Small-Dose Inhaled Nitric Oxide Attenuates Hemodynamic Changes After Pulmonary Air Embolism in Dogs (original) (raw)
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European Heart Journal. Acute Cardiovascular Care, 2020
BackgroundInhaled nitric oxide (iNO) effectively reduces right ventricular afterload when administered in the immediate phase of acute pulmonary embolism (PE) in preclinical animal models. In a porcine model of intermediate-risk PE, we aimed to investigate whether iNO has pulmonary vasodilator efficacy both in the immediate and prolonged phase of acute PE.MethodsAnesthetized pigs (n = 18) were randomized into three subgroups. An acute PE iNO-group (n = 6) received iNO at 40 ppm at one, three, six, nine and 12 hours after onset of PE. Vehicle animals (n = 6) received PE, but no active treatment. A third group of sham animals (n = 6) received neither PE nor treatment. Animals were evaluated using intravascular pressures, respiratory parameters, biochemistry and intracardiac pressure-volume measurements.ResultsThe administration of PE increased mean pulmonary artery pressure (mPAP) (vehicle vs sham; 33.3 vs 17.7 mmHg, p < 0.0001), pulmonary vascular resistance (vehicle vs sham; 847....
Inhaled nitric oxide improves hemodynamics during a venous air infusion (VAI) in dogs
Intensive Care Medicine, 1999
Objective: To evaluate the hemodynamic effects of inhaled nitric oxide (NO) during a venous air infusion (VAI) in dogs. We also addressed the question of whether NO therapy changes thromboxane (Tx) A2 release and nitrate/nitrite production during a VAI. Design: Prospective trial. Setting: University laboratory. Interventions: Anesthetized mongrel dogs received a VAI (0.2 ml × kg–1× min–1) after the measurement of baseline hemodynamics. Control dogs (n = 8) received no further treatment. After 30 min of VAI, NO 3 ppm inhalation was initiated (n = 7) for 30 min, followed by 30 min without NO inhalation, and then a final 30 min of NO 40 ppm treatment. Hemodynamic variables were registered and arterial and mixed venous blood samples were drawn for gas analysis and for the determinations of serum TxB2 (by enzyme-linked immunosorbent assay) and nitrate/nitrite (by high-performance liquid chromatography) levels. Results: The cardiac index increased 24 % and the pulmonary vascular resistance index decreased 30 % during both periods of NO inhalation. Arterial oxygen tension and arterial oxygen saturation were slightly lower after NO therapy. Nitrate/nitrite concentrations were unaltered in the control group and there were no differences between the arterial and mixed venous serum nitrate/nitrite levels. Nitrite concentrations remained below 1 μM in both groups of animals, but the nitrate concentration increased after inhalation of 40 ppm NO. Serum TxB2 increased after 60 min of VAI in the control group, but there was no increase in NO-treated animals (all p < 0.05) Conclusions: Nitrate/nitrite concentrations were unaltered after VAI in dogs. NO therapy attenuated TxA2 release and improved hemodynamics, but not blood oxygenation, in dogs with a VAI. There were no differences between the responses to 3 ppm and 40 ppm NO.
Lung, 2006
Acute pulmonary embolism increases pulmonary vascular resistance and may lead to acute right ventricular failure and cardiocirculatory collapse and respiratory failure, possibly resulting in substantial morbidity and mortality. Inhaled nitric oxide (NO) dilates pulmonary blood vessels and has been used to reduce pulmonary vascular resistance in patients with chronic thromboembolic pulmonary hypertension and acute respiratory distress syndrome. This case series describes our experience with inhaled NO administered to four patients suffering from acute massive pulmonary embolism following abdominal surgery. The four described patients recovering from small bowel resection, pancreatoduodenectomy, hemipelvectomy, or recent gastrointestinal bleeding had severe respiratory and hemodynamic deterioration due to pulmonary embolism. Each received inhaled NO (20-25 ppm) via the inspiratory side of the breathing circuit of the ventilator. Pulmonary and systemic blood pressures, heart rate, and lung gas exchange improved in all the patients within minutes after the initiation of NO administration. Inhaled NO may be useful in treating acute massive pulmonary embolism. This potential application warrants further investigation.
Inhaled nitric oxide is not a negative inotropic agent in a porcine model of pulmonary hypertension
The Journal of Thoracic and Cardiovascular Surgery, 1997
Background: Reports of pulmonary edema complicating inhaled nitric oxide therapy in patients with chronic heart failure and pulmonary hypertension have raised the concern that inhaled nitric oxide may have negative inotropic effects. Methods and results: We investigated the effect of multiple doses of inhaled nitric oxide (20, 40 and 80 ppm) on left ventricular contractile state in 10 open-chest pigs. Pressure-volume loops were generated during transient preload reduction to determine the end-systolic pressure-volume relationship and the stroke work-end-diastolic volume relation. Inhaled nitric oxide had no effect on systemic vascular resistance, cardiac output, end-systolic pressure-volume relationship or stroke workend-diastolic volume relation under normal conditions. After induction of pulmonary hypertension (intravenous thromboxane A z analog), inhalation of nitric oxide (80 ppm) resulted in a reduction in pulmonary vascular resistance (mean-standard error of the mean) from 10.4-3 to 6.5-2 Wood units (p < 0.001) and in pulmonary artery pressure from 44-4 to 33-4 mm Hg (p < 0.05). Left ventricular end-diastolic volume rose from 53-9 ml to 57-10 ml (p = 0.02). No statistically significant change in cardiac output or systemic vascular resistance was observed. Inhaled nitric oxide had no effect on end-systolic pressure-volume relationship or stroke work-end-diastolic volume relation. Conclusions: In a porcine model of pulmonary hypertension, inhaled nitric oxide does not impair left ventricular contractile function. Therefore the cause of pulmonary edema observed in some patients receiving inhaled nitric oxide is not due to a negative inotropic action of this therapy. (J Thorac Cardiovasc Surg 1997; 114:461-6) nhaled nitric oxide (NO) is currently being used in a number of clinical situations to selectively reduce 12 pulmonary vascular resistance. ' When given by the inhaled route, NO reduces pulmonary vascular resistance while leaving systemic vascular resistance From the Departments of Surgery, a Anesthesiology, b and Medicine,
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...
Nitric Oxide Inhalation Decreases Pulmonary Artery Remodeling in the Injured Lungs of Rat Pups
Circulation Research, 2000
Vascular injury causes the muscularization of peripheral pulmonary arteries, which is more pronounced in the infant than in the adult lung. Although inhaled NO gas attenuates pulmonary artery remodeling in hypoxic rats, whether or not it protects the lung by mitigating vasoconstriction is unknown. This investigation tested whether inhaled NO decreases the muscularization of injured pulmonary arteries in rat pups by modulating vascular tone. One week after monocrotaline administration, the percentage of muscularized rat pup lung arteries was increased by Ͼ3-fold. Nevertheless, monocrotaline exposure did not cause right ventricular hypertrophy, pulmonary hypertension, or vasoconstriction. In addition, it did not increase the expression of markers of inflammation (interleukin-1, intercellular adhesion molecule-1, and E-selectin) or of platelet-mediated thrombosis (GPIb␣). Continuous inhalation of 20 ppm NO gas prevented the neomuscularization of the pulmonary arteries in pups with lung injury. Moreover, a 3-fold increase in cell proliferation and 30% decrease in cell numbers in pulmonary arteries caused by monocrotaline exposure was prevented by NO inhalation. These data indicate that inhaled NO protects infants against pulmonary remodeling induced by lung injury by mechanisms that are independent of pulmonary tone, inflammation, or thrombosis. (Circ Res. 2000;87:140-145.) Key Words: inhaled nitric oxide Ⅲ pulmonary hypertension Ⅲ proliferation Ⅲ congenital heart disease Ⅲ bronchopulmonary dysplasia
European Journal of Pharmacology, 1993
Nitric oxade (10 ppm) inhaled by pigs before or during endotoxln shock induced by an infusion of E coh lipopolysacchande Nitric oxade inhalation selectively attenuated pulmonary hypertension during endotoxln infusion without influencing mean arterml blood pressure and cardtac output Upon cessation of nitric oxade inhalation, pulmonary artery pressure rapidly increased to levels seen m endotoxm-treated controls The oxygenation and pH of arterial blood were significantly higher m the ammals receiving mtnc oxide A marked increase m arterial plasma noradrenahne and neuropept~de Y was seen m endotorantreated control pigs whde m the mtnc oxide-treated pigs this increase was markedly reduced The increase In arterial plasma endothehn-1 was not influenced by mtric orade inhalation Infusion of L-arglnme (substrate for mtnc oxide synthesis) also attenuated the pulmonary hypertension but was not selectwe for the pulmonary vasculature L-Nltro-arglnme (a nitric oxide synthesis inhibitor) lnltmted a rapid but brief elevahon of arterial blood pressure and of pulmonary artery pressure as well as a reduction m cardiac output Nitric oxade inhalation selectively reduces pulmonary hypertension in porcine endotoxln shock and improves arterial oxygenation and pH with a marked attenuation of sympathetic actwatlon Nitric oxide (NO), Endotoxan shock, Pulmonary hypertension, Adult respiratory distress syndrome (ARDS), Endothehn, Noradrenahne, Neuropeptlde Y
Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series
Respiratory …, 2012
Inhaled nitric oxide (INO) has been shown to preferentially lower resistance in the pulmonary vasculature. The relative selectiveness of INO in accomplishing this effect makes it an attractive drug to administer as salvage therapy in patients with acute right ventricular failure secondary to pulmonary embolism. We describe 4 cases in which INO was used as a temporizing agent to decrease right ventricular after-load following massive near-fatal pulmonary embolism. All 4 patients survived to hospital discharge. Key words: massive pulmonary embolism; acute cor pulmonale; right heart failure; inhaled nitric oxide. [Respir Care 2012;57 :444 -448.