Hemodynamic Effects of Angiotensin and Renin Inhibition in Dogs with Acute Left Ventricular Failure

Sweet, Charles S.; Ludden, C. T.; Frederick, C. M.; Ribeiro, Lair G.T.

doi:10.1016/s0002-9343(84)80052-2

Cited by 25 publications

(9 citation statements)

References 30 publications

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“…The effects of failure on preload are demonstrated by increase in left ventricular end-diastolic pressure and pulmonary capillary wedge pressure. These hemodynamic changes are the same as those reported by others who have used the same experimental model [30][31][32].…”

Section: Discussionsupporting

confidence: 87%

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Hall

Karlberg

1986

Res. Exp. Med.

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Acute left ventricular failure was induced in anesthetized dogs by left coronary embolization. Treatment with the converting enzyme inhibitor enalaprilat (MK-422) was then given. Hemodynamic registrations confirmed the development of left ventricular failure. Plasma concentrations of angiotensin II and aldosterone rose significantly. Treatment with enalaprilat was accompanied by significant reductions in heart preload and afterload and in plasma hormone concentrations.

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Section: Discussionsupporting

confidence: 87%

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Hall

Karlberg

1986

Res. Exp. Med.

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“…These results are similar to those of Sweet et al [26,27] who have been working with the same model. Leddy et al [17], examining conscious dogs in acute left ventricular failure, found no hemodynamic effect at all after ACE-inhibition.…”

Section: Discussionsupporting

confidence: 91%

“…The dose of enalaprilat used in this study equals the one used by Sweet et al [26,27]. Data presented by the same research group [11] indicate that this dose is sufficient to inhibit about 90% of the hypertensive response to infused angiotensin I.…”

Section: Discussionmentioning

confidence: 86%

Effect of ACE-inhibition on tissue blood flow during acute left ventricular failure in the dog

1987

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Anesthetized dogs in acute left ventricular failure were treated with the ACE-inhibitor enalaprilat (MK-422). ACE-inhibition produced a fall in the mean blood pressure and a redistribution of cardiac output to the brain, right ventricle, upper gastrointestinal tract, and the inner and middle part of the renal cortex. The flow to the spleen, adrenals, skin, muscle, fat, lower gastrointestinal tract, and outer renal cortex did not change significantly. The differential sensitivity of the tissues to ACE-inhibition is most likely due to differences in sensitivity to circulating angiotensin II.

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“…Studies are currently under way to confirm our impression that angiotensin II increases myocardial contrac tility. This would be consistent with studies on isolated myocardial muscle strips from adult animals and studies on the failing heart [12][13][14], However, in intact normoxemic adult animals the cardiac output routinely falls with angiotensin II infusion because of baroreceptor reflexes [15,16]. Interestingly, angiotensin II blunts the baroreceptor re flexes in conscious animals, but not enough to allow cardiac output to increase [15,16].…”

Section: Discussionsupporting

confidence: 84%

Hemodynamic Responses to Angiotensin II in the Newborn Lamb

Goetzman¹,

Bennett²

1991

Dev Pharmacol Ther

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Angiotensin II is known to increase both pulmonary and systemic arteriolar tone in adult animals. Its influence on these vascular beds shortly after birth is less well understood. Therefore, we studied the effects of infusions of angiotensin II (0.1 μg/kg/min) on pulmonary and systemic hemodynamics in 13 anesthesized newborn lambs. Systemic vascular resistance increased significantly from a mean of 0.079 ± 0.03 to 0.094 ± 0.04 mm Hg/ml/min during angiotensin II infusion while the mean pulmonary vascular resistance was unchanged at 0.024 ± 0.01 mm Hg/ml/min. Interestingly, cardiac output increased significantly by 18.9% during angiotensin II infusion. During hypoxemia produced by ventilating with 10-12% oxygen, the responses to angiotensin II infusion were similar to those obtained during normoxia. The absence of an effect on pulmonary vascular resistance and the increase in cardiac output were not predicted based on results reported for older animals. The mechanisms responsible for these age-related differences are unknown. Our findings have implications regarding the potential clinical use of angiotensin II as a modulator of blood pressure in the hypotensive newborn.

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Hemodynamic Effects of Angiotensin and Renin Inhibition in Dogs with Acute Left Ventricular Failure

Cited by 25 publications

References 30 publications

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Plasma concentrations of angiotensin II and aldosterone during acute left ventricular failure in the dog. Effect of converting enzyme inhibition

Effect of ACE-inhibition on tissue blood flow during acute left ventricular failure in the dog

Hemodynamic Responses to Angiotensin II in the Newborn Lamb

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