Stress failure of pulmonary capillaries in racehorses with exercise-induced pulmonary hemorrhage

1993 ◽  
Vol 75 (3) ◽  
pp. 1097-1109 ◽  
Author(s):  
J. B. West ◽  
O. Mathieu-Costello ◽  
J. H. Jones ◽  
E. K. Birks ◽  
R. B. Logemann ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Soft Tissues ◽  
Pulmonary Hemorrhage ◽  
Ultrastructural Changes ◽  
Radius Of Curvature ◽  
Alveolar Wall ◽  
Ultrastructural Studies ◽  
Pulmonary Capillaries ◽  
Exercise Induced

Bleeding into the lungs in thoroughbreds is extremely common; there is evidence that it occurs in essentially all horses in training. However, the mechanism is unknown. We tested the hypothesis that exercise-induced pulmonary hemorrhage (EIPH) is caused by stress failure of pulmonary capillaries. Three thoroughbreds with known EIPH were galloped on a treadmill, and after the horses were killed with intravenous barbiturate the lungs were removed, inflated, and fixed for electron microscopy. Ultrastructural studies showed evidence of stress failure of pulmonary capillaries, including disruptions of the capillary endothelial and alveolar epithelial layers, extensive collections of red blood cells in the alveolar wall interstitium, proteinaceous fluid and red blood cells in the alveolar spaces, interstitial edema, and fluid-filled protrusions of the endothelium into the capillary lumen. The appearances were consistent with the ultrastructural changes we have previously described in rabbit lungs at high capillary transmural pressures. Actual breaks in the endothelium and epithelium were rather difficult to find, and they were frequently associated with platelets and leukocytes that appeared to be plugging the breaks. The paucity of breaks was ascribed to their reversibility when the pressure was lowered and to the fact that 60–70 min elapsed between the gallop and the beginning of lung fixation. Capillary wall stress was calculated from pulmonary vascular pressures measured in a companion study (Jones et al. FASEB J. 6: A2020, 1992) and from measurements of the thickness of the blood-gas barrier and the radius of curvature of the capillaries. The value was as high as 8 x 10(5) dyn/cm2 (8 x 10(4) N/m2), which exceeds the breaking stress of most soft tissues. We conclude that stress failure of pulmonary capillaries is the mechanism of EIPH.

Blood flow switching among pulmonary capillaries is decreased during high hematocrit

2004 ◽  
Vol 97 (2) ◽  
pp. 522-526 ◽  
Author(s):  
William A. Baumgartner ◽  
Amanda J. Peterson ◽  
Robert G. Presson ◽  
Nobuhiro Tanabe ◽  
Eric M. Jaryszak ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Average Distance ◽  
Substantial Part ◽  
Alveolar Wall ◽  
Capillary Perfusion ◽  
Capillary Networks ◽  
Pulmonary Capillaries ◽  
Pulmonary Capillary ◽  
Alveolar Capillary

Pulmonary capillary perfusion within a single alveolar wall continually switches among segments, even when large-vessel hemodynamics are constant. The mechanism is unknown. We hypothesize that the continually varying size of plasma gaps between individual red blood cells affects the likelihood of capillary segment closure and the probability of cells changing directions at the next capillary junction. We assumed that an increase in hematocrit would decrease the average distance between red blood cells, thereby decreasing the switching at each capillary junction. To test this idea, we observed 26 individual alveolar capillary networks by using videomicroscopy of excised canine lung lobes that were perfused first at normal hematocrit (31–43%) and then at increased hematocrit (51–62%). The number of switches decreased by 38% during increased hematocrit ( P < 0.01). These results support the idea that a substantial part of flow switching among pulmonary capillaries is caused by the particulate nature of blood passing through a complex network of tubes with continuously varying hematocrit.

scholarly journals Efficacy of nasal strip and furosemide in mitigating EIPH in Thoroughbred horses

2001 ◽  
Vol 91 (3) ◽  
pp. 1396-1400 ◽  
Author(s):  
Casey A. Kindig ◽  
Paul McDonough ◽  
Gus Fenton ◽  
David C. Poole ◽  
Howard H. Erickson
Keyword(s):  
Bronchoalveolar Lavage ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Pulmonary Hemorrhage ◽  
Additional Benefit ◽  
Thoroughbred Horses ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Maximal Effort ◽  
Treatment Order

The purpose of this investigation was to study the effects of an equine nasal strip (NS), furosemide (Fur), and a combination of both (NS + Fur) on exercise-induced pulmonary hemorrhage (EIPH) at speeds corresponding to near-maximal effort. Five Thoroughbreds (526 ± 25 kg) were run on a flat treadmill from 7 to 14 m/s in 1 m · s−1 · min−1 increments every 2 wk (treatment order randomized) under control (Con), Fur (1 mg/kg iv 4 h prior), NS, or NS + Fur conditions. During each run, pulmonary arterial (Ppa) and esophageal (Pes) pressures were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) 30 min postrun. Furosemide (Fur and NS + Fur trials) reduced peak Ppa ∼7 mmHg compared with Con ( P < 0.05) whereas NS had no effect ( P > 0.05). Maximal Pes swings were not different among groups ( P > 0.05). NS significantly diminished EIPH compared with the Con trial [Con, 55.0 ± 36.2; NS, 30.8 ± 21.8 × 106 red blood cells (RBC)/ml BAL fluid; P < 0.05]. Fur reduced EIPH to a greater extent than NS (5.2 ± 3.0 × 106 RBC/ml BAL; P < 0.05 vs. Con and NS) with no additional benefit from NS + Fur (8.5 ± 4.2 × 106 RBC/ml BAL; P > 0.05 vs. Fur, P < 0.05 vs. Con and NS). In conclusion, although both modalities (NS and Fur) were successful in mitigating EIPH, neither abolished EIPH fully as evaluated via BAL. Fur was more effective than NS in constraining the severity of EIPH. The simultaneous use of both interventions appears to offer no further gain with respect to reducing EIPH.

Anti-inflammatory agent, dexamethasone, does not affect exercise-induced arterial hypoxemia in Thoroughbreds

2002 ◽  
Vol 93 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan ◽  
Tracy Depuy ◽  
Sarah Humphrey
Keyword(s):  
Pulmonary Hemorrhage ◽  
Exercise Duration ◽  
Pulmonary Injury ◽  
Arterial Hypoxemia ◽  
Inflammatory Agent ◽  
Pulmonary Capillaries ◽  
Anti Inflammatory ◽  
Gas Measurements ◽  
Exercise Induced ◽  
Chemical Mediators

In view of the suggestion that pulmonary injury-induced release of histamine and/or other chemical mediators from airway inflammatory and mast cells contribute to the exercise-induced arterial hypoxemia (EIAH) in human athletes, we examined the effects of pretreatment with a potent anti-inflammatory agent, dexamethasone, on EIAH and desaturation of hemoglobin in horses. Seven healthy, sound, exercise-trained Thoroughbreds were studied in the control (no medications) experiments, followed in 7 days by intravenous dexamethasone (0.11 mg·kg−1·day−1for 3 consecutive days) studies. Blood-gas measurements were made at rest and during incremental exercise leading to maximal exertion at 14 m/s on a 3.5% uphill grade. Galloping at this workload induced pulmonary hemorrhage in all horses in both treatments, thereby indicating that stress failure of pulmonary capillaries had occurred. In both treatments, significant EIAH, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but significant differences between the control and dexamethasone treatments were not discerned. The failure of pretreatment with dexamethasone to significantly affect EIAH suggests that pulmonary injury-evoked airway inflammatory response may not play a major role in EIAH in racehorses. However, our observations in both treatments that EIAH developed quickly (being evident at 30 s of exertion) and that its severity remained unaffected by increasing exercise duration (to 120 s) suggest that EIAH has a functional basis, probably related to significant shortening of the transit time for blood in the pulmonary capillaries as cardiac output increases dramatically.

scholarly journals Heinz Body Anemia—An Ultrastructural Study. I. Heinz Body Formation

Blood ◽  
1965 ◽  
Vol 25 (6) ◽  
pp. 885-896 ◽  
Author(s):  
RICHARD A. RIFKIND ◽  
DAVID DANON
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Structural Changes ◽  
Regular Sequence ◽  
Ultrastructural Changes ◽  
Drug Induced ◽  
Heinz Bodies ◽  
Heinz Body

Abstract The ultrastructural changes in red blood cells exposed to phenylhydrazine, either in vivo or in vitro, are described. There is an age-dependent gradient of red cell sensitivity to this drug which includes the more mature reticulocytes as well as the population of circulating erythrocytes. Oxidative denaturation of hemoglobin and the formation of Heinz bodies, which constitute the major drug-induced lesion, are accompanied by a regular sequence of structural changes commencing in the central cytoplasm of erythrocytes and the drug-sensitive reticulocytes. These early changes often appear in close associaion with clusters of mitochondria. The initial morphologic lesion has an apparently crystalline structure and the significance of this stage is discussed. Heinz bodies grow by coalescence and condensation and finally come to lie just beneath the cell surface. Here they result in considerable distortion of cell shape and deformation of the plasma membrane. Thus, phenylhydrazine administration produces in red blood cells extensive ultrastructural alterations both in hemoglobin and in the cell membrane which may have considerable bearing on the fate of these cells in the circulation.

scholarly journals Red Blood Cell Aging as a Homeostatic Response to Exercise-Induced Stress

2019 ◽  
Vol 9 (22) ◽  
pp. 4827 ◽  
Author(s):  
Joames K. Freitas Leal ◽  
Dan Lazari ◽  
Coen C.W.G. Bongers ◽  
Maria T.E. Hopman ◽  
Roland Brock ◽  
...  
Keyword(s):  
Blood Cell ◽  
Red Blood Cells ◽  
Red Blood Cell ◽  
Blood Cells ◽  
Molecular Mechanisms ◽  
Moderate Intensity ◽  
Cell Aging ◽  
Moderate Intensity Exercise ◽  
Induced Stress ◽  
Exercise Induced

Our knowledge on the molecular mechanisms of red blood cell aging is mostly derived from in vitro studies. The Four Days Marches of Nijmegen in the Netherlands, the world’s largest yearly walking event, constitutes a unique possibility to study the effect of mechanical and biochemical stressors occurring during moderate-intensity exercise on red blood cell aging in vivo. Therefore, longitudinal measurements were performed of biophysical, immunological, and functional red blood cell characteristics that are known to change during aging. Our data show that moderate-intensity exercise induces the generation of a functionally improved red blood cell population with a higher deformability and a decreased tendency to aggregate. This is likely to be associated with an early removal of the oldest red blood cells from the circulation, as deduced from the (dis)appearance of removal signals. Thus, the physiological red blood cell aging process maintains homeostasis in times of moderate-intensity exercise-induced stress, probably by accelerated aging and subsequent removal of the oldest, most vulnerable red blood cells.

Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses

1997 ◽  
Vol 82 (5) ◽  
pp. 1584-1592 ◽  
Author(s):  
Eric K. Birks ◽  
Odile Mathieu-Costello ◽  
Zhenxing Fu ◽  
Walter S. Tyler ◽  
John B. West
Keyword(s):  
High Pressures ◽  
Autologous Blood ◽  
Pulmonary Hemorrhage ◽  
Capillary Endothelium ◽  
Gas Barrier ◽  
Thoroughbred Racehorses ◽  
Pulmonary Capillaries ◽  
Thoroughbred Horses ◽  
Exercise Induced ◽  
Very High

Birks, Eric K., Odile Mathieu-Costello, Zhenxing Fu, Walter S. Tyler, and John B. West. Very high pressures are required to cause stress failure of pulmonary capillaries in Thoroughbred racehorses. J. Appl. Physiol. 82(5): 1584–1592, 1997.—Thoroughbred horses develop extremely high pulmonary vascular pressures during galloping, all horses in training develop exercise-induced pulmonary hemorrhage, and we have shown that this is caused by stress failure of pulmonary capillaries. It is known that the capillary transmural pressure (Ptm) necessary for stress failure is higher in dogs than in rabbits. The present study was designed to determine this value in horses. The lungs from 15 Thoroughbred horses were perfused with autologous blood at Ptm values (midlung) of 25, 50, 75, 100 and 150 mmHg, and then perfusion fixed, and samples (dorsal and ventral, from caudal region) were examined by electron microscopy. Few disruptions of capillary endothelium were observed at Ptm ≤ 75 mmHg, and 5.3 ± 2.2 and 4.3 ± 0.7 breaks/mm endothelium were found at 100 and 150 mmHg Ptm, respectively. Blood-gas barrier thickness did not change with Ptm. At low Ptm, interstitial thickness was greater than previously found in rabbits but not in dogs. We conclude that the Ptm required to cause stress failure of pulmonary capillaries is between 75 and 100 mmHg and is greater in Thoroughbred horses than in both rabbits and dogs.

Effects of Exercise Training on the Distribution of Metallic Mercury in Mice

1994 ◽  
Vol 13 (8) ◽  
pp. 524-528 ◽  
Author(s):  
Nobuhiro Shimojo ◽  
Yoshihiro Arai
Keyword(s):  
Exercise Training ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Mercury Content ◽  
Whole Body ◽  
Mercury Vapour ◽  
Entire Body ◽  
Significant Difference ◽  
Exercise Induced ◽  
Induced Changes

1 The purpose of this study was to correlate exercise induced changes of antioxidant enzymes with the distribution of mercury after mercury vapour exposure in mice. 2 Exercise training consisted of swimming (1 h/day for 5 days/week) for 9 weeks. After 9 weeks of training, swim-trained mice showed significantly elevated levels of catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSHpx ) in their red blood cells, CAT and GSHpx in their kidneys and SOD in the liver. 3 Exercised mice (Ex) and non-exercised mice (N.Ex) were exposed to mercury vapour (3.5 mg m-3) for 1 h. Mercury concentrations were assayed in the . blood, brain, heart, lungs, liver and kidneys along with the mercury content of the entire body. The whole body mercury content showed no significant difference in any measurement (immediately, 24 h and 48 h after mercury exposure) between the Ex and N.Ex groups. Mercury concentrations in the Ex group were significantly higher than the N.Ex group in the heart, whole blood, red blood cells and the brain at 24 and 48 h; and in the plasma and kidneys at 24 h. 4 It was concluded that exercise training is a factor in distribution changes of mercury after exposure to mercury vapour, though it is not a factor in the total absorption and excretion of mercury.

scholarly journals УЛЬТРАМІКРОСКОПІЧНІ ПРОЯВИ У СТРУКТУРІ ПІДНИЖНЬОЩЕЛЕПНОЇ СЛИННОЇ ЗАЛОЗИ НАПРИКІНЦІ 2-ГО ТИЖНЯ ЕКСПЕРИМЕНТАЛЬНОГО ОПІОЇДНОГО ВПЛИВУ

World Science ◽  
2020 ◽  
Vol 1 (4(56)) ◽  
pp. 4-7
Author(s):  
Mykhalevych Marta
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Salivary Gland ◽  
Connective Tissue ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Acinar Cells ◽  
Ultrastructural Changes ◽  
Submandibular Salivary Gland ◽  
Perivascular Edema

This publication demonstrates the ultrastructural changes of the submandibular salivary gland under the opioid effect at the 2nd week of the experimental research.After 14 days of experimental opioid effect, we found the destructive changes in the organelles of exocrinocytes of acinar cells, as well as dyscirculatory processes. Capillary lumen was enlarged, overflowing with red blood cells. In the endothelium of the capillaries also noted the expansion of the granular endoplasmic reticulum. Small vacuoles appeared in the cytoplasm of endothelial cells. Single mitochondria located in the area of the endothelial cytoplasmic organelles are swollen. Due to the development of perivascular edema, the underlying connective tissue substance around the capillaries was impregnated with electron-illuminated transudate masses.

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