Muitos equinos participantes de provas de corrida, ao exame endoscópico, apresentam evidências de ocorrência de Hemorragia Pulmonar Induzida pelo Exercício (HPIE). A HPIE trata-se de um sangramento de origem pulmonar que ocorre em equinos durante atividade física intensa e pela alta prevalência, muitas vezes associada aos equinos de corrida. Considerando, baseado nos estudos realizados, que o principal mecanismo descrito no desenvolvimento dos quadros de HPIE envolve o aumento da pressão transmural, resultante do aumento da pressão pulmonar causada pelo exercício físico, a furosemida parece ter papel importante na atenuação destes fatores, o que suporta a sua utilização nestes animais. Foram avaliados 21 equinos da raça Puro Sangue Inglês, atletas de distintas modalidades (corrida e polo), com e sem HPIE em dois momentos, antes (T0) e 4 horas após a administração da furosemida (T1) na dose de 0,5 mg/kg. Os animais foram submetidos a exame ecocardiográfico nos dois momentos, e também a colheita de sangue para avaliação hematológica e bioquímica. Ao exame ecocardiográfico foram consideradas as seguintes variáveis: FC, DC, VEj, FEj, VSFVE, VDFVE, FS, SIV, PLVE, DVE em sístole e diástole, AEs, Ao, AE:Ao, TEVE, E-S, e pico de velocidade do fluxo na artéria pulmonar. Para os exames laboratoriais foram consideradas as seguintes variáveis: He, Hb, Ht, VCM, HCM, CHCM, Leu, Neu, Linf, Mon, Plaq, AST, GGT, Alb, Pt, BT e BD. O uso da furosemida exerceu influência sobre os índices ecocardiográficos estudados de animais sem HPIE alterando a velocidade do fluxo da artéria pulmonar e o TEVE. Os demais parâmetros ecocardiográficos estudados bem como os parâmetros hemáticos não apresentaram alteração significativa, exceção feita aos valores de ureia e creatinina que aumentaram em T1, em função da hemoconcentração, sendo significantemente maiores no grupo sem HPIE. / Many racehorses at endoscopic examination after race present evidence of Exercise Induced Pulmonary Hemorrhage (HPIE). HPIE is a bleeding that occurs from pulmonary origin in horses during intense physical activity, often associated, by the high prevalence, to the racehorses, being able to present itself in many other equines, since undergoing intense physical exercise. Considering, based on previous studies, that the main mechanism involved in the development of HPIE involves the increase of the transmural pressure, resulting from the increase of the pulmonary pressure caused by the physical exercise, furosemide seems to play an important role in the attenuation of these factors, which supports their use in these animals. Twenty-one Thoroughbred horses, athletes, with and without HPIE were evaluated at two moments, before (T0) and 4 hours after furosemide administration (T1) at a dose of 0.5 mg / kg. All equines were submitted to echocardiographic examination at both moments, as well as blood sampling for hematological and biochemical evaluation. Echocardiographic examination showed the following variables: FC, DC, VEj, FEj, VSFVE, VDFVE, FS, SIV, PLVE, DVE, AEs, Ao, AE:Ao, TEVE, E-S, and flow in the pulmonary artery. For the laboratory tests, the following variables were considered: He, Hb, Ht, VCM, HCM, CHCM, Leu, Neu, Linf, Mon, Plaq, AST, GGT, Alb, Pt, BT and BD. Furosemide influenced some echocardiographic indexes of non-HPIE animals, altering the velocity of pulmonary artery flow and TEVE. All others echocardiographic and hematological parameters did not present any influence of furosemide administration, although urea and creatinine values have increased in T1 due to the hemoconcentration in non-HPIE group.

Muitos equinos participantes de provas de corrida, ao exame endoscópico, apresentam evidências de ocorrência de Hemorragia Pulmonar Induzida pelo Exercício (HPIE). A HPIE trata-se de um sangramento de origem pulmonar que ocorre em equinos durante atividade física intensa e pela alta prevalência, muitas vezes associada aos equinos de corrida. Considerando, baseado nos estudos realizados, que o principal mecanismo descrito no desenvolvimento dos quadros de HPIE envolve o aumento da pressão transmural, resultante do aumento da pressão pulmonar causada pelo exercício físico, a furosemida parece ter papel importante na atenuação destes fatores, o que suporta a sua utilização nestes animais. Foram avaliados 21 equinos da raça Puro Sangue Inglês, atletas de distintas modalidades (corrida e polo), com e sem HPIE em dois momentos, antes (T0) e 4 horas após a administração da furosemida (T1) na dose de 0,5 mg/kg. Os animais foram submetidos a exame ecocardiográfico nos dois momentos, e também a colheita de sangue para avaliação hematológica e bioquímica. Ao exame ecocardiográfico foram consideradas as seguintes variáveis: FC, DC, VEj, FEj, VSFVE, VDFVE, FS, SIV, PLVE, DVE em sístole e diástole, AEs, Ao, AE:Ao, TEVE, E-S, e pico de velocidade do fluxo na artéria pulmonar. Para os exames laboratoriais foram consideradas as seguintes variáveis: He, Hb, Ht, VCM, HCM, CHCM, Leu, Neu, Linf, Mon, Plaq, AST, GGT, Alb, Pt, BT e BD. O uso da furosemida exerceu influência sobre os índices ecocardiográficos estudados de animais sem HPIE alterando a velocidade do fluxo da artéria pulmonar e o TEVE. Os demais parâmetros ecocardiográficos estudados bem como os parâmetros hemáticos não apresentaram alteração significativa, exceção feita aos valores de ureia e creatinina que aumentaram em T1, em função da hemoconcentração, sendo significantemente maiores no grupo sem HPIE. / Many racehorses at endoscopic examination after race present evidence of Exercise Induced Pulmonary Hemorrhage (HPIE). HPIE is a bleeding that occurs from pulmonary origin in horses during intense physical activity, often associated, by the high prevalence, to the racehorses, being able to present itself in many other equines, since undergoing intense physical exercise. Considering, based on previous studies, that the main mechanism involved in the development of HPIE involves the increase of the transmural pressure, resulting from the increase of the pulmonary pressure caused by the physical exercise, furosemide seems to play an important role in the attenuation of these factors, which supports their use in these animals. Twenty-one Thoroughbred horses, athletes, with and without HPIE were evaluated at two moments, before (T0) and 4 hours after furosemide administration (T1) at a dose of 0.5 mg / kg. All equines were submitted to echocardiographic examination at both moments, as well as blood sampling for hematological and biochemical evaluation. Echocardiographic examination showed the following variables: FC, DC, VEj, FEj, VSFVE, VDFVE, FS, SIV, PLVE, DVE, AEs, Ao, AE:Ao, TEVE, E-S, and flow in the pulmonary artery. For the laboratory tests, the following variables were considered: He, Hb, Ht, VCM, HCM, CHCM, Leu, Neu, Linf, Mon, Plaq, AST, GGT, Alb, Pt, BT and BD. Furosemide influenced some echocardiographic indexes of non-HPIE animals, altering the velocity of pulmonary artery flow and TEVE. All others echocardiographic and hematological parameters did not present any influence of furosemide administration, although urea and creatinine values have increased in T1 due to the hemoconcentration in non-HPIE group.

Doctor of Philosophy / Department of Anatomy and Physiology / David C. Poole / Exercise-induced pulmonary hemorrhage (EIPH) or epistaxis has been recognized in racehorses since the 16th century. Since this time, great strides have been made in terms of identifying the lungs as the source of the hemorrhage via the endoscope, utilization of bronchoalveolar lavage to quantify the hemorrhage, and the discovery of successful treatments such as furosemide and the nasal strip that ameliorate, but do not abolish EIPH. It has been determined that, in addition to extremely high pulmonary arterial pressures and the negative intrapleural pressures being the major physiologic forces causing pulmonary capillary stress failure, other factors have the potential for influencing the severity of EIPH including locomotory impact trauma, inflammatory airway disease (IAD), upper airway obstruction, coagulation anomalies, and high blood viscosity. It has been hypothesized that EIPH is detrimental to performance and this was recently confirmed by Hinchcliff et al. in 2004. EIPH is a complex multi-factorial condition with much still unknown about the etiology, best method for diagnosis, and most effective form of treatment. Chapter one of this dissertation determined the effectiveness of a novel treatment, concentrated equine serum, in ameliorating EIPH via reduction of IAD. Chapter two refuted the hypothesis that herbal formulations commonly used in the field with anecdotal success would decrease EIPH by correcting coagulation deficits during exercise, as scientific efficacy was not evident, at least at the dose and duration used in our investigation. Chapter three addressed the dogma that EIPH only occurs during maximal intensity exercise, and in demonstrating significant EIPH during sub-maximal exercise, emphasized the role that the airways play in contributing to the initiation and severity of EIPH. Chapter four examined the occurrence and severity of EIPH in the horse’s canine counterpart, the racing Greyhound. The demonstrated presence of mild EIPH in the Greyhound, a physiologically similar yet different athlete in comparison to the horse sheds new light on the etiology of this condition in both species. The results of these investigations have advanced the frontiers of our knowledge concerning EIPH. Specifically, they have generated novel information on the mechanistic bases of EIPH and have provided evidence supporting additional treatment options for reducing the severity of EIPH in horses.