1994
DOI: 10.1093/japr/3.3.244
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Effect of Age of Exposure and Dietary Acidification or Alkalinization on Broiler Pulmonary Hypertension Syndrome

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Cited by 35 publications
(20 citation statements)
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“…Increases in the pulmonary arterial pressure theoretically can be attributed to increases in cardiac output as well as to increases in the resistance to blood flow through the pulmonary vasculature Wideman, 2000;Wideman et al, 2007; Figure 1A). Fast growth, full-feeding, acclimation to cool environmental temperatures, heat stress, hypoxemia, hypercapnia, and metabolic acidosis all clearly contribute to the pathogenesis of pulmonary hypertension in broilers by increasing the cardiac output, either directly by increasing the metabolic demand for O 2 , or indirectly by dilating the systemic arterioles and thereby increasing venous return (Peacock et al, 1989;Reeves et al, 1991;Owen et al, 1994;Fedde et al, 1998;Wideman et al, 1998aWideman et al, ,c, 1999aWideman et al, ,b, 2000Wideman et al, , 2003aWideman, 1999;). Comparisons of PAH-susceptible and PAH-resistant broilers do not consistently reveal differences in cardiac output, but PAH-susceptible broilers consistently have higher pulmonary arterial pressures and pulmonary vascular resistances compared with PAH-resistant broilers Wideman, 2001, 2006c;Wideman et al, , 2006Wideman et al, , 2007Bowen et al, 2006a;Lorenzoni et al, 2008).…”
Section: Pulmonary Vascular Resistancementioning
confidence: 99%
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“…Increases in the pulmonary arterial pressure theoretically can be attributed to increases in cardiac output as well as to increases in the resistance to blood flow through the pulmonary vasculature Wideman, 2000;Wideman et al, 2007; Figure 1A). Fast growth, full-feeding, acclimation to cool environmental temperatures, heat stress, hypoxemia, hypercapnia, and metabolic acidosis all clearly contribute to the pathogenesis of pulmonary hypertension in broilers by increasing the cardiac output, either directly by increasing the metabolic demand for O 2 , or indirectly by dilating the systemic arterioles and thereby increasing venous return (Peacock et al, 1989;Reeves et al, 1991;Owen et al, 1994;Fedde et al, 1998;Wideman et al, 1998aWideman et al, ,c, 1999aWideman et al, ,b, 2000Wideman et al, , 2003aWideman, 1999;). Comparisons of PAH-susceptible and PAH-resistant broilers do not consistently reveal differences in cardiac output, but PAH-susceptible broilers consistently have higher pulmonary arterial pressures and pulmonary vascular resistances compared with PAH-resistant broilers Wideman, 2001, 2006c;Wideman et al, , 2006Wideman et al, , 2007Bowen et al, 2006a;Lorenzoni et al, 2008).…”
Section: Pulmonary Vascular Resistancementioning
confidence: 99%
“…Sustained pulmonary vasoconstriction attributable to hypoxia is responsible for increasing the incidence of PAH in commercial broilers reared at high altitudes, particularly when accompanied by subthermoneutral environmental temperatures that increase the cardiac output and induce the release of stress hormones. Exposure to hypobaric hypoxia has been used extensively as a research model for triggering PAH under experimental conditions (Burton and Smith, 1967;Burton et al, 1968;Cueva et al, 1974;Sillau et al, 1980;Sillau and Montalvo, 1982;Owen et al, 1990Owen et al, , 19941995a,b,c;Yersin et al, 1992;Beker et al, 1995;Wideman et al, 2000;Odom et Putative sympathetic (adrenergic) and parasympathetic (cholinergic) nerve terminals have been observed in association with the interparabronchial arterioles of avian lungs (Akester, 1971;Bennett, 1971;King et al, 1978). Epinephrine and norepinephrine constrict avian pulmonary arteries, and intravenously administered epinephrine elicits immediate pulmonary vasoconstriction accompanied by pulmonary hypertension (Somlyo and Woo, 1967;Wideman, 1999;Villamor et al, 2002;Lorenzoni and Ruiz-Feria, 2006;Ruiz-Feria, 2009;Bautista-Ortega and Ruiz-Feria, 2010).…”
Section: Mediators Of Pulmonary Vasoconstrictionmentioning
confidence: 99%
“…Várias fontes de sódio foram estudadas e foi concluído que o cloreto de amônio (BRANTON et al, 1986;SHLOSBERG et al, 1998) e o cloreto de sódio (SHLOSBERG et al, 1998) favoreceram a acidose e conseqüentemente, a ascite; já o bicarbonato de sódio (BOTTJE & HARRISON, 1985) e o carbonato de sódio (OWEN et al, 1994) favoreceram a alcalose.…”
Section: Genética E Ambienteunclassified
“…Conversely, Bergsjù and Kaldhusdal (1994) reported that the mycotoxin deoxynivalenol did not affect ascites status of broilers. The manipulation of dietary components to produce an acidi®ed ration has been implicated in an increase in ascites syndrome (Owen et al, 1994;Summers, 1996;Groves, 1997). Birds subjected to metabolic acidosis through HCl injection (as with acidi®ed rations) also experienced an increase in ascites (Wideman et al, 1998a).…”
Section: Nutrients and Other Dietary Compounds That Increase Ascites mentioning
confidence: 99%
“…Ubiquinone (coenzyme Q) has been shown to be bene®cial in decreasing ascites incidence (Nakamura et al, 1996). The manipulation of dietary components to produce an alkalinized ration has been implicated in a decrease in ascites syndrome (Owen et al, 1994;Summers, 1996;Groves, 1997). The addition of a Yucca schidigera extract, which functions as a urease inhibitor, decreased ascites incidence possibly through lowering intestinal ammonia and gut turn-over Balog et al, 1994;Walker, 1994a,b).…”
Section: Nutrients and Other Dietary Compounds That Decrease Ascites mentioning
confidence: 99%