Why the study?
Do various vasoactive agents and volume loading improve cardiac output in a goat model of acute pulmonary hypertension?
Do various vasoactive agents and volume loading improve cardiac output in a goat model of acute pulmonary hypertension?
In a goat model of acute pulmonary hypertension, volume loading with Ringer's lactate appears to be the optimal treatment to restore cardiac output without undesirable increases in heart rate.
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Volume loading may optimize output without tachycardia in experimental acute PH; leaves open translation to patients.
In eight anesthetized ventilated goats, the hemodynamic effect of isoproterenol (ISU), dopamine (DOP), norepinephrine (NE), nitroglycerin (NTG), and Ringer's lactate (RL) infusion was evaluated after inducing acute pulmonary hypertension (PHN) to decrease cardiac output. Therapy with ISU significantly (p less than .05) increased cardiac output, but also increased transmural right ventricular end-diastolic pressure (RVEDPTM) and heart rate (HR) and decreased stroke volume (SV) and right ventricular ejection fraction (RVEF). NE increased cardiac output, mean arterial pressure (MAP), systemic vascular resistance (SVR), and RVEF. DOP decreased pulmonary vascular resistance (PVR) and increased cardiac output, MAP, and RVEF, but also significantly increased HR. NTG increased cardiac output and RVEF while decreasing SVR and PVR. Intravascular volume expansion by RL infusion increased cardiac output, SV, and RVEDPTM and decreased HR and PVR. The results of this study indicate that volume loading may be the treatment of choice to restore cardiac output in the face of acute PHN. NE and NTG may be effective as an adjunct therapy. Although ISU and DOP increase cardiac output, the concomitant elevation in HR is undesirable.
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Mathru et al. (1986) studied this question.
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