Reduction In Pulmonary Artery Pressure Research Articles

Decrease in pulmonary artery pressure after administration of thoracic epidural anesthesia in a patient with Marfan syndrome awaiting aortic valve replacement procedure

Thoracic epidural anesthesia is an adjunct to general anesthesia in cardiac surgery. Decrease in heart rate and blood pressure are frequently seen beneficial effects. There are several other hemodynamic effects of thoracic epidural anesthesia such as decrease in systemic vascular resistance, cardiac index, left ventricular stroke work index among others. However, the effect of thoracic epidural anesthesia on pulmonary artery pressure (PAP) has not been studied extensively in humans. Thoracic epidural anes-thesia decreased pulmonary artery pressure in experimen-tally induced pulmonary hypertension in animals. The mechanisms involved in such reduction are ill understood. We describe in this report, a significant reduction in PAP in a patient with Marfan's syndrome scheduled to under-go aortic valve replacement. The possible mechanisms of decrease in pulmonary artery pressure in the described case are, decrease in the venous return to the heart, decrease in the systemic vascular resistance, decrease in the right ventric-ular function and finally, improvement in myocardial contraction secondary to all the above. The possibility of Marfan's syndrome contributing to the decrease in PAP appears remote. The authors present this case to generate discussion about the possible mechanisms involved in thoracic epidural anesthesia producing beneficial effects in patients with secondary pulmonary hypertension. Thoracic epidural anesthesia appears to decrease pulmonary artery pressure by a combination of several mechanisms, some unknown to us. This occurrence, if studied and understood well could be put to clinical use in pulmonary hypertensives.

Treatment of Pulmonary Arterial Hypertension: Great Expectations!

> “Take nothing on its looks; take everything on evidence. There’s no better rule.” > > — Charles Dickens, Great Expectations Pulmonary arterial hypertension (PAH) is a serious, progressive, often fatal condition characterized by increased pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR)1,2. Patients with PAH experience dyspnea and exercise limitation — and as right ventricular (RV) failure develops, edema, exertional chest pain, syncope, and increased risk of death. PAH is most commonly idiopathic (IPAH) or associated with an underlying connective tissue disease (CTD-PAH), such as scleroderma1. In both IPAH and CTD-PAH patients, median survival is less than 3 years in the absence of therapy3,4,5. Research advances in our understanding of the pathobiology of PAH have led to the study, approval, and availability of many novel PAH-specific medications. These include prostanoid analogs (i.e., intravenous epoprostenol, subcutaneous/intravenous treprostinil), endothelin receptor antagonists (i.e., ambrisentan, bosentan), and phosphodiesterase type-5 inhibitors (i.e., sildenafil, tadalafil)2,6. What are the expectations of this array of therapies on the part of patients with PAH and their physicians? The published evidence, typically short-term, 3 to 4-month, randomized controlled trials of all these therapies, demonstrates benefit in both IPAH and CTD-PAH7. A majority of patients have small reductions in PAP and PVR, increased cardiac output, decreased symptoms, and increased exercise capacity, as measured by 6-minute walk test (6-MWT). New York Heart Association/World Health Organization (NYHA/WHO) functional class will improve in about one-third of patients, and objectively measured quality of life (QOL) may also improve2,6,7. A metaanalysis of published randomized controlled trials of PAH-specific therapies also confirmed a small, short-term survival benefit7. Thus, based on the evidence, patients with PAH and their physicians expect symptomatic benefit and improved functional capacity, important components … Address correspondence to Dr. S. Mehta, Division of Respirology, London Health Sciences Center, Victoria Hospital, Room E1.325, 800 Commissioner’s Road East, London, ON N6A 5W9, Canada. E-mail: sanjay.mehta{at}lhsc.on.ca

Progenitor cells in pulmonary vascular remodeling.

Pulmonary hypertension is characterized by cellular and structural changes in the walls of pulmonary arteries. Intimal thickening and fibrosis, medial hypertrophy and fibroproliferative changes in the adventitia are commonly observed, as is the extension of smooth muscle into the previously non-muscularized vessels. A majority of these changes are associated with the enhanced presence of α-SM-actin+ cells and inflammatory cells. Atypical abundances of functionally distinct endothelial cells, particularly in the intima (plexiform lesions), and also in the perivascular regions, are also described. At present, neither the origin(s) of these cells nor the molecular mechanisms responsible for their accumulation, in any of the three compartments of the vessel wall, have been fully elucidated. The possibility that they arise from either resident vascular progenitors or bone marrow–derived progenitor cells is now well established. Resident vascular progenitor cells have been demonstrated to exist within the vessel wall, and in response to certain stimuli, to expand and express myofibroblastic, endothelial or even hematopoietic markers. Bone marrow–derived or circulating progenitor cells have also been shown to be recruited to sites of vascular injury and to assume both endothelial and SM-like phenotypes. Here, we review the data supporting the contributory role of vascular progenitors (including endothelial progenitor cells, smooth muscle progenitor cells, pericytes, and fibrocytes) in vascular remodeling. A more complete understanding of the processes by which progenitor cells modulate pulmonary vascular remodeling will undoubtedly herald a renaissance of therapies extending beyond the control of vascular tonicity and reduction of pulmonary artery pressure.

Regulation of the Pulmonary Circulation in the Fetus and Newborn

During the development of the pulmonary vasculature in the fetus, many structural and functional changes occur to prepare the lung for the transition to air breathing. The development of the pulmonary circulation is genetically controlled by an array of mitogenic factors in a temporo-spatial order. With advancing gestation, pulmonary vessels acquire increased vasoreactivity. The fetal pulmonary vasculature is exposed to a low oxygen tension environment that promotes high intrinsic myogenic tone and high vasocontractility. At birth, a dramatic reduction in pulmonary arterial pressure and resistance occurs with an increase in oxygen tension and blood flow. The striking hemodynamic differences in the pulmonary circulation of the fetus and newborn are regulated by various factors and vasoactive agents. Among them, nitric oxide, endothelin-1, and prostaglandin I(2) are mainly derived from endothelial cells and exert their effects via cGMP, cAMP, and Rho kinase signaling pathways. Alterations in these signaling pathways may lead to vascular remodeling, high vasocontractility, and persistent pulmonary hypertension of the newborn.

Not hearing is believing: novel insight into cardiopulmonary function using agitated contrast and ultrasound

the advancement of science depends heavily on the development and successful application of new techniques. Progress in ultrasound technology has allowed researchers in physiology to examine many important parameters noninvasively, including cerebral blood flow velocity, pulmonary artery systolic

Activation of endothelial BKCa channels causes pulmonary vasodilation

BackgroundLarge-conductance Ca2+-activated K+ (BKCa) channels cause hyperpolarization and can regulate vascular tone. In this study, we evaluated the effect of endothelial BKCa activation on pulmonary vascular tone. MethodsThe presence of BKCa channels in lung microvascular endothelial cells (LMVEC) and rat lung tissue was confirmed by RT-PCR, immunoblotting and immunohistochemistry. Isolated pulmonary artery (PA) rings and isolated ventilated-perfused rat lungs were used to assay the effects of BKCa channel activation on endothelium-dependent vasodilation. ResultsImmunoblotting and RT-PCR revealed the presence of BKCa channel α- and β4-subunits in LMVEC. Immunohistochemical staining showed BKCa channel α-subunit expression in vascular endothelium in rat lungs. In arterial ring studies, BKCa channel activation by NS1619 enhanced endothelium-dependent vasodilation that was attenuated by tetraethylammonium and iberiotoxin. In addition, activation of BKCa channels by C-type natriuretic peptide caused endothelial-dependent vasodilation that was blocked by iberiotoxin, L-NAME, and lanthanum. Furthermore, BKCa activation by NS1619 caused a dose-dependent reduction in PA pressures that was attenuated by L-NAME. In vitro, BKCa channel activation in LMVEC caused hyperpolarization and increased NO production. ConclusionsPulmonary endothelium expresses BKCa channels. Activation of endothelial BKCa channels causes hyperpolarization and NO mediated endothelium-dependent vasodilation in micro- and macrovasculature in the lung.

Update on the clinical utility of sildenafil in the treatment of pulmonary arterial hypertension

Sildenafil is an orally administered phosphodiesterase type 5 inhibitor that is approved for the treatment of pulmonary arterial hypertension (PAH). The hemodynamic effects of sildenafil are mitigated primarily via potentiating the effects of endogenous nitric oxide, leading to smooth muscle cell relaxation and reductions in pulmonary arterial pressures and pulmonary vascular resistance. When added to standard background therapy in patients with idiopathic or associated PAH from congenital heart disease, anorexigen use, or connective tissue disease, sildenafil treatment results in improved exercise capacity as measured by 6 minute walk distance, improved hemodynamics, and favorable changes in quality of life. Sildenafil use is contraindicated with concomitant nitrate administration, and caution should be exercised when used in combination with antihypertensive agents due to risks of precipitating hypotension. Side effects are generally mild, and include flushing, headaches, and epistaxis. The combination of sildenafil with intravenous epoprostenol is safe and well tolerated, and further improves exercise capacity. Sildenafil is approved only for treatment of PAH, and although emerging data suggest a potential role in treating other types of pulmonary hypertension, larger trials are required to confirm these findings.

Anomalous Origin of the Left Coronary Artery from the Right Pulmonary Artery Presenting Following Relief of Left Heart Obstruction: A Distinct and Predictable Clinico-Pathological Syndrome

Pre-operative recognition of significant abnormalities of the coronary arteries is important in a variety of congenital cardiac conditions. Failure to diagnose anomalous origin of the coronary artery from the pulmonary artery during repair of other anomalies is important because reduction in pulmonary artery pressure will reduce myocardial perfusion pressure. We report two cases of the rare association of anomalous origin of the left coronary artery from the right pulmonary artery, aortic coarctation, and mitral stenosis. Definitive imaging of coronary artery anatomy by echocardiography or other modalities should form a routine part of diagnostic assessment in all congenital heart disease patients but particularly those with left heart obstruction.

Pulmonary Arterial Hypertension in Patients With Transcatheter Closure of Secundum Atrial Septal Defects

Pulmonary arterial hypertension (PAH) may develop in patients with atrial septal defects (ASD); however, little is known about associated risk factors and its evolution after transcatheter ASD closure. We conducted a cohort study on 215 adults with attempted transcatheter ASD closure from 1999 to 2006. Patients were classified according to baseline systolic pulmonary artery pressures as having no (I, <40 mm Hg), mild (II, 40 to 49 mm Hg), moderate (III, 50 to 59 mm Hg), or severe (IV, >or=60 mm Hg) PAH. Independent predictors of moderate or severe PAH were older age (odds ratio [OR], 1.10 per year; P<0.0001), larger ASD (OR, 1.13 per millimeter; P=0.0052), female sex (OR, 3.9; P=0.0313), and at least moderate tricuspid regurgitation (OR, 3.6; P=0.0043). At 15 (interquartile range, 8 to 43) months post-ASD closure, patients with higher baseline pressures were more likely to experience a >or=5-mm Hg decrease (33.7%, 73.9%, 79.2%, and 100.0% in groups I to IV, P<0.0001), with a larger magnitude of reduction (0, 8, 17, and 22 mm Hg; P<0.0001). However, normalization of pressures (<40 mm Hg) occurred less frequently in patients with more advanced PAH (90.2%, 71.7%, 66.7%, and 23.5%, P<0.0001). Among patients with moderate or severe PAH, independent predictors of normalization were lower baseline pressures (OR, 0.91 per mm Hg; P=0.0418) and no more than mild tricuspid regurgitation (OR, 0.14; P=0.0420). In adults with ASDs, severity of PAH is modulated by age, sex, defect size, and degree of tricuspid regurgitation. Patients with moderate or severe PAH may benefit from substantial reductions in pulmonary artery pressures after transcatheter ASD closure, although the PAH values remain elevated in a sizeable proportion.

The effect of adenoidectomy on right ventricular performance in children

Objective Several studies have shown a reduction in pulmonary artery pressure (PAP) after adenoidectomy in children suffering form upper airway obstruction caused by adenoid hypertrophy (AH). However, it is not clear whether this would be significantly reflected on right ventricle output (RVO). Methods Our aim was to determine if there were any detectable changes in RV performance parameters after adenoidectomy in children with AH. Thirty children with AH (female/male: 11/19) aged between 2.5 and 12 years (median: five years) were included in this study. Adenoidectomy was performed under sinuscopic guide using adenoid curette and microdebrider. All children were examined by echocardiography one day before and one month after adenoidectomy. Velocity time integral of tricuspid valve flow (VTItv) and pulmonary valve flow (VTIpa); E/ A ratio of tricuspid valve flow; RV end-diastolic diameter (RVEDd) and left ventricle fraction shortening (FS) were measured. Heart rate (HR) was also recorded. Results Preoperatively VTItv, VTIpa, E/ A ratio, RVEDd, FS, and HR were 18.6 ± 3.0 cm, 20.8 ± 3.1 cm, 1.21 ± 0.31, 11.5 ± 2.1 mm, 35.1 ± 4.3%, and 112 ± 19, respectively. Postoperatively VTItv, VTIpa, E/ A ratio, RVEDd, FS, and HR were 21.5 ± 2.5 cm, 24.4 ± 4.3 cm, 1.44 ± 0.32, 9.3 ± 2.6 mm, 33.9 ± 3.5%, and 104 ± 28, respectively. There were significant differences between preoperative and postoperative VTItv ( p = 0.03), VTIpa ( p = 0.01), E/ A ratios ( p = 0.04), and RVEDd ( p = 0.01). FS and HR were not significantly different. Conclusions This study illustrated that in children suffering from AH, relieving upper airway obstruction by adenoidectomy may result in improvement of RV filling and RVO, associated with the reduction in PAP.

Sildenafil therapy in secondary pulmonary hypertension: Is there benefit in prolonged use?

Background Sildenafil is of benefit to selected patients with pulmonary hypertension due to parenchymal lung or cardiac disease. We present data from patients with secondary pulmonary hypertension, comparing their right heart catheter results and six minute walking distance to time on treatment. Methods 25 patients with symptomatic secondary pulmonary hypertension received sildenafil 50 mg tds in a 5-year period. Underlying causes were chronic inoperable thromboembolic disease (11), COPD (6), interstitial lung disease (5) and valvular heart disease (3). Their cardio-pulmonary haemodynamics were measured with right heart catheterization prior to treatment, post-treatment at 2, 6 and 12 months and subsequently depending upon clinical need. Six-minute walk distance was also measured. Results Patient age range was 40 to 83 (median 70.5) years. Time of treatment to latest right heart catheter was 2 to 60 (median 17) months and 8 to 61 (median 34) months to clinic follow-up or death. There was a significant reduction in six-minute walk distance from baseline to long term (> 12 months) follow-up ( p = 0.002). Pulmonary vascular resistance was significantly reduced from baseline to 12 months ( p = 0.049). The mean pulmonary arterial (PA) pressure was significantly reduced at long-term follow-up ( p = 0.009). 20 patients had an improved PA pressure with treatment. In those with a worsening PA pressure, two had an improvement in cardiac output and six minute walk distance, two had stable cardiac output at 20 and 21 months, and one had measurements taken during a significant illness. Three patients, who had a reduction in PA pressure, subsequently died of progression of underlying illness at 8 months, from myocardial infarction at 34 months, and from aspergillus pneumonia at 59 months. Conclusion Long-term use of sildenafil in patients with secondary forms of pulmonary hypertension is associated with a sustained improvement in cardio-pulmonary haemodynamics. Lack of improvement may be attributed to other factors apart from treatment failure, such as underlying disease progression or unrelated concurrent illness at time of assessment.

Obstructive Sleep Apnea and Pulmonary Hypertension

Obstructive sleep apnea (OSA) is associated with repetitive nocturnal arterial oxygen desaturation and hypercapnia, large intrathoracic negative pressure swings, and acute increases in pulmonary artery pressure. Rodents when exposed to brief, intermittent hypoxia for several hours per day to mimic OSA developed pulmonary vascular remodeling and sustained pulmonary hypertension and right ventricular hypertrophy within a few weeks. Until recently, however, it was unclear whether episodic nocturnal hypoxemia associated with OSA was sufficient to cause similar changes in humans. This controversy appears to have been resolved by several recent studies that have shown (a) pulmonary hypertension in 20% to 40% of patients with OSA in the absence of other known cardiopulmonary disorders and (b) reductions in pulmonary artery pressure in patients with OSA after nocturnal continuous positive airway pressure (CPAP) treatment. The pulmonary hypertension associated with OSA appears to be mild and may be due to a combination of precapillary and postcapillary factors including pulmonary arteriolar remodeling and hyperreactivity to hypoxia and left ventricular diastolic dysfunction and left atrial enlargement. Although measurable changes in the structure and function of the right ventricle have been reported in association with OSA, the clinical significance of these changes is uncertain. Right ventricular failure in OSA appears to be uncommon and is more likely if there is coexisting left-sided heart disease or chronic hypoxic respiratory disease.

Inhaled nitric oxide versus aerosolized iloprost for the treatment of pulmonary hypertension with left heart disease*

To determine the effects of inhaled nitric oxide (NO) and aerosolized iloprost on pulmonary hemodynamics and lung edema formation in a rat model of pulmonary hypertension due to congestive heart failure (CHF). Prospective, randomized, controlled study. Research laboratory. One hundred sixty male Sprague-Dawley rats. CHF was induced by supracoronary aortic banding whereas sham-operated rats served as controls. CHF rats or controls inhaled NO, aerosolized iloprost, or 0.9% NaCl for 3 minutes each. Additional CHF groups received intravenous infusions of iloprost, sodium nitroprusside, or 0.9% NaCl. For prolonged drug administration over 150 minutes, NO was inhaled continuously whereas aerosolized iloprost was administered for 3 minutes each at 45-minute intervals. Dose-response relations in rats with CHF showed a maximal pulmonary-selective reduction in blood pressure at 20 ppm NO and 2.5 microg/mL aerosolized iloprost, with iloprost therapy resulting in a greater decrease in pulmonary arterial pressure (PAP). At these doses, both vasodilators decreased pulmonary vascular resistance and increased venous oxygen saturation (Svo2) in the absence of systemic hemodynamic effects. No pulmonary or systemic effects were detected in rats with CHF inhaling 0.9% NaCl or in control rats inhaling NO or iloprost. Intravenous infusion of iloprost or sodium nitroprusside not only reduced pulmonary but also systemic vascular resistance. During prolonged inhalation, NO caused a stable reduction in PAP, whereas PAP decreased even further during repetitive iloprost inhalations. After 150 minutes, iloprost-treated rats had a higher Svo2 and lesser edema as compared with animals with CHF inhaling NO or untreated rats with CHF, although differences in wet/dry weight ratio did not reach statistical significance (p < 0.06). Inhaled vasodilators may offer an effective, safe, and pulmonary-selective strategy for the treatment of pulmonary hypertension in left heart disease, and inhaled iloprost may be superior to NO in this condition.

Continuous epoprostenol therapy and septal defect closure in a patient with severe pulmonary hypertension

A 31-year-old woman with exertional dyspnea diagnosed as having atrial septal defect (ASD) with severe pulmonary hypertension (PH). Intravenous epoprostenol therapy was started to improve PH. Although pulmonary arterial pressure decreased, her symptoms remained in class III of WHO functional class, probably because of exacerbation of the left-to-right shunt caused by the reduction of pulmonary vascular resistance (PVR). Transcatheter atrial septal closure was therefore performed. Soon after the procedure, additional reduction in pulmonary arterial pressure was achieved. Her symptoms improved and oxygen inhalation was discontinued. One year after the procedure, although intravenous epoprostenol was still required, her symptoms had improved to class I of WHO functional class without exacerbation of PH. Transcatheter atrial septal closure after lowering PVR by intravenous epoprostenol would be a novel therapy for patients with ASD accompanied by PH.

Effect of tonsillectomy and/or adenoidectomy on pulmonary arterial pressure in adults

Abstract The aim of the study was to determine the mean pulmonary pressure in adult with hypertrophic tonsils and adenoids and to clarify whether tonsillectomy and adenoidectomy has any effect on mean pulmonary arterial pressure of these adult. The study was carried out on 50 patients with diagnosis of upper airway obstruction resulting from hypertrophied tonsils and adenoids (group1). 25 adults were assigned as control with similar age and sex distribution (group2). For study subjects Routine general Examinations, BMI, ECG, Chest X ray, Arterial blood gases and Echocardiography were done. Mean pulmonary arterial pressure was measured by using Doppler Echocardiography preoperatively and mean 3–4 months postoperatively in all subjects. Elevated PAP (pulmonary artery pressure) was found in 15 patients (30%) in group 1 preoperatively. Mean PAP was 28.34 ±5.11 mmHg preoperative in group 1 and 19.84 ± 5.0 mmHg in group 2 (p &lt;0.001). PAP decrease to 22.38 ±4.28 mmHg postoperatively in group 1 (p &lt;0.001). Arterial oxygen saturation (spo2%) increase from 93.5 ± 1.9% preoperatively to 95.3 ± 1.3% post operatively (p &lt; 0.001). percent reduction of PAP postoperatively correlates to age (t=−2.3, p= 0.02), preoperative PAP (p =0.01) but no correlation was found with BMI. In conclusions, this Study showed that obstructed adenoid and hypertrophy of tonsils causes higher mean pulmonary artery pressure in adult &amp; revealed that tonsil&amp; adenoid is effective therapeutic measure in such patients. With early intervention is necessary to avoid progressive cardiopulmonary disease.

Total anomalous pulmonary venous drainage beyond childhood

We studied the anatomic characteristics and results of surgery in 27 patients with total anomalous pulmonary venous drainage who were 15 years or older between January 1997 and July 2007. Mean age was 19.7+/-11.6 years (15-48 years). The anatomic subtypes were supracardiac (n=15), cardiac (n=7), and mixed (n=5). Fourteen patients were in NYHA class II and 13 were in NYHA class III. Eleven patients had severe and the rest had moderate pulmonary arterial hypertension; six patients had significant right ventricular dysfunction. All patients underwent complete repair. A small inter-atrial communication was left open in four patients and in two patients, a fenestrated unidirectional valved patch was used to close the atrial septal defect. There were no early or late deaths. Follow-up was 3-127 months (mean 61.2+/-36.1 months). Twenty patients were in NYHA class I and seven were in class II. Echocardiography showed normal right and left ventricular function in all patients with reduction of pulmonary arterial pressures in 26 patients. One patient underwent radiofrequency ablation for new onset atrial flutter. Surgery can be safely undertaken in a few naturally selected group of patients with total anomalous pulmonary venous drainage who survive beyond childhood.

Pulmonary haemodynamic changes in patients with severe COPD

Worsening gas exchange during exercise and during exacerbations of COPD contributes to systemic hypoxaemia and reduces quality of life. However, pulmonary haemodynamic changes under such conditions are not well understood. Right heart catheterization was performed in six patients with severe COPD (%FEV(1) < 50%) during rest, exercise and during an exacerbation. Pulmonary artery pressure (Ppa) was slightly elevated at rest. The Ppa, as well as pulmonary artery wedge pressure (Pawp) and cardiac index were significantly increased during bicycle ergometer exercise. In contrast, pulmonary vascular resistance increased significantly during an exacerbation accompanied by a slightly increased Ppa. Supplemental oxygen resulted in significant decreases in Ppa and Pawp during exercise and Ppa during exacerbations. In patients with COPD, haemodynamic changes in the pulmonary circulation may differ during exercise and with exacerbations. Supplementary oxygen is beneficial and associated with reductions in pulmonary arterial pressures.

Significant improvement of portopulmonary hypertension after 1-week terlipressin treatment

Cirrhosis associated with moderate and severe portopulmonary hypertension carries a poor prognosis. Optimal management has not yet been defined. Current treatment options, such as prostacyclin analogues, endothelin antagonists, and phosphodiesterase-5 inhibitors, are characterized by slow onset of action and various adverse effects, particularly in patients with advanced cirrhosis. Here, we report the significant reduction of pulmonary arterial pressure after 1-week terlipressin treatment in a patient with concomitant hepato-renal syndrome. Terlipressin could be a novel and safe treatment for portopulmonary hypertension.

Pulmonary Hemodynamic Responses to Intravenous Prostaglandin E2 in Broiler Chickens

Prostaglandin E(2) (PGE(2)) affects pulmonary arterial pressure (PAP), pulmonary vascular resistance (PVR), and respiratory rate (RR) in mammals, but no information previously was available regarding avian pulmonary responses to PGE(2). Two experiments were conducted in which 45- to 55-d-old male broiler chickens were infused i.v. with PGE(2) at the lowest rate (30 mug/min for 4 min) that reliably reduced PAP during pilot studies. When compared with preinfusion (control) values in experiment 1, PGE(2) reduced PAP from 19 +/- 1 to 16 +/- 1 mmHg (P < 0.001) and reduced mean systemic arterial pressure from 111 +/- 6 to 81 +/- 5 mmHg (P < 0.001) but did not significantly reduce heart rate (HR; control: 338 +/- 9 beats/min; PGE(2): 320 +/- 12 beats/min; P > 0.05). Infusing PGE(2) also reduced the RR from 57 +/- 2 to 46 +/- 4 breaths/min (P < 0.001) and reduced the percentage saturation of hemoglobin with oxygen (%HbO(2)) from 85 +/- 2 to 77 +/- 3%HbO(2) (P < 0.001). After the PGE(2) infusion ceased, the PAP, mean systemic arterial pressure, RR, and %HbO(2) recovered within 8 min to levels that did not differ from preinfusion control values. In experiment 2, an ultrasonic flow probe was surgically implanted on 1 pulmonary artery to measure cardiac output (CO). When compared with preinfusion control values, PGE(2) reduced CO from 140 +/- 6 to 111 +/- 5 mL/kg of BW x min (P < 0.001), reduced PAP from 25 +/- 2 to 21 +/- 1 mmHg (P < 0.001), and reduced RR from 49 +/- 4 to 35 +/- 4 breaths/min (P < 0.001). The reduction in CO was caused by a reduction in HR from 305 +/- 9 to 260 +/- 9 beats/min without a significant reduction in stroke volume (control: 0.46 +/- 0.02 mL/kg of BW x beat; PGE(2): 0.43 +/- 0.02 mL/kg of BW x beat; P = 0.158). After the PGE(2) infusion ceased the CO, PAP, RR, and HR recovered within 9 min to levels that did not differ from preinfusion control values. The PVR, calculated as PAP/CO, was not altered by PGE(2) (control: 0.18 +/- 0.01 relative resistance units; PGE(2): 0.20 +/- 0.02 relative resistance units; P > 0.723). These results indicate that in broilers PGE(2) reduced PAP by reducing CO rather than by acting as a pulmonary vasodilator to lower PVR. The PGE(2)-induced reductions in PAP would benefit broilers that are susceptible to pulmonary hypertension syndrome by reducing their right ventricular overload; however, the reductions in CO and RR combined with the onset of systemic arterial hypoxemia would accelerate the pathophysiological progression leading to terminal pulmonary hypertension syndrome.

2007 in Review: A Dozen Steps Forward in Anesthesiology

Summary These 12 articles represent an inspiring collection ofadvances in our specialty. Yet another dozen could easilyhave been chosen, including: ● Long-term neuroprotection from isoflurane: Sakai et al .A NESTHESIOLOGY 2007; 106:92–9 ● The first human application of a novel local anesthetic:Rodriquez-Navarro et al .A NESTHESIOLOGY 2007; 106:339–45 ● Application of monitoring to measure in real time end-tidal concentrations of systemically administereddrugs: Takita et al .A NESTHESIOLOGY 2007; 106:659–64and Hornuss et al .A NESTHESIOLOGY 2007; 106:665–4 ● ASA practice guidelines for obstetric anesthesia: Con-nis et al .A NESTHESIOLOGY 2007; 106:843–63 ● The safety of low dose droperidol in the peri-operativeperiod: Nuttall et al .A NESTHESIOLOGY 2007; 106:531–6 ● Moving neuromuscular monitoring electrodes 2 cmmedially reduces the incidence of postoperative nau-sea and vomiting as much as pharmacologic therapy:Arnberger et al .A NESTHESIOLOGY 2007; 107:903–8 ● Laboratory studies suggesting a drug used orally totreat Alzheimer’s disease might also be used to treatchronic pain: Clayton