Mean Pulmonary Capillary Pressure Research Articles

Underrated value of repeated right heart catheterization in pulmonary hypertension with heart failure-a case of persisted pulmonary arterial hypertension after treatment for biventricular failure.

Pulmonary hypertension (PH) is a common complication of left heart disease and its presence in patients with heart failure predicts worse clinical outcomes. Specific agents targeting pulmonary arterial hypertension (PAH) have been developed over the last few years, but the efficacy of these agents in pulmonary hypertension due to left heart disease (PH-LHD) is uncertain. We report a case of idiopathic pulmonary arterial hypertension (IPAH) initially presented with biventricular failure, which was misdiagnosed as PH-LHD. A 31-year-old man who had a history of recurrent hemoptysis was referred to our center with biventricular failure. Right heart catheterization (RHC) showed elevated mean pulmonary arterial pressure (mPAP) and pulmonary capillary wedge pressure (PCWP). He was diagnosed as having PH-LHD, specifically combined post-capillary and precapillary PH (CpcPH). We treated him for 2 years with diuretics, a beta blocker, an angiotensin-converting enzyme (ACE) inhibitor, and sildenafil, which was added to treat CpcPH. A follow-up echocardiography showed that biventricular function had improved, but not PH. A second RHC revealed elevated mPAP and normal PCWP, which made us change the diagnosis to IPAH. In conclusion, it is important to perform repeated RHC in CpcPH patients after the improvement of left heart dysfunction to distinguish CpcPH from IPAH.

Right ventriculo-arterial coupling in repaired Fallot patients with pulmonary valve regurgitation before and after pulmonary valve implantation: a CMR study

Background Right ventricular-pulmonary arterial coupling plays an important role in the occurrence of right ventricular failure. Ventricular-arterial coupling is defined as Ea/ Emax. Ea is the effective arterial elastance and an index of the post-load, and includes vascular resistances, vessel compliance, vascular impedance, systolic and diastolic time intervals. Ea = (arterial end-systolic pressure/stroke volume), where arterial end-systolic pressure = (mean pulmonary arterial pressure wedge capillary pressure). The role of wedge capillary pressure can be considered negligible in subjects with normal pulmonary artery pressure and normal left ventricular (LV) function. Therefore, the formula can be simplified to Ea = (mean pulmonary arterial pressure/stroke volume). Emax is the maximal systolic ventricular elastance. This is a loadindependent index. It occurs at the end of the systole and is given by the formula Emax = [end-systolic pressure/(end-systolic volume volume (theorical) at zero load)]. Volume at zero load can be considered negligible, and end-systolic pressure can be approximated by mean pulmonary arterial pressure. Therefore Emax = (mean pulmonary artery pressure/end-systolic volume). Consequently, Ea/Emax = [(mean pulmonary artery pressure/ stroke volume)/(end-systolic volume/mean pulmonary artery pressure)] and results in Ea/Emax = (end-systolic volume/stroke volume). Optimal ventricular-arterial coupling is when Ea/Emax=1. Objective of this study is to evaluate by CMR the right ventricular-arterial coupling before and after surgical or transcatheter pulmonary valve implantation (PVI) in subjects who underwent surgery for tetralogy of Fallot (ToF) and have pulmonary valve (PV) regurgitation and/ or stenosis.

1843 High Frequency Oscillation and Prone Position in the Experimental Model of Ards - Changes of Pressure Hemodynamic Parameters

Background and AimsHigh frequency oscillation (HFO) and prone position ventilation have their places in the treatment of an inhomogeneous pulmonary pathology of ARDS. Possible benefits of early used HFO include...

Aquatic therapies in patients with compromised left ventricular function and heart failure

With water immersion, gravity is partly eliminated, and the water exerts a pressure on the body surface. Consequently there is a blood volume shift from the periphery to the central circulation, resulting in marked volume loading of the thorax and heart. This paper presents a selection of published literature on water immersion, balneotherapy, aqua exercises, and swimming, in patients with left ventricular dysfunction (LVD) and/or stable chronic heart failure (CHF). Based on exploratory studies, central hemodynamic and neurohumoral responses of aquatic therapies will be illustrated. Major findings are: 1. In LVD and CHF, a positive effect of therapeutic warm-water tub bathing has been observed, which is assumed to be from afterload reduction due to peripheral vasodilatation caused by the warm water. 2. In coronary patients with LVD, at low-level water cycling the heart is working more efficiently than at lowlevel cycling outside of water. 3. In patients with previous extensive myocardial infarction, upright immersion to the neck resulted in temporary pathological increases in mean pulmonary artery pressure (mPAP) and mean pulmonary capillary pressures (mPCP). 4. Additionally, during slow swimming (20-25m/min) the mPAP and/or PCP were higher than during supine cycling outside water at a 100W load. 5. In CHF patients, neck- deep immersion resulted in a decrease or no change in stroke volume. 6. Although patients are hemodynamically compromised, they usually maintain a feeling of well-being during aquatic therapy. Based on these findings, clinical indications for aquatic therapies are proposed and ideas are presented to provoke further research.

Effect of Altitude on the Heart and the Lungs

This review focuses on the effects of altitude exposure from 1 to several days or weeks as occurs in tourists, trekkers, and mountaineers who visit high altitude and normally reside near sea level. We briefly review the acute physiological adjustments and early acclimatization that occur in the cardiovascular system and the lungs of healthy individuals. These ensure life-sustaining oxygen delivery to the tissues despite a reduction in the partial pressure of inspired oxygen between 20% and 60% at 2500 and 8000 m, respectively. One of the acute adjustments, hypoxic pulmonary vasoconstriction (HPV), may be disadvantageous in those with a vigorous response and lead to 2 potentially lethal illnesses, high-altitude pulmonary edema (HAPE) and subacute mountain sickness (SAMS), which we present in more detail. Finally, on the basis of knowledge about the acute physiological adjustments and acclimatization and, when available, a review of the literature, we discuss the high-altitude tolerance of patients with coronary artery disease, congestive heart failure, arrhythmias, systemic hypertension, and pulmonary hypertension. ### Circulation The major effects of acute hypoxia on the heart and lung are shown in Figure 1. Hypoxia directly affects the vascular tone of the pulmonary and systemic resistance vessels and increases ventilation and sympathetic activity via stimulation of the peripheral chemoreceptors.1 Interactions occur between the direct effects of hypoxia on blood vessels and the chemoreceptor-mediated responses in the systemic and pulmonary circulation. Figure 1. Effects of hypoxia on systemic and pulmonary circulation. Unraveling the underlying mechanisms of the hypoxic vasodilatation of systemic arterioles is an active area of research. Several mechanisms appear to regulate local oxygen delivery according to the needs of the tissues2,3; for instance, the release of ATP from red blood cells and the generation of NO by various ways appear to regulate local oxygen delivery according to the needs …

Exercise in Heart Failure: Should Aqua Therapy and Swimming Be Allowed?

Although exercise training is established as an integrated part of treatment regimes in both patients with transmural myocardial infarction (MI) and chronic congestive heart failure (CHF), there is no consensus yet on the appropriateness of water exercises and swimming. One reason is the lack of information concerning both central hemodynamic volume and pressure responses during immersion in these patients. This paper presents explorative studies on changes in cardiac dimensions and central hemodynamics during graded immersion and swimming in patients with moderate and/or severe MI and in patients with moderate and/or compensated severe CHF. For comparison purposes, healthy subjects were assessed. Measurements were performed by using Swan-Ganz right heart catheterization, subxiphoidal echocardiography, and Doppler-echocardiography. The major findings were: 1) Indicators of an increase in preload were seen in patients with moderate and severe MI. In both patient groups, upright immersion to the neck and supine body position at rest in the water resulted in abnormal mean pulmonary artery pressure (PAm) and mean pulmonary capillary pressures (PCPm), respectively. During low-speed swimming (20-25 m.min(-1)), the PAm and/or PCPm were higher than during supine cycle ergometry at a load of 100 W. 2) Left ventricular overload and decrease and/or no change in stroke volume occurred in patients with severe CHF who were immersed up to the neck. 3) Patient's well-being was maintained despite hemodynamic deterioration. The acute responses during immersion and swimming suggest the need for additional studies on long-term changes in cardiac dimensions and central hemodynamic in both patients with severe MI and severe CHF who undergo a swimming program, compared with nonswimming patients with MI and CHF of similar etiology and severity of disease.

Two-chamber contractile silhouette predicts severity of pre-operative hemodynamics in patients undergoing trisvr surgery

Surgical left ventricular (LV) remodeling (TRISVR) is a procedure that both reduces LV volume and restores an elliptical LV endoventricular shape in patients with ischemic cardiomyopathy and low ejection fraction. Analysis of preoperative (pre-op) RAO 30° LV angiographic silhouettes has value in the selection of patients for TRISVR surgery. This report correlates pre-op contractile silhouette Types I-III with pre-op hemodynamic measurements affecting TRISVR surgical risk.Two-chamber LV contractile silhouette types describe residual regional LV chamber contractile function by identifying remaining contractile areas. The above three types of silhouettes uniquely described 61 of 68 consecutive patients undergoing TRISVR surgery. Patients underwent pre-op cardiac catheterization and transthoracic echocardiography with assessment of chamber volume, mean pulmonary artery pressure (PAP), mean pulmonary capillary pressure (Pcw), contractile EF% (regional EF% of most contractile areas), chamber EF%, and the presence and severity of mitral regurgitation (MR).

Intravenous pentoxifylline does not enhance the pulmonary haemodynamic efficacy of frusemide in strenuously exercising thoroughbred horses.

The present study was carried out to examine whether pentoxifylline administration to horses premedicated with frusemide would attenuate the exercise-induced pulmonary arterial, capillary and venous hypertension to a greater extent than frusemide alone, thereby affecting the occurrence of exercise-induced pulmonary haemorrhage (EIPH). Using established techniques, we determined right heart and pulmonary vascular pressures in 6 healthy, sound Thoroughbred horses at rest and during exercise performed at maximal heart rate at a workload of 14 m/s on 3.5% uphill grade in the control (no medications), frusemide (250 mg i.v., 4 h pre-exercise)-control, and the frusemide (250 mg i.v., 4 h pre-exercise) + pentoxifylline (8.5 mg/kg bwt i.v., 15 min preexercise) treatments. Sequence of the 3 treatments was randomised for every horse and 7 days were allowed between them. In the control study, galloping at 14 m/s on 3.5% uphill grade elicited significant right atrial as well as pulmonary arterial, capillary and venous hypertension and all horses experienced EIPH as detected by the presence of fresh blood in the trachea on endoscopic examination. Frusemide administration was not attended by changes in heart rate at rest or during exercise. Although in the frusemide-control experiments, a significant reduction in mean pulmonary arterial, capillary and wedge pressures was observed both at rest and during galloping at 14 m/s on 3.5% uphill grade, all horses still experienced EIPH. Pentoxifylline administration to standing horses premedicated with frusemide caused nervousness, muscular fasciculations, sweating and tachycardia. Although these symptoms had largely abated within 15 min, there were no significant changes in the right atrial or pulmonary vascular pressures. Exercise in the frusemide + pentoxifylline experiments also caused significant right atrial as well as pulmonary arterial, capillary and venous hypertension, but these data were not found to be significantly different from the frusemide-control experiments. All horses in the frusemide + pentoxifylline experiments also experienced EIPH. In conclusion, our data indicate that pentoxifylline (8.5 mg/kg bwt i.v., 15 min pre-exercise) is ineffective in modifying the pulmonary haemodynamic effects of frusemide in exercising horses. It should be noted, however, that we did not examine whether erythrocyte plasticity was altered by the administration of pentoxifylline. Since the intravascular force exerted onto the blood-gas barrier of exercising horses premedicated with frusemide remained unaffected by pentoxifylline administration, it is concluded that concomitant pentoxifylline administration is unlikely to offer additional benefit to horses experiencing EIPH.

Partial liquid ventilation reduces fluid filtration of isolated rabbit lungs with acute hydrochloric acid-induced edema.

Hydrochloric acid aspiration increases pulmonary microvascular permeability. The authors tested the hypothesis that partial liquid ventilation has a beneficial effect on filtration coefficients in acute acid-induced lung injury. Isolated blood-perfused rabbit lungs were assigned randomly to one of four groups. Group 1 (n = 6) served as a control group without edema. In group 2 (n = 6), group 3 (n = 6), and group 4 (n = 6), pulmonary edema was induced by intratracheal instillation of hydrochloric acid (0.1 N, 2 ml/kg body weight). Filtration coefficients were determined 30 min after this injury (by measuring loss of perfusate after increase of left atrial pressure). Group 2 lungs were gas ventilated, and group 3 lungs received partial liquid ventilation (15 ml perfluorocarbon/kg body weight). In group 4 lungs, the authors studied the immediate effects of bronchial perfluorocarbon instillation on ongoing filtration. Intratracheal instillation of hydrochloric acid markedly increased filtration coefficients when compared with non-injured control lungs (2.3 +/- 0.7 vs. 0.31 +/- 0.08 ml.min(-1). mmHg(-1).100 g(-1) wet lung weight, P < 0.01). Partial liquid ventilation reduced filtration coefficients of the injured lungs (to 0.9 +/- 0.3 ml.min(-1).mmHg(-1).100 g(-1) wet lung weight, P = 0.022). Neither pulmonary artery nor capillary pressures (determined by simultaneous occlusion of inflow and outflow of the pulmonary circulation) were changed by hydrochloric acid instillation or by partial liquid ventilation. During ongoing filtration, bronchial perfluorocarbon instillation (5 ml/kg body weight) immediately reduced the amount of filtered fluid by approximately 50% (P = 0.027). In the acute phase after acid injury, partial liquid ventilation reduced pathologic fluid filtration. This effect started immediately after bronchial perfluorocarbon instillation and was not associated with changes in mean pulmonary artery, capillary, or airway pressures. The authors suggest that in the early phase of acid injury, reduction of fluid filtration contributes to the beneficial effects of partial liquid ventilation on gas exchange and lung mechanics.

Clenbuterol administration does not enhance the efficacy of furosemide in attenuating the exercise-induced pulmonary capillary hypertension in Thoroughbred horses.

The stimulation of pulmonary beta2-adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol-a beta2-adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise-induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre-exercise)-control, and furosemide (250 mg i.v., 4 h pre-exercise)+clenbuterol (0.8 microg/kg i.v., 11 min pre-exercise) experiments. The sequence of these treatments was randomized for every horse, and 7 days were allowed between them. Using catheter-tip-transducers whose in-vivo signals were referenced at the point of the left shoulder, pulmonary vascular pressures were determined at rest, sub-maximal exercise, and during galloping at 14.2 m/s on a 3.5% uphill grade--a workload that elicited maximal heart rate. In the control study, incremental exercise resulted in progressive significant (P<0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P<0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide-control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P<0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P<0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P<0.05), but these data were not different from the furosemide-control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood-gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.

Clenbuterol administration does not enhance the efficacy of furosemide in attenuating the exercise‐induced pulmonary capillary hypertension in Thoroughbred horses

The stimulation of pulmonary β2‐adrenergic receptors causes a decrease in vascular resistance. Thus, the present study was carried out to examine whether concomitant administration of clenbuterol—a β2‐adrenergic receptor agonist, to horses premedicated with furosemide would attenuate the exercise‐induced pulmonary capillary hypertension to a greater extent than furosemide alone, and in turn, affect the occurrence of exercise‐induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise‐trained Thoroughbred horses. All horses were studied in the control (no medications), furosemide (250 mg i.v., 4 h pre‐exercise)‐control, and furosemide (250 mg i.v., 4 h pre‐exercise)+clenbuterol (0.8 μg/kg i.v., 11 min pre‐ exercise) experiments. The sequence of these treatments was randomized for every horse, and 7 days were allowed between them. Using catheter‐tip‐transducers whosein‐vivosignals were referenced at the point of the left shoulder, pulmonary vascular pressures were determined at rest, sub‐maximal exercise, and during galloping at 14.2 m/s on a 3.5% uphill grade—a workload that elicited maximal heart rate. In the control study, incremental exercise resulted in progressive significant (P&lt;0.05) increments in heart rate, right atrial as well as pulmonary arterial, capillary and venous (wedge) pressures, and all horses experienced EIPH. Furosemide administration caused a significant (P&lt;0.05) reduction in mean right atrial as well as pulmonary capillary and venous pressures of standing horses. Although exercise in the furosemide‐control experiments also caused right atrial and pulmonary vascular pressures to increase significantly (P&lt;0.05), the increment in mean pulmonary capillary and wedge pressures was significantly (P&lt;0.05) attenuated in comparison with the control study, but all horses experienced EIPH. Clenbuterol administration to standing horses premedicated with furosemide caused tachycardia, but significant changes in right atrial or pulmonary vascular pressures were not discerned at rest. During exercise in the furosemide+clenbuterol experiments, heart rate, mean right atrial as well as pulmonary arterial, capillary and wedge pressures increased significantly (P&lt;0.05), but these data were not different from the furosemide–control experiments, and all horses experienced EIPH as well. Thus, it was concluded that clenbuterol administration is ineffective in modifying the pulmonary hemodynamic effects of furosemide in standing or exercising horses. Because the intravascular force exerted onto the blood–gas barrier of horses premedicated with furosemide remained unaffected by clenbuterol administration, it is believed that concomitant clenbuterol administration is unlikely to offer additional benefit to healthy horses experiencing EIPH.

Intravenous pentoxifylline does not affect the exercise‐induced pulmonary arterial, capillary or venous hypertension in Thoroughbred horses

The present study was carried out to examine whether intravenously administered pentoxifylline—a phosphodiesterase inhibitor which increases red blood cell deformability and decreases blood viscosity—would attenuate the magnitude of exercise‐induced pulmonary capillary hypertension in healthy, fit Thoroughbred horses and in turn, diminish the occurrence of exercise‐induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise‐trained Thoroughbred horses. Hemodynamic data were collected at rest, and during exercise performed at 8 and 14 m/sec on 3.5% uphill grade in the control (no medications) and the pentoxifylline (8.5 mg/kg, i.v.) experiments. The sequence of treatments was randomized for every horse and 7 days were allowed between treatments. Galloping at 14 m/sec on 3.5% uphill grade elicited maximal heart rate. In both treatments, simultaneous measurements of phasic and mean right atrial and pulmonary arterial, capillary and wedge pressures were made using catheter‐tip‐manometers whose signals were carefully referenced at the point of the left shoulder. In the control study, exercise resulted in progressive significant increments in heart rate, right atrial and pulmonary arterial, capillary and venous pressures; thereby, confirming that exercising Thoroughbreds develop significant pulmonary hypertension. All horses experienced exercise‐induced pulmonary hemorrhage (EIPH) in the control experiments. Pentoxifylline administration to standing horses caused anxiety, tachycardia, muscular fasciculations/tremors and mild sweating, but statistically significant changes in right atrial and pulmonary arterial, capillary and venous pressures were not detected. Exercise in the pentoxifylline treatment also resulted in progressive significant increments in heart rate and right atrial as well as pulmonary vascular pressures, but these data were not statistically significantly different from those in the control study and the incidence of EIPH remained unchanged. Thus, it was concluded that i.v. pentoxifylline is ineffective in attenuating the exercise‐induced pulmonary arterial, capillary and venous hypertension in healthy, fit Thoroughbred horses.

Intravenous pentoxifylline does not affect the exercise-induced pulmonary arterial, capillary or venous hypertension in Thoroughbred horses.

The present study was carried out to examine whether intravenously administered pentoxifylline-a phosphodiesterase inhibitor which increases red blood cell deformability and decreases blood viscosity-would attenuate the magnitude of exercise-induced pulmonary capillary hypertension in healthy, fit Thoroughbred horses and in turn, diminish the occurrence of exercise-induced pulmonary hemorrhage (EIPH). Experiments were carried out on six healthy, sound, exercise-trained Thoroughbred horses. Hemodynamic data were collected at rest, and during exercise performed at 8 and 14 m/sec on 3.5% uphill grade in the control (no medications) and the pentoxifylline (8.5 mg/kg, i.v.) experiments. The sequence of treatments was randomized for every horse and 7 days were allowed between treatments. Galloping at 14 m/sec on 3.5% uphill grade elicited maximal heart rate. In both treatments, simultaneous measurements of phasic and mean right atrial and pulmonary arterial, capillary and wedge pressures were made using catheter-tip-manometers whose signals were carefully referenced at the point of the left shoulder. In the control study, exercise resulted in progressive significant increments in heart rate, right atrial and pulmonary arterial, capillary and venous pressures; thereby, confirming that exercising Thoroughbreds develop significant pulmonary hypertension. All horses experienced exercise-induced pulmonary hemorrhage (EIPH) in the control experiments. Pentoxifylline administration to standing horses caused anxiety, tachycardia, muscular fasciculations/tremors and mild sweating, but statistically significant changes in right atrial and pulmonary arterial, capillary and venous pressures were not detected. Exercise in the pentoxifylline treatment also resulted in progressive significant increments in heart rate and right atrial as well as pulmonary vascular pressures, but these data were not statistically significantly different from those in the control study and the incidence of EIPH remained unchanged. Thus, it was concluded that i.v. pentoxifylline is ineffective in attenuating the exercise-induced pulmonary arterial, capillary and venous hypertension in healthy, fit Thoroughbred horses.

Pulmonary capillary pressure in horses undergoing alteration of pleural pressure by imposition of various upper airway resistive loads.

We hypothesized that changes in pleural pressure induced by resistive breathing would affect transmural pulmonary artery, pulmonary capillary, and pulmonary wedge pressures. Seven horses were assigned to exercise with each of 4 upper respiratory resistive loads in random order at intervals of at least 2 days: 1) control--no added resistive loads; 2) inspiratory resistive load (Iobst)--left laryngeal hemiplegia; 3) expiratory resistive load (Eobst)--one-way valve in the right nostril; and 4) combined inspiratory and expiratory resistive loads (CIEobst)--left nostril occlusion. On each occasion, the horses performed an incremental exercise protocol consisting of exercise episodes of 3 min duration at 75, 90, and 100% of maximal heart rate (HRmax). Pulmonary artery and oesophageal pressures were recorded continuously. Subsequent analysis was carried out on the pulmonary arterial pressure signal with the oesophageal pressure signal subtracted, hence the pulmonary vascular pressures in this paper approximate transmural pressures. Pulmonary vascular pressures, heart rate, and arterial blood gas tensions were measured at each level of exercise. Pulmonary capillary and pulmonary wedge pressures were determined from the pulmonary artery waveform after dynamic occlusion of a branch of the pulmonary artery. During exercise, peak expiratory oesophageal pressure was more positive in horses with Eobst and CIEobst (adjusted means = 43, and 39 mmHg, respectively) compared with control (adjusted mean = 23 mmHg) (P = 0.0001). Peak inspiratory oesophageal pressure was more negative in horses at exercise with Iobst and CIEobst (adjusted means = -42 and -39 mmHg, respectively) compared with control (adjusted mean = -26 mmHg) (P = 0.0012). Eobst was associated with an increase in mean oesophageal pressure while Iobst was associated with a decrease in mean oesophageal pressure. There were significant increases in mean pulmonary artery pressure in horses with CIEobst (adjusted means = 82 mmHg) and in pulmonary wedge pressure in horses with CIEobst and Iobst (adjusted means = 51, and 55 mmHg, respectively) when compared to control (73 and 42 mmHg, respectively) (P = 0.0001). Pulmonary capillary pressure was significantly increased in horses with CIEobst or Iobst (adjusted means = 61 mmHg, 63 mmHg, respectively) when compared to control (adjusted mean = 50 mmHg)(P = 0.0001). At maximal exercise intensity with inspiratory obstruction, the mean oesophageal (pleural) pressure was -17 mmHg while the mean pulmonary capillary pressure was 77 mmHg. The latter exceeds the reported 75 mmHg threshold for capillary failure in horses. We conclude that inspiratory resistive breathing can lead to a significant increase in transmural pulmonary capillary pressure which may contribute to loss of capillary integrity and rupture.

Partial liquid ventilation combined with inhaled nitric oxide in acute respiratory failure with pulmonary hypertension in piglets.

This study was a prospective, randomized, controlled design to evaluate gas exchange, lung mechanics, and pulmonary hemodynamics during partial liquid ventilation (PLV) combined with inhaled nitric oxide (NO) in acute respiratory failure (ARF) with pulmonary hypertension (PH). ARF with PH was induced in 12 piglets weighing 9.7-13.7 kg by repeated lung lavages and the continuous infusion of the stable endoperoxane analog of thromboxane. Thereafter the animals were randomly assigned either for PLV or conventional mechanical ventilation (CMV) at a fractional concentration of inspired O2 (Fio2) of 1.0. Perfluorocarbon (PFC) liquid (30 mL kg-1) was instilled into the endotracheal tube over 5 min followed by 5 mL kg-1h-1. All animals were treated with different concentrations of NO (1-10-20 ppm) inhaled in random order. Continuous monitoring included ECG, right atrial (Pra), mean pulmonary artery (Ppa), pulmonary capillary (Ppc'), and mean arterial (Pa) pressures, arteria oxygen saturation, and mixed venous oxygen saturation measurements. During PLV Pao2/Fio2 increased significantly from 8.2 +/- 0.4 kPa to 34.8 +/- 5.1 kPa (p < 0.01), whereas Pao2/FiO2 remained constant at 9.5 +/- 0.4 kPa during CMV. The infusion of the endoperoxane analog resulted in a sudden decrease of Pao2/Fio2 from 34.8 +/- 5.1 kPa to 14.1 +/- 0.4 kPa (p < 0.01) in the PLV group and from 9.5 +/- 0.4 kPa to 6.9 +/- 0.2 kPa (p < 0.05) in the control group. Inhaled NO significantly improved oxygenation in both groups (Pao2/Fio2: 45.7 +/- 5.3 kPa during PLV and 25.9 +/- 4.7 kPa during CMV). During inhalation of NO mean Ppa decreased significantly from 7.8 +/- 0.26 kPa to 4.2 +/- 0.26 kPa (p < 0.01) in the PLV group and from 7.4 +/- 0.26 kPa to 5.1 +/- 0.13 kPa (p < 0.01) in the control group. As documented in the literature PLV significantly improves oxygenation and lung mechanics in severe ARF. In addition, when ARF is associated with severe PH, the combined treatment of PLV and inhaled NO improves pulmonary hemodynamics resulting in better oxygenation.

Pulmonary vascular pressures of exercising thoroughbred horses with and without endoscopic evidence of EIPH.

Exercise-induced pulmonary hemorrhage (EIPH) is a common occurrence in racehorses. The objective of this study was to compare pulmonary vascular pressures of healthy Thoroughbred horses with and without postexertion endoscopically detectable fresh blood in the trachea. The nasopharynx, larynx, and trachea (down to the carina) of horses were examined weekly with an endoscope 55-60 min postexertion, and the diagnosis of EIPH was confirmed by the presence of fresh blood in the trachea. Measurements of heart rate and right atrial, pulmonary arterial, and pulmonary arterial wedge pressures were made during quiet rest and during treadmill exercise performed at 14.5 m/s on a 5% uphill grade. This workload elicited maximal heart rate of the horses. Mean pulmonary capillary pressure was estimated to be halfway between the mean pulmonary arterial pressure and the mean pulmonary arterial wedge pressure. These data from 7 healthy sound exercise-trained horses that were positive on 12 consecutive occasions (at 1-wk intervals) for the postexercise presence of fresh blood in the trachea were compared with those in 8 healthy horses that were consistently negative for the evidence of fresh blood in the trachea on postexercise endoscopic examination over 12-16 wk. The heart rate and the right heart and/or pulmonary vascular pressures in the two groups of horses were similar at rest. Exercise was attended by a large significant (P < 0.05) increase in these pressures and heart rate in both groups. However, statistically significant differences between endoscopically EIPH-positive and endoscopically EIPH-negative horses for heart rate and right atrial and pulmonary vascular pressures were not found during exercise. Thus these data revealed that the magnitude of exercise-induced right atrial as well as pulmonary arterial, capillary, and venous hypertension in endoscopically EIPH-positive horses that are otherwise healthy is quite similar to that in endoscopically EIPH-negative horses during comparable exertion.

Pulmonary capillary pressure during exercise in horses

The object of this study was to relate pulmonary capillary pressure to arterial and wedge pressures during exercise. Pulmonary vascular pressures were measured in six standardbred horses exercising at speeds equivalent to 75, 90, and 100% of maximal heart rate. Vascular pressures were measured with transducer-tip catheters and expressed relative to esophageal pressure. Pulmonary capillary pressure was estimated by the arterial-occlusion technique modified for exercise. Mean pulmonary arterial, capillary and wedge pressures increased from 30.5 +/- 6.3, 17.8 +/- 4.3, and 13.4 +/- 1.6 mmHg, respectively, at rest, to 70.5 +/- 5.2, 42.1 +/- 5.3, and 38.4 +/- 5.6 mmHg, respectively, at maximal exercise. The largest part of the increase occurred during the first level of exertion. With exercise, the pressure across the lung barely doubled at a time when the cardiac output would have increased at least fivefold. Thus the absolute resistance in both pre- and postcapillary segments must have decreased. The capillary and wedge pressures rose similarly, whereas the difference between them did not change with exertion. The fractional resistance of the precapillary segment increased with exercise. The postcapillary resistance, initially 28% of the total pulmonary vascular resistance, fell to 9% at maximal exercise. The rise (to approximately 45 mmHg) in pulmonary capillary pressure with exertion is consistent with an increase in transvascular filtration.

Leukotoxin, 9,10-epoxy-12-octadecenoate causes edematous lung injury via activation of vascular nitric oxide synthase.

We examined the mechanism of leukotoxin, 9,10-epoxy-12-octadecenoate (Lx)-induced lung injury in blood-free, physiological salt solution-perfused rat lungs under constant flow conditions. Mean pulmonary arterial (Ppa) and pulmonary capillary pressure (Pcap, estimated by the double-occlusion method), wet lung weight (WLW), pulmonary capillary filtration coefficient (Kfc), lung perfusate lactate dehydrogenase (LDH) activity, and nitrite levels were assessed. Bolus injection of Lx (200 microM) caused insidious and significant lung weight gain, which was not associated with remarkable elevation of Ppa or Pcap but was associated with an increase of perfusate LDH activity and nitrite levels. Lx (20 microM) elevated Kfc, indicating that Lx had affected pulmonary vascular permeability. Because Lx causes endothelium dependent pulmonary vasodilation, we studied the effect of NG-monomethyl-L-arginine (L-NMMA), NG-monomethyl-D-arginine (D-NMMA), superoxide dismutase (SOD), human oxyhemoglobin (oxyHb), and methylene blue (MB) on Lx-induced lung injury. L-NMMA, SOD, and oxyHb, but not MB or D-NMMA, protected the lungs against Lx (200 microM)-induced injury. Lx increased pulmonary vascular permeability and caused lung injury. Because both nitric oxide synthase inhibitors and SOD inhibited the Lx-induced lung injury, it is possible that peroxynitrite is involved in the mechanism whereby Lx causes lung injury.

Pulmonary vascular pressures of thoroughbreds increase rapidly and to a higher level with rapid onset of high-intensity exercise than slow onset.

Previous studies of pulmonary vascular pressures have utilised gradual incremental step exercise protocols, but in competitive racing at the track, horses perform rapid acceleration high-intensity exercise. The rate of rise in pulmonary vascular pressures under conditions of quick onset high-intensity exercise is unknown. Catheter mounted manometers, whose in vivo signals were matched with pressure signals obtained via transducers connected to fluid-filled lumens from same cardiovascular sites, were used to compare right heart and pulmonary vascular pressures in 8 healthy Thoroughbreds performing 2 separate exercise protocols on a high speed treadmill (gradually incremental vs. rapid acceleration exercise protocol where the belt speed was raised from 8 m/s to 15 m/s in 8 s). Heart rate, right atrial and pulmonary vascular pressures at rest were similar for the 2 protocols. Rapid acceleration of horses from 8 to 15 m/s was attended by an equally rapid escalation in the right heart and pulmonary vascular pressures such that these pressures reached their zenith as belt speed approached 15 m/s. Although exercise at 15 m/s resulted in similar heart rate in the 2 protocols, the mean +/- s.e. values of mean right atrial pressure, mean pulmonary artery pressure, mean pulmonary artery wedge pressure and mean pulmonary capillary pressure (91.5 +/- 3.9 mmHg) in the rapid acceleration exercise were significantly (P < 0.05) higher than respective values at 15 m/s in the gradual incremental step exercise protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary vascular pressures of strenuously exercising Thoroughbreds after administration of flunixin meglumine and furosemide

Summary High-intensity exercise results in a dramatic increase in mean pulmonary capillary blood pressure of horses, and administration of furosemide 4 hours before exertion significantly attenuates this exercise-induced increment. To test whether this effect of furosemide is mediated via release of prostaglandins, right atrial and pulmonary vascular pressures were measured in 8 healthy, sound, exercise-trained Thoroughbreds at rest and during incremental-step exercise on a treadmill. Horses were studied on 3 separate occasions: after IV administration of saline (0.9% NaCl) solution, after administration of furosemide (250 mg, IV, 4 hours before exercise) alone, and after administration of flunixin meglumine (1.1 mg/kg, IV, q 8 h for 3 days) and furosemide (250 mg, IV, 4 hours before exercise; last dose of flunixin meglumine was administered 90 seconds after furosemide injection). Experiments on each horse were separated by at least 7 days and were performed in random order. At rest and at the highest workload (14.5 m/s on a 5% uphill incline), mean pulmonary capillary blood pressure recorded after administration of furosemide alone was not significantly different from that recorded after administration of flunixin meglumine and furosemide. However, these values were significantly (P&lt; 0.05) less than corresponding values of mean pulmonary capillary blood pressure recorded after administration of saline solution. Thus, it was concluded that furosemide-induced attenuation of the increment in pulmonary capillary blood pressure during strenuous exercise is probably not mediated via prostaglandin production.