher dose caused substantially greater common and internal carotid hyperaemia than did (±)-dobutamine, possibly indicating a selective and additional effect of human a-CGRP on cranial blood flow. Furthermore, there were no adverse cardiovascular effects following infusion of human a-CGRP.

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Central and Regional Vascular Hemodynamics Following Intravenous Milrinone in the Conscious Rat

Cited by 26 publications

References 0 publications

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Influence of levosimendan, pimobendan, and milrinone on the regional distribution of cardiac output in anaesthetized dogs

Effects of RS-1893, a novel cardiotonic agent, on central and peripheral hemodynamics in anesthetized rats.

Differential effects of (±)‐dobutamine and human α‐CGRP on cardiac and on regional haemodynamics in conscious Long Evans rats

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