The effect of herbal supplementation on the severity of exercise-induced pulmonary haemorrhage

2005 ◽  
Vol 2 (1) ◽  
pp. 17-25 ◽  
Author(s):  
TS Epp ◽  
P McDonough ◽  
DJ Padilla ◽  
JH Cox ◽  
DC Poole ◽  
...  
Keyword(s):  
Platelet Function ◽  
Blood Gases ◽  
Pulmonary Haemorrhage ◽  
Exercise Tests ◽  
Arterial Blood ◽  
Thoroughbred Horses ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Complete Blood Counts ◽  
Herbal Formulations

AbstractExercise-induced pulmonary haemorrhage (EIPH) is a serious condition that affects the health and possibly the performance of all racehorses. However, only two treatments, furosemide and the Flair™ equine nasal strip, both of which reduce capillary transmural pressure, have been successful in reducing EIPH. Alternatively, transient impairment of platelet function and coagulation during exercise has been considered an additional contributor to EIPH. Consequently, herbal formulations designed to enhance platelet function, and hence coagulation, are hypothesized to reduce EIPH. To investigate the validity of this hypothesis, five Thoroughbred horses completed three maximal incremental exercise tests on a 10% inclined treadmill in a randomized cross-over design experiment. Treatments included twice daily oral administration (for 3 days) of a placebo (PL; cornstarch) and two herbal formulas, Yunnan Paiyao (YP) or Single Immortal (SI). Blood samples for coagulation profiles, complete blood counts and biochemistry profiles were collected before each exercise test. During each test, pulmonary arterial pressure, oxygen uptake, arterial blood gases, plasma lactate and time-to-fatigue were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) at 30–60 min post-exercise. The herbal formulations were not effective in decreasing EIPH (×106 red blood cells ml−1 BAL fluid: PL, 27.1±11.6; YP, 33.2±23.4; SI, 35.3±15.4, P>0.05) or in changing any of the other variables measured with the exception of time-to-fatigue, which was slightly but significantly prolonged by Single Immortal compared with placebo and Yunnan Paiyao (PL, 670±9.6 s; YP, 665±5.5 s; SI, 685±7.9 s, P<0.05). Thus, these results do not support the use of these herbal formulations in the prevention of EIPH.

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

Acute and chronic pulmonary vasoconstriction after left lung autotransplantation in conscious dogs

1992 ◽  
Vol 73 (2) ◽  
pp. 603-609 ◽  
Author(s):  
P. A. Murray ◽  
R. S. Stuart ◽  
C. D. Fraser ◽  
D. M. Fehr ◽  
B. B. Chen ◽  
...  
Keyword(s):  
Left Lung ◽  
Blood Gases ◽  
Conscious Dogs ◽  
Specific Effects ◽  
Vascular Regulation ◽  
Post Surgery ◽  
Pulmonary Vasoconstriction ◽  
Arterial Blood ◽  
Pulmonary Arterial ◽  
Active Flow

We investigated the acute and chronic effects of left lung autotransplantation (LLA) on the left pulmonary vascular pressure-flow (LP/Q) relationship in conscious dogs. Continuous LP/Q plots were generated in chronically instrumented conscious dogs 2 days, 2 wk, 1 mo, and 2 mo after LLA. Identically instrumented normal conscious dogs were studied at equal time points post-surgery. LLA had little or no effect on baseline systemic hemodynamics or blood gases. In contrast, compared with normal conscious dogs, striking active flow-independent pulmonary vasoconstriction was observed 2 days post-LLA. The slope of the LP/Q relationship was increased from a normal value of 0.275 +/- 0.021 to 0.699 +/- 0.137 mmHg.ml-1.min-1.kg-1 2 days post-LLA. Pulmonary vasoconstriction of similar magnitude was also observed on a chronic basis at 2 wk, 1 mo, and even 2 mo post-LLA. Pulmonary vasoconstriction post-LLA was not due to fixed resistance at the left pulmonary arterial or venous anastomotic sites. Finally, systemic arterial blood gases were unchanged when total pulmonary blood flow was directed to exclusively perfuse the transplanted left lung. Thus, LLA results in both acute and chronic pulmonary vasoconstriction in conscious dogs. LLA should serve as a useful stable experimental model to assess the specific effects of surgical transplantation on pulmonary vascular regulation.

Exercise-induced hypoxemia in older athletes

1994 ◽  
Vol 76 (1) ◽  
pp. 120-126 ◽  
Author(s):  
C. Prefaut ◽  
F. Anselme ◽  
C. Caillaud ◽  
J. Masse-Biron
Keyword(s):  
Blood Gases ◽  
Blood Gas Analysis ◽  
Gas Analysis ◽  
Lung Water ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Older Athletes ◽  
Level Of Training ◽  
Exercise Induced ◽  
Arterial Po2

To determine whether exercise induces hypoxemia in highly trained older “master” athletes (MA), as it does in certain elite endurance-trained young athletes (YA), 10 MA (65.3 +/- 2.6 yr), 10 control subjects (CS; 68.3 +/- 2.2 yr), and 10 endurance-trained YA (23.3 +/- 1.1 yr) performed an incremental exercise test. During testing, blood samples for arterial blood gas analysis were drawn during the last 20 s of each load. Lung exchanges were measured using a breath-by-breath automated exercise device. Exercise-induced hypoxemia (EIH) appeared in all MA and 8 of 10 YA, whereas there were no changes in the blood gases of CS. In MA, arterial PO2 decreased significantly from 40% of maximal O2 uptake onward and was associated with a significant increase in the ideal alveolar-arterial O2 difference from 60% onward. The MA also showed a lower ventilation for a given absolute load compared with CS. In all subjects arterial PCO2 rose slightly but significantly during the work, but this increase was most marked in MA. The EIH differed between MA and YA in the following ways: 1) all MA showed a drop in arterial PO2 during exercise, 2) this drop appeared earlier and was significantly greater for a given load in MA, and 3) EIH appeared at a lower level of training regimen in MA. This hypoxemia was at first isolated, probably at least partially due to relative hypoventilation, and then was associated with a widened ideal alveolar-arterial O2 difference, which may have been due to an increase in extravascular lung water.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Do We Need Exercise Tests to Detect Gas Exchange Impairment in Fibrotic Idiopathic Interstitial Pneumonias?

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Benoit Wallaert ◽  
Lidwine Wemeau-Stervinou ◽  
Julia Salleron ◽  
Isabelle Tillie-Leblond ◽  
Thierry Perez
Keyword(s):  
Gas Exchange ◽  
Cardiopulmonary Exercise Testing ◽  
Blood Gases ◽  
Oxygen Desaturation ◽  
Walk Test ◽  
Diffusing Capacity ◽  
Arterial Blood Gases ◽  
Exercise Tests ◽  
Cardiopulmonary Exercise ◽  
Arterial Blood

In patients with fibrotic idiopathic interstitial pneumonia (f-IIP), the diffusing capacity for carbon monoxide (DLCO) has been used to predict abnormal gas exchange in the lung. However, abnormal values for arterial blood gases during exercise are likely to be the most sensitive manifestations of lung disease. The aim of this study was to compare DLCO, resting PaO2, P(A-a)O2at cardiopulmonary exercise testing peak, and oxygen desaturation during a 6-min walk test (6MWT). Results were obtained in 121 patients with idiopathic pulmonary fibrosis (IPF,n=88) and fibrotic nonspecific interstitial pneumonias (NSIP,n=33). All but 3 patients (97.5%) had low DLCO values (<LLN) whereas only 66.6% had low KCO; 42 patients (65%) exhibited resting hypoxemia (<75 mmHg); 112 patients (92.5%) exhibited a high P[(A-a)O2], peak (>35 mmHg) and 100 (83%) demonstrated significant oxygen desaturation during 6MWT (>4%). Interestingly 27 patients had low DLCO and normal P(A-a)O2, peak and/or no desaturation during the 6MWT. The 3 patients with normal DLCO also had normal PaO2, normal P(A-a)O2, peak, and normal oxygen saturation during 6MWT. Our results demonstrate that in fibrotic IIP, DLCO better defines impairment of pulmonary gas exchange than resting PaO2, exercise P(A-a)O2, peak, or 6MWT SpO2.

Effects of a specific endothelin-1A antagonist on exercise-induced pulmonary haemorrhage (EIPH) in Thoroughbred horses

2006 ◽  
Vol 38 (S36) ◽  
pp. 198-203 ◽  
Author(s):  
D. J. PADILLA ◽  
T. S. EPP ◽  
P. McDONOUGH ◽  
D. J. MARLIN ◽  
H. H. ERICKSON ◽  
...  
Keyword(s):  
Pulmonary Haemorrhage ◽  
Thoroughbred Horses ◽  
Exercise Induced

l-NAME does not affect exercise-induced pulmonary hypertension in Thoroughbred horses

1998 ◽  
Vol 84 (6) ◽  
pp. 1902-1908 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz
Keyword(s):  
Nitric Oxide ◽  
Heart Rate ◽  
Nitric Oxide Synthase ◽  
Venous Blood ◽  
Right Atrial ◽  
Maximal Heart Rate ◽  
Thoroughbred Horses ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Oxide Synthase

The present study was carried out to examine the effects of nitric oxide synthase inhibition with N ω-nitro-l-arginine methyl ester (l-NAME) on the right atrial as well as on the pulmonary arterial, capillary, and venous blood pressures of horses during rest and exercise performed at maximal heart rate (HRmax). Experiments were carried out on seven healthy, sound, exercise-trained Thoroughbred horses. Using catheter-tip manometers, with signals referenced at the point of the shoulder, we determined phasic and mean right atrial and pulmonary vascular pressures in two sets of experiments [control (no medications) and l-NAME (20 mg/kg iv given 10 min before exercise studies)]. The studies were carried out in random order 7 days apart. Measurements were made at rest and during treadmill exercise performed on a 5% uphill grade at 6, 8, and 14.2 m/s. Exercise on a 5% uphill grade at 14.2 m/s elicited HRmax and could not be sustained for >90 s. In quietly standing horses,l-NAME administration caused a significant rise in right atrial, as well as pulmonary arterial, capillary, and venous pressures. This indicates that nitric oxide synthase inhibition modifies the basal pulmonary vasomotor tone. In both treatments, exercise caused progressive significant increments in right atrial and pulmonary vascular pressures, but the values recorded in the l-NAME study were not different from those in the control study. The extent of exercise-induced tachycardia was significantly decreased in thel-NAME study at 6 and 8 m/s but not at 14.2 m/s. Thus, l-NAME administration may not modify the equine pulmonary vascular tone during exercise at HRmax. However, as indicated by a significant reduction in heart rate,l-NAME seems to modify the sympathoneurohumoral response to submaximal exercise.

Sign in / Sign up

Export Citation Format

Share Document