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    Abstract
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    Materials and Me...
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JANAK MEHTA AWARD Table of Contents   
Year : 2010  |  Volume : 13  |  Issue : 2  |  Page : 138-144
Acute hemodynamic effects of inhaled nitroglycerine, intravenous nitroglycerine, and their combination with intravenous dobutamine in patients with secondary pulmonary hypertension


1 Department of Cardiac Anesthesiology, All India Institute of Medical Sciences (AIIMS), New Delhi, India
2 Department of CTVS, CN Center, All India Institute of Medical Sciences (AIIMS), New Delhi, India

Click here for correspondence address and email

Date of Submission13-Dec-2009
Date of Acceptance13-Mar-2010
Date of Web Publication3-May-2010
 

   Abstract 

Objectives: The presence of pulmonary artery hypertension (PAH) affects the prognosis of patients; therefore, it is important to treat it. The aim of this study is to compare the acute hemodynamic effects of inhaled nitroglycerine (iNTG), intravenous nitroglycerine (IV NTG) alone and their combination with intravenous dobutamine (IV DOB) during the early postoperative period, in patients with PAH undergoing mitral valve or double valve replacement surgery. Materials and Methods: In the study, 40 patients with secondary PAH were administered iNTG 2.5 μg/kg/min, IV NTG 2.5 μg/kg/min, a combination of iNTG 2.5 μg/kg/min + IV DOB 10 μg/kg/min, and IV NTG 2.5 μg/kg/min + IV DOB 10 μg/kg/min for 10 minutes each following valve replacement surgery, in random order. The hemodynamic parameters were recorded before (T0) and immediately after the intervention. (T1). Results: iNTG effectively decreased mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance index (PVRI), and the PVR / SVR ratio, without affecting arterial pressures, systemic vascular resistance or mixed venous oxygen saturation (SvO 2 ). IV NTG produced both systemic and pulmonary vasodilation along with a significant fall in SvO 2 . The combination of iNTG and IV DOB caused a significant decrease in mPAP and PVRI, with no significant change in SVRI, PVR / SVR ratio, and SvO 2 . A combination of IV NTG + IV DOB caused both pulmonary and systemic vasodilatation with a significant decrease in SvO 2 . None of the drugs caused any significant change in the cardiac index. Conclusion: All drugs were of similar efficacy in reducing the pulmonary vascular resistance index. Only iNTG produced selective pulmonary vasodilatation, while IV NTG and its combination with IV dobutamine had a significant concomitant systemic vasodilatory effect.

Keywords: Inhaled nitroglycerine, intravenous nitroglycerine, intravenous dobutamine, pulmonary artery hypertension

How to cite this article:
Mandal B, Kapoor PM, Chowdhury U, Kiran U, Choudhury M. Acute hemodynamic effects of inhaled nitroglycerine, intravenous nitroglycerine, and their combination with intravenous dobutamine in patients with secondary pulmonary hypertension. Ann Card Anaesth 2010;13:138-44

How to cite this URL:
Mandal B, Kapoor PM, Chowdhury U, Kiran U, Choudhury M. Acute hemodynamic effects of inhaled nitroglycerine, intravenous nitroglycerine, and their combination with intravenous dobutamine in patients with secondary pulmonary hypertension. Ann Card Anaesth [serial online] 2010 [cited 2020 Mar 29];13:138-44. Available from: http://www.annals.in/text.asp?2010/13/2/138/62946



   Introduction Top


Pulmonary artery hypertension (PAH) is a common complication of valvular heart disease. Its presence and severity is associated with an increased risk of right ventricular failure (RVF) following valve surgery, thereby leading to greater morbidity and mortality.

Vasodilator drugs, for example, intravenous (IV) sodium-nitroprusside (SNP), nitroglycerine (NTG), prostaglandin; inhaled nitric oxide (iNO), iloprost, NTG, SNP, and inodilators such as dobutamine and milrinone have been used to prevent and treat RVF in patients with PAH, after valve surgery.

Inhaled nitroglycerine (iNTG) has proved to be successful in decreasing pulmonary artery pressure (PAP) after Mitral Valve Replacement (MVR) without causing hypotension. [1],[2] Also, it is effective in children with congenital heart disease with PAH. [3] iNTG also exerts a favorable effect on oxygenation as it does not inhibit hypoxic pulmonary vasoconstriction (HPV), thereby preventing any increase in intrapulmonary shunt fraction. [1],[4]

In cardiac surgical patients the combination of IV NTG and dobutamine in a low dose, 5 - 10 μg/kg/min, is routinely used for decreasing PAP and increasing cardiac output (CO). However, the hemodynamic effects of a combination therapy of iNTG and low dose IV dobutamine in patients undergoing valve surgery have not yet been addressed.

IV NTG not only decreases PAP and systemic arterial pressure, but also inhibits HPV, thereby causing ventilation-perfusion (V/Q) mismatch, resulting in poorer oxygenation. [2],[5] Dobutamine has been shown to increase CO and improve oxygen transport and oxygenation in patients with massive pulmonary embolism. [6],[7],[8]

Therefore, we hypothesized that a combination of iNTG with IV dobutamine will not only produce a decrease in PAP, but also an increase in CO and improvement in oxygenation. Hence, we undertook this study to compare the acute hemodynamic effects of iNTG, IV NTG, iNTG + IV dobutamine, and IV NTG + IV dobutamine, in patients with valvular heart disease and PAH undergoing MVR or double valve replacement (DVR) surgery.


   Materials and Methods Top


This study was conducted at the Cardiothoracic Center of the All India Institute of Medical Sciences; with the approval of the Hospital Ethics Committee and informed consent from the patients. A total of 40 adult patients of either sex, undergoing elective MVR or DVR surgery for valvular heart disease and PAH [mean PAP (mPAP) > 25 mmHg] were enrolled in the study. All the drugs were administered to the same group of patients to decrease the confounding factors, because of the different pathophysiology in different disease conditions.

An additional prerequisite was to ensure stable postoperative hemodynamic conditions to allow repetitive withdrawal of vasodilator substances for reassessment of baseline values and to avoid the necessity for hemodynamic interventions such as volume substitution or a change in inotropic support.

Exclusion criteria

The patients with contraindications for pulmonary artery catheterization, emergency surgery, redo surgeries, history of chronic obstructive pulmonary disease, left ventricular ejection fraction < 40 %, post bypass mPAP< 25 mmHg, unstable hemodynamics, increased mediastinal bleeding, high inotropic requirement, mechanical circulatory assistance, and echocardiographic evidence of significant tricuspid regurgitation were excluded from this study.

Anesthesia management

All patients were premedicated with morphine 0.1 mg/kg and promethazine 0.5 mg/kg intramuscularly 30 - 45 minutes prior to induction of anesthesia. Anesthesia was induced with IV fentanyl (2 - 3 μg/kg), thiopentone (3 - 5 mg/kg) titrated to effect, midazolam (1 - 2 mg), and the trachea was intubated following vecuronium bromide (0.1 mg/kg). The anesthesia was maintained with intermittent fentanyl, midazolam, vecuronium, and sevoflurane (2 - 3%) in oxygen and air (50:50).

Continuous hemodynamic monitoring in the patient included pulse oximetry, electrocardiography (lead II, V 5 ), systemic arterial pressure through 20 G radial artery cannula, central venous pressure through a triple lumen (7.5 Fr., Arrow International, Inc 2400, Bernville road, Reading, PA 19605, USA), and pulmonary artery pressure using 7.5 Fr thermodilution pulmonary artery catheter (Swan- Ganz catheter, Edward Life Sciences LLC Irvine, CA, USA) via the right internal jugular vein, and transesophageal echocardiography (TEE). The same monitoring, except TEE, continued into the post surgical intensive care unit.

All the patients underwent MVR or DVR under mild hypothermia with standard cardiopulmonary bypass according to the institutional protocol. Intraoperatively, IV NTG 0.5 - 1 μg/kg/min and IV dopamine 5 - 10 μg/kg/min were infused, to facilitate weaning from cardiopulmonary bypass. Patients with a low heart rate were paced using atrial or atrioventricular sequential pacing.

The study was performed in the intensive care unit (ICU) within the first eight hours after surgery. IV NTG was discontinued 60 minutes before the initial baseline measurements. During the study period all the patients were sedated with fentanyl (2 μg/kg. hr -1 ) and paralyzed with vecuronium and the study was continued. The patients were mechanically ventilated with a constant tidal volume of 10 ml/kg and the respiratory rate was adjusted to maintain a pH of 7.35 - 7.45, a paCO 2 of 35 - 45 mmHg, and fiO 2 60%, using a servo 900C ventilator (Servo 900 C, Siemens Elema, Lund, Sweden). No hemodynamic interventions other than the initiation and withdrawal of study groups were performed during the study period. The iNTG was nebulized using 6 l/min of medical air with the help of the CIRRUS Jet Nebulizer (Intersurgical Respiratory Systems, Berkshire, UK) attached to the inspiratory limb of the ventilator.

A complete profile of hemodynamic parameters was noted before each individual drug administration (baseline T 0 ) and after inhalation of NTG (2.5 μg/kg/min for 10 minutes; 25 μg/kg for over 10 minutes), IV NTG (2.5 μg/kg/min for 10 minutes), a combination of iNTG (2.5 μg/kg/min) + IV Dobutamine (10 μg/kg/min) for 10 minutes, and IV NTG (2.5 μg/kg/min) + IV Dobutamine (10 μg/kg/min) for 10 minutes. After stopping the study drug, a minimum period of 20 minutes or until PAP returned to within 5% of the baseline value was allowed after each vasodilator was stopped, before the second set of drugs was administered.

The hemodynamic parameters measured included mean arterial pressure (MAP) (mmHg), mean pulmonary artery pressure (mPAP) (mmHg), pulmonary capillary wedge pressure (PCWP) (mmHg), central venous pressure (CVP) (mmHg), cardiac index (CI) (l/min/m 2 ), heart rate (HR) (per min), PVRI (dynes.sec/cm 5 .m 2 ), SVRI (dynes.sec/cm 5 .m 2 ), and PVR / SVR ratio (P/R). The cardiac output was estimated using three to four iced saline injections, randomly distributed throughout the respiratory cycle, using a cardiac output monitor; SIRECUST 1261 (Siemen's, Danvers, MA, 01923, USA). The mean of these readings was taken as the cardiac output each time. CI, SVRI, and PVRI were derived from the measured hemodynamic variables using the standard formulae. Arterial and mixed venous blood samples were drawn at baseline and after each drug administration, to measure the mixed venous oxygen saturation (SvO 2 ).

After the study was completed, the patients were maintained on IV NTG and IV dopamine and / or dobutamine as per the patient's requirement and routine ICU care was provided according to the institute protocol.

Statistical analysis was performed using STATA- 9 software. Continuous data were presented as mean ± SD and median (range). The t-test and Wilcoxon signed-rank tests were used for comparison of continuous variables depending on normality. A P value < 0.05 was considered to be statistically significant.


   Results Top


The patient characteristics are presented in [Table 1] and the hemodynamic parameters measured are illustrated in [Table 2].

iNTG challenge

iNTG caused a significant decrease in mPAP, PVRI, and P/R without significant modifications in the other hemodynamic parameters, such as, MAP, CVP, PCWP, HR, SVRI, CI, and SvO 2 [Table 2].

IV NTG challenge


Nitroglycerine infusion caused a significant decrease in MAP, mPAP, PCWP, CVP, PVRI, and SVRI, and an increase in HR with no change in CI or P/R. This was associated with a significant decrease in SvO 2 [Table 2].

iNTG with IV dobutamine challenge

The combination of iNTG and IV dobutamine caused a significant decrease in mPAP , PVRI, and MAP with no significant change in CVP, PCWP, CI, HR , SVRI, P/R, and SvO 2 [Table 2].

IV NTG with IV dobutamine challenge

The combination of IV NTG and IV dobutamine caused a significant decrease in MAP, mPAP, PCWP, CVP, PVRI, and SVRI, with no significant change in P/R. There was a significant decrease in SvO 2 [Table 2].

Comparison of treatments


The mPAP was significantly reduced for all drugs, with a maximal decrease for iNTG (-19%) followed by IV NTG (-18%). A significant decrease in PVRI was found with all drugs, iNTG (-26%), IV NTG (-25%), iNTG + IV DOB (-16%), and IV NTG + IV DOB (-24%).

A significant decrease in SVRI was found with IV NTG (-21%) and IV NTG + IV DOB (-17%), while there was no significant change in SVRI with iNTG or iNTG + IV DOB.

The median PVR / SVR ratio (P/R) decreased significantly with iNTG (-24%), while it increased with IV DOB + IV NTG (+ 29%).

The SvO 2 increased with iNTG and iNTG + IV DOB, although it was not statistically significant, but SvO 2 decreased significantly with IV NTG and IV NTG + IV DOB.

There was no significant change in CI with any of the drugs. The MAP decreased significantly with IV NTG and IV NTG + IV DOB. There was no significant change in the heart rate with either of the drugs, although higher heart rates were seen in patients receiving a combination of IV NTG + IV Dobutamine. There was a significant decrease in PCWP and CVP with the use of IV NTG and the combination of IV NTG + IV Dobutamine, while there was no change with iNTG or iNTG + IV Dobutamine.


   Discussion Top


The pathophysiological mechanisms contributing to PAH in the longstanding valvular disease include:

  • Increased left arterial pressure ; back pressure on pulmonary circulation
  • Vascular remodeling in response to chronic obstruction (fixed component)
  • Pulmonary arterial vasoconstriction (reactive component).
PAH is usually reflex in origin in the immediate postbypass period. Cardiopulmonary bypass itself contributes to an increase in mPAP. Several days or even weeks might be required for the increased PVR to return to normal after surgery. The reactive component of PAH is amenable to prevention and treatment with the aid of pulmonary vasodilators, thereby reducing the risk of RVF in the immediate postbypass period.

Vasodilator agents are one of the therapeutic options in the treatment of PAH. Inhalation of nitric oxide (NO) is a popular treatment modality. NO inhalation may have adverse reactions and the clinical use requires an expensive and complicated system. NTG gets metabolized to NO, which is a potent smooth muscle relaxant in the vascular endothelial cells. Inhaled nitroglycerine is cheap, convenient to administer and gives rise to a higher local concentration of NO. [9],[10]

In our study iNTG in a dose of 2.5 μg/kg/min produced a significant decrease in mPAP and PVRI, without significant changes in MAP, CVP, PCWP, HR, SVRI, and CI. We found the onset of action to be within 3 - 5 minutes and the effect lasted for about 20 - 30 minutes. These results are similar to those of Yurtseven et al. who showed that in patients with PAH undergoing MVR, inhalation of NTG in a dose of 2.5 μg/kg/min, nebulized by a 2 - l gas flow of 40% oxygen and air mixture, produced a significant reduction in mPAP and PVR, without reducing MAP, CVP, PCWP, HR, CI, or SVR. The onset of action in their study was also within 3 - 5 minutes, but the effect lasted around 60 minutes after a single dose of nebulization. [1]

In another study Yurtseven et al. found that in patients with PAH undergoing MVR, inhaled NTG in a dose of 20 μg/kg nebulized by 2-l air jet, effectively reduced mPAP and PVR without affecting MAP, SVR, or CO. [2] Omar et al. investigated the effects of inhalational NTG in PAH resulting from congenital heart disease and reported decreases in SPAP and mPAP as a result of NTG administration; however, HR, SBP, and MAP were not affected. [11] Goyal et al. studied the efficacy of NTG inhalation in reducing PAH in children with congenital heart disease. With a dose of 2.5 μg/kg/mg for 10 minutes there was a significant decrease in systolic, diastolic, and mean PAP as well as PVRI, without it affecting the systemic hemodynamics and they postulated that it could be used as a therapeutic modality for acute reduction of PAH in children with congenital heart disease. [3] In a study by Gong et al., in dogs with experimentally induced PAH, inhalation of nebulized NTG decreases mPAP, dPAP, and sPAP without affecting SBP, DBP, MAP, SVR or CO. [12]

In our study the median PVR / SVR ratio decreased with inhaled NTG (24%), (p < 0.001) indicating selectivity to the pulmonary vasculature. The selective pulmonary vasodilatation did not lead to inhibition of HPV, hence the higher SvO 2 with iNTG.

We found that IV NTG in a dose of 2.5 μg/kg/min infusion produced a significant decrease in MAP, mPAP, PCWP, CVP, PVRI, and SVRI, and an increase in HR, with no change in CI, PVR / SVR ratio. The above-mentioned results proved the effectiveness of IV NTG as a pulmonary vasodilator. Besides, IV NTG induced significant reductions in the outflow impedance of both ventricles (decreased PVRI and SVRI) and decreased right and left cardiac filling pressures (CVP, PCWP). Also it did not cause a significant change in the PVR / SVR ratio, further indicating a lack of pulmonary selectivity. The vasodilator effect of IV NTG was accompanied by a worsening in arterial oxygenation as documented by a significant decrease in mixed venous oxygen saturation (SvO 2 ), probably due to the inhibition of HPV leading to an increased shunt fraction. This was similar to the results seen by Schmid et al., who studied the effect of inhaled NO 40 ppm and IV NTG in a dose of 3 - 5 μg/kg/min, in patients with severe PAH after cardiac surgery, and found that iNO and IV NTG had similar efficacy in reducing PVR. iNO induced selective pulmonary vasodilation while NTG had a significant concomitant systemic vasodilatory effect. iNO led to an increase in cardiac index while NTG had no effect on CI or RV performance. [5]

Bando et al. compared nitroglycerine infusion and inhalation in doses of 1 and 2.5 μg/kg/min, respectively, in dogs with HPV, and reported that NTG inhalation in doses of 2.5 μg/kg/min decreases MAP, mPAP, and PVR, but did not affect the cardiac output. The same doses of NTG infusion did not decrease mPAP, but decreased MAP. They concluded that inhalation of NTG is more effective in pulmonary circulation when compared to NTG infusion. We have also found that inhaled NTG improves oxygenation, whereas, IV NTG decreases paO 2 by inhibiting HPV. [4] In our study mPAP and PVRI were significantly reduced with iNTG and IV NTG. iNTG caused a significant decrease in the PVR / SVR ratio without decrease in MAP and SVRI, whereas, IV NTG caused a significant decrease in MAP and SVR, with no changes in the PVR / SVR ratio, indicating greater pulmonary selectivity, without systemic hypotension with iNTG as compared to IV NTG. We also observed an increase in SvO 2 with iNTG and a decrease in SvO 2 with IV NTG suggesting possible inhibition of HPV with IV NTG.

Vizza et al. studied the acute hemodynamic effect of iNO, dobutamine, and a combination of the two in patients with mild-to-moderate secondary pulmonary artery hypertension awaiting lung transplant. They found that iNO (40 ppm) decreased mPAP, increased paO 2 , and significantly decreased Qs/Qt (venous admixture). Dobutamine 10 μg/kg/min for 10 minutes produced an increase in CI and mPAP with a decrease in paO 2 as a result of high Qs/Qt. A combination of these two drugs produced an increase in CI without mPAP modification and an increase in paO 2 and Qs/Qt. [8]

The above-mentioned results document the effectiveness of IV dobutamine to treat PAH. IV dobutamine produces a decrease in right cardiac filling pressures (CVP) and increases the contractility of the right ventricle, thus decreasing right ventricular end diastolic volume. It significantly decreases PVRI, thereby, decreasing right ventricular afterload and increases SVI and right ventricular output. Although dobutamine produces a significant decrease in PVRI, it also causes an increase in CI, thereby increasing mPAP. This can be attributed mainly to the recruitment of vessels rather than to its vasodilator effect. It does not cause a significant change in the PVR / SVR ratio, indicating no pulmonary selectivity. In our study we did not see any decrease in SvO 2 with IV dobutamine used in combination with iNTG, probably because the vascular recruitment occurred in well-ventilated lung areas, unlike the study by Vizza et al., who studied the lung transplant patients with severe, underlying lung pathology. [8]

Ducas J. et al. studied the general hemodynamic effects of dopamine and dobutamine in dogs with acute pulmonary hypertension complicated by a decrease in cardiac output (CO). Both dopamine and dobutamine increased CO (p < 0.05) and decreased PVR (p < 0.05). Ventricular filling pressures were not affected. Pulmonary- pressure flow plots suggested that these findings were not a result of vasodilatation. They concluded that both before and after the induction of pulmonary hypertension, dopamine and dobutamine improved CO without affecting a pulmonary vascular tone. [13]

Majerus TC. et al. studied that in dosages of 2 - 15 μg/kg/min, dobutamine has been seen to increase cardiac output (mainly through stroke volume), reduce systemic vascular resistance, lower central venous and pulmonary artery wedge pressures, improve renal blood flow, and relieve signs and symptoms of congestive heart failure. In higher dosages it can increase heart rate and induce arrhythmias. [14]

In our study the combination of iNTG and IV dobutamine caused a significant decrease in MAP, mPAP, and PVRI, with no significant change in CVP, PCWP, CI, HR, SVRI, PVR / SVR ratio or SvO 2 . To the best of our knowledge, the interaction of iNTG and IV dobutamine in pulmonary circulation has not been previously reported. The combination of both these drugs produces a decrease in mPAP, PVRI, but no change in CI. This suggests that the increase in CI induced by dobutamine is counterbalanced by the concomitant pulmonary vasodilatation induced by iNTG. The combination also increased SvO 2, indicating a favorable effect on oxygenation.

The combination of IV NTG and IV dobutamine produces a significant decrease in MAP, mPAP, PVRI, PCWP, CVP, SVRI, and SvO 2, with no significant change in CI or PVR/SVR ratio. The combination of these drugs produces a greater decrease in the left ventricular preload and afterload indicated by a decrease in PCWP and SVRI. This reflexly incites a greater increase in HR, although it is not statistically significant. The combination has also produced a significant decrease in SvO 2 following the inhibition of HPV by IV NTG, combined with an increased oxygen demand by IV dobutamine, in our study.

Limitations

The patients with RV dysfunction were not included in this study. Hence, the actual effect of iNTG in the management of RV dysfunction could not be assessed. The actual dose of the drug reaching the lungs, after nitroglycerine inhalation, could not be predicted. The pediatric patients who had greater hemodynamic perturbations secondary to PAH were also not included in this study.


   Conclusion Top


Inhaled nitroglycerine is a cheap, convenient to administer, selective pulmonary vasodilator without systemic adverse effects. iNTG can be used to treat PAH either alone on in combination with intravenous dobutamine. iNTG is a better alternative than IV NTG in patients with PAH undergoing valvular surgery. The inhaled route may be even more beneficial in the management of patients with RV dysfunction, secondary to PAH, especially because of the lack of systemic vasodilatory effect. The combination of intravenous nitroglycerine and dobutamine may be helpful in the setting of PAH with biventricular dysfunction, but caution has to be maintained when using this combination in patients with lung pathology, because of systemic hypotension and inhibition of HPV.

 
   References Top

1.Yurtseven N, Karaca P, Kaplan M, Ozkul V, Tuygun AK, Aksoy T, et al. Effect of nitroglycerine inhalation on patients with pulmonary hypertension undergoing mitral valve replacement surgery. Anesthesiology 2003;99:855-8.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]  
2.Yurtseven N, Karaca P, Uysal G, Ozkul V, Cimen S, Tuygun AK, et al. A comparison of the acute hemodynamic effects of inhaled nitroglycerine and Iloprost in patients with pulmonary hypertension undergoing mitral valve surgery. Ann Thorac Cardiovasc Surg 2006;12:319-23.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Goyal P, Kiran U, Chauhan S, Juneja R, Choudhary M. Efficacy of nitroglycerine inhalation in reducing pulmonary arterial hypertension in children with congenital heart disease. Br J Anesth 2006;97:208-14.  Back to cited text no. 3      
4.Bando M, Ishii Y, Kitamura S, Ohno S. Effects of inhalation of nitroglycerine on hypoxic pulmonary vasoconstriction. Respiration 1998;65:63-70.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Schmid ER, Bόrki C, Engel MH, Schmidlin D, Tornic M, Seifert B. Inhaled nitric oxide versus intravenous vasodilators in severe pulmonary hypertension after cardiac surgery. Anesth Analg 1998;89:1108-15.  Back to cited text no. 5      
6.Jardin F, Genevray B, Brun-Ney D, Margairaz A. Dobutamine: A hemodynamic evaluation in pulmonary embolism shock. Crit Care Med 1985;13:1009-12.  Back to cited text no. 6  [PUBMED]    
7.Manier G, Castaing Y. Influence of cardiac output on oxygen exchange in acute pulmonary embolism. Am Rev Resp Dis 1992;145:130-6.  Back to cited text no. 7  [PUBMED]    
8.Vizza CD, Rocca GD, Roma AD, Iacoboni C, Pierconti F, Venuta F, et al. Acute Hemodynamic effects of inhaled nitric oxide, dobutamine and a combination of the two in patients with mild to moderate secondary pulmonary hypertension. Crit Care 2001;5:355-61.  Back to cited text no. 8  [PUBMED]  [FULLTEXT]  
9.Archer SL, Huang JM, Hampl V, Nelson DP, Shultz PJ, Weir EK. Nitric oxide and cGMP cause vasorelaxation by activation of a charybdotoxin - sensitive K channel by c GMP dependent protein kinase. Proc Natl Acad Sci USA 1994;91:7583-7.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Marks GS, McLaughlin BE, Nakatsu K, Brien JF. Direct evidence for nitric oxide formation from glycerile trinitrate during incubation with intact bovine pulmonary artery. Can J Physiol Pharmacol 1992;70:308-11.  Back to cited text no. 10  [PUBMED]    
11.Omar HA, Gong F, Sun MY, Einzig S. Nebulized nitroglycerine in children with pulmonary hypertension secondary to congenital heart disease. W V Med 1999;95:74-5.  Back to cited text no. 11      
12.Gong F, Shiraishi H, Kikuchi Y, Hoshina M, Ichihashi K, Sato Y, et al. Inhalation of nebulized nitroglycerine in dogs with experimental pulmonary hypertension induced by U46619. Pediatr Int 2000;42:255-8.  Back to cited text no. 12  [PUBMED]  [FULLTEXT]  
13.Ducas J, Stitz M, Gu S, Schick U, Prewitt RM. Pulmonary vascular pressure-flow characteristics. Effects of dopamine and dobutamine before and after pulmonary embolism. Am Rev Respir Dis 1992;146:307-12.  Back to cited text no. 13      
14.Majerus TC, Dasta JF, Bauman JL, Danziger LH, Ruffolo RR Jr. Dobutamine: ten years later. Pharmacotherapy 1989;9:245-59.  Back to cited text no. 14  [PUBMED]    

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Correspondence Address:
Banashree Mandal
Department of Cardiac Anesthesiology, Max Devki Devi Heart and Vascular Institute, New Delhi-110 017
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.62946

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    Tables

  [Table 1], [Table 2]

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