[Designing equipment--a few view points].
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Dental Equipment↗
Biomedical subjects
S Lundin
Publications and source records attributed to S Lundin.
Acute vasodepressor effect in normotensive rats following extracorporal perfusion of the declipped kidney of two-kidney, one clip hypertensive rats.
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Animals↗
Vasodilator therapy after heart transplantation: effects of inhaled nitric oxide and intravenous prostacyclin, prostaglandin E1, and sodium nitroprusside.
BACKGROUND: Vasodilator therapy is frequently needed to treat pulmonary hypertension after heart transplantation. In the present study, the effects of intravenous sodium nitroprusside, prostacyclin, prostaglandin E1, and inhaled nitric oxide (5, 10, and 20 parts per million) on central hemodynamics, right ventricular function, and pulmonary selectivity were evaluated shortly after heart transplantation. METHODS: Hemodynamic measurements were made after surgery in the intensive care unit. The intravenous vasodilators were compared at equipotent infusion rates. Effects of inhaled nitric oxide were measured after 10 minutes inhalation at each dose level. RESULTS: Cardiac output, stroke volume, right ventricular end-diastolic volume, and central filling pressures were highest with prostacyclin (16 +/- 2 ng/kg/min) compared with both prostaglandin E1 (202 +/- 27 ng/kg/min) and sodium nitroprusside (1.0 +/- 0.2 microgram/kg/min). Systemic and pulmonary vascular resistance were lowest with prostacyclin. None of the intravenous vasodilators induced a selective pulmonary vasodilation. In contrast, nitric oxide inhalation induced a selective decrease in pulmonary vascular resistance, with no change in systemic vascular resistance. Cardiac output increased with nitric oxide, whereas mean pulmonary arterial pressure, transpulmonary pressure gradient, and central venous pressure decreased, with the most pronounced effect at an inhaled concentration of 20 parts per million. CONCLUSIONS: Prostacyclin is the best choice for intravenous vasodilator therapy after heart transplantation. However, inhaled nitric oxide is the only selective pulmonary vasodilator, which should be used in cases of pulmonary hypertension and severe right ventricular failure associated with systemic hypotension.
Administration, Inhalation↗
Inhaled nitric oxide in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance.
The reversibility of elevated pulmonary vascular resistance in heart transplant candidates is currently evaluated with intravenous vasodilators. The aim of this study was to evaluate the effects of increased concentrations of inhaled nitric oxide (20, 40, and 80 ppm) on central hemodynamics and right ventricular function in heart transplant candidates with elevated pulmonary vascular resistance (> 2.5 Wood units). Comparison was made with intravenous vasodilators, sodium nitroprusside, and prostacyclin in doses that lowered the mean arterial pressure by about 15%. Inhalation of nitric oxide did not change systemic or pulmonary arterial pressure, cardiac output, right ventricular function, or systemic vascular resistance. Pulmonary capillary wedge pressure increased and transpulmonary pressure gradient and pulmonary vascular resistance decreased (-34% +/- 4% and -36% +/- 4%, respectively; p < 0.01) during 20 ppm nitric oxide, with no further effects at higher doses. Prostacyclin and sodium nitroprusside decreased pulmonary vascular resistance (-50% +/- 6% and -33% +/- 5%; p < 0.01). Prostacyclin reduced to some extent (p = 0.08) transpulmonary pressure gradient, which was not seen during sodium nitroprusside infusion. Systemic vascular resistance decreased during both sodium nitroprusside (-37% +/- 5%) and prostacyclin (-44% +/- 4%) infusion. The pulmonary vascular resistance/systemic vascular resistance ratio, used as an index of pulmonary selectivity, was decreased by nitric oxide (p < 0.01) but not by the intravenous vasodilators. Metabolic data indicate that inhaled nitric oxide is metabolized in the same way as that formed endogenously. In conclusion, inhaled nitric oxide is a selective pulmonary vasodilator that can be used safely in the hemodynamic evaluation of heart transplant candidates with elevated pulmonary vascular resistance.
Administration, Inhalation↗