Inhaled nitric oxide is not a negative inotropic agent in a porcine model of pulmonary hypertension (original) (raw)
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2010
We sought to compare the responses of patients with pulmonary hypertension from primary and secondary causes (PPH and SPH, respectively) to inhaled nitric oxide (iNO) in the cardiac catheterization laboratory. BACKGROUND Pulmonary hypertension can lead to right ventricular pressure overload and failure. Although vasodilators are effective as therapy in patients with PPH, less is known about their role in adults with SPH. Inhaled nitric oxide can accurately predict the response to other vasodilators in PPH and could be similarly utilized in SPH.
The Journal of physiology, 1994
1. The actions of inhibitors of the release or action of nitric oxide (NO) on pulmonary vascular resistance (PVR) were investigated in lungs isolated from pig, sheep, dog and man. 2. In pig, sheep and human lungs perfused with Krebs-dextran solution, both N omega-nitro-L-arginine methyl ester (L-NAME; 10(-5) M) and Methylene Blue (10(-4) M) increased basal PVR. This increase was reversed by sodium nitroprusside (10(-5) M). In pig lungs N omega-monomethyl-L-arginine (10(-4) M) increased PVR by 154%. This increase was partially reversed by L-arginine (10(-3) M). L-NAME had no effect in dog lungs. 3. Pulmonary artery pressure-flow (PPA/Q) relationships were studied over a wide range of flows. In pigs, sheep and human lungs perfused with Krebs-dextran solution, L-NAME increased the PPA/Q slope. This increase was reversed by sodium nitroprusside. In dog lungs L-NAME had no effect. 4. In blood-perfused lungs, the respective responses to L-NAME were similar to those observed with saline. A...
European Journal of Anaesthesiology, 1996
Summary intravenous nitroglycerine, inhaled nitric oxide increased arterial PaO 2 from 5.3 to 5.9 kPa (P=0.02). Pulmonary hypertension is usually treated with intra-Both treatments diminished central venous pressure venous (i.v.) vasodilators, but their use is limited by and left atrial pressure, suggesting a possible cardiac systemic effects. In the current study, we compared effect. Inhaled nitric oxide was shown to be a potent the effects of inhaled nitric oxide and intravenous pulmonary vasodilator which attenuated pulmonary nitroglycerine on pulmonary and systemic haemohypertension and improved arterial oxygenation withdynamic responses as well as on gas exchange measout important direct effects on systemic pressure in urements in anaesthetized pigs whose pulmonary porcine hypoxia-induced pulmonary hypertension. pressure was increased by hypoxia (FiO 2 =15%). Both treatments reduced pulmonary pressure to the control Keywords: nitric oxide, nitroglycerine, pulmonary hylevel. Inhaled nitric oxide did not affect systemic arpertension, systemic arterial pressure, cardiac effect, terial pressure but intravenous nitroglycerine depig. creased it from 126.2 to 108.8 mmHg (P=0.04). Unlike
Veterinary Research Communications, 2007
Pirrone, F., Albertini, M., Mazzola, S., Pastore, C., Clement, M.G., Benfatto, M.C., Aldini, G. and Carini, M., 2007. Intravenous infusion of nitric oxide in experimental pulmonary hypertension: biotransformation and haemodynamics. Veterinary Research Communications, 31(Suppl. 1), 185–187
Nitric oxide and pulmonary arterial pressures in pulmonary hypertension
Free Radical Biology and Medicine, 2004
Decreased production of vasodilator substances such as nitric oxide (NO) has been proposed as important in development of pulmonary arterial hypertension (PAH). We hypothesize that NO measured over time serves as a non invasive marker of severity of PAH and response to therapy. We prospectively and serially measured exhaled NO and carbon monoxide (CO), a vasodilator and anti-inflammatory product of heme oxygenases, in 17 PAH patients in conjunction with hemodynamic parameters over 2 years. Although pulmonary artery pressures and NO were similar in all patients at entry to the study, NO increased in the 12 individuals who survived to complete the study, and correlated with change in pulmonary artery pressures. In contrast, CO did not change or correlate with hemodynamic parameters. Investigation of NO-oxidant reaction products in PAH in comparison to controls suggests that NO synthesis is impaired in the lung and that reactive oxygen species may be involved in the pathophysiology of pulmonary hypertension. Endogenous NO is inversely related to pulmonary artery pressure in PAH, with successful therapy of PAH associated with increase in NO. D
Pediatric Cardiology, 2002
The purpose of this study was to evaluate the hemodynamic eects of inhaled nitric oxide in oxygen (NO + O 2 ) in patients with pulmonary hypertension. Eighteen patients (median age 31.5 months) with pulmonary hypertension inhaled through a mask 100% O 2 and 20 parts per million NO + inspired O 2 fraction (FiO 2 ) at 0.4. Hemodynamic measurements were made at baseline and after O 2 and NO + O 2 administration. The pulmonary vascular resistance index decreased after inhalation of O 2 and NO + O 2 (p = 0.0018 and p = 0.0003, respectively), the decrease being signi®cantly greater after NO + O 2 (p = 0.0311). Concerning the transpulmonary pressure gradient, a reduction occurred in values after O 2 and NO + O 2 inhalation when compared with baseline values (p = 0.0014 and p = 0.0008). In patients with congenital heart disease, an increase occurred in pulmonary blood¯ow after O 2 (p = 0.0089) and NO + O 2 (p = 0.0019) compared with baseline values, and an increase also occurred in the pulmonary/systemic blood¯ow ratio after NO + O 2 (p = 0.0017). The main side eect related to NO + O 2 was pulmonary congestion in 3 patients. Low doses of NO combined with O 2 demonstrated a selective pulmonary vasodilator response in patients with pulmonary hypertension. Despite its use for testing pulmonary reactivity, inhalation of NO + O 2 should be carefully administered because of the potential risk of pulmonary congestion.
Critical care (London, England), 1997
BACKGROUND: In order to test the hypothesis that inhaled nitric oxide (NO) reverses the pulmonary hypertension induced by alphaalpha-diaspirin crosslinked hemoglobin (alphaalphaHb), were studied anesthetized pigs that were administered with a total dose of 200 mg/kg of 10% alphaalphaHb. Inhaled NO (5 ppm) was administered for 10 min, and then discontinued for 10 min. This cycle was then repeated with 10 ppm inhaled NO. RESULTS: alphaalphaHb caused pulmonary arterial pressure (PAP) to increase from 27 +/- 1.7 to 40 +/- 3.0 mmHg (P<0.05) and dynamic lung compliance to decrease from 29+/- 1.5 to 23+/- 1.6 ml/cmH2O (P < 0.05). After both doses of inhaled NO, but particularly 10 ppm, PAP was reduced (P < 0.05) and lung compliance increased (P < 0.05) from the alphaalphaHb levels. When inhaled NO was discontinued PAP again increased and lung compliance decreased to levels significantly different from baseline (P < 0.05). CONCLUSION: We conclude that cell-free hemoglobin-ind...
Pediatric Research, 2005
Persistent pulmonary hypertension of the newborn is characterized by elevated pulmonary vascular resistance after birth leading to right-to-left shunting and systemic arterial hypoxemia. Inhaled nitric oxide (NO) is effective in reducing the need for extracorporeal membrane oxygenation, but it has potential toxicities, especially in an oxygen-rich environment. A number of other NO-based molecules have been given by inhalation, but their structure-function relationships have not been established. Recent studies have raised the idea that toxic and beneficial properties can be separated. We synthesized a novel organic nitrate [ethyl nitrate (ENO 2 )], tested it in vitro, and administered it to hypoxic piglets. ENO 2 lowered pulmonary artery pressure and raised the PO 2 in arterial blood but did not alter systemic vascular resistance or methemoglobin levels. In addition, we tested the effect of ENO 2 in the presence of the thiol glutathione, both in vivo and in vitro, and found its action to be enhanced. Although ENO 2 is less potent than inhaled NO on a doseequivalency basis, pretreatment of hypoxic animals with glutathione, which may be depleted in injured lungs, led to a markedly enhanced effect (largely mitigating the difference in potency).