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Titolo:
Ascites in poultry: recent investigations
Autore:
Currie, RJW;
Indirizzi:
Ross Breeders Ltd, Newbridge EH28 8SZ, Midlothian, Scotland Ross Breeders Ltd Newbridge Midlothian Scotland EH28 8SZ othian, Scotland
Titolo Testata:
AVIAN PATHOLOGY
fascicolo: 4, volume: 28, anno: 1999,
pagine: 313 - 326
SICI:
0307-9457(199908)28:4<313:AIPRI>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
PULMONARY-HYPERTENSION SYNDROME; SERUM TROPONIN-T; RIGHT-VENTRICULAR HYPERTROPHY; BROILER-CHICKENS; NITRIC-OXIDE; ALPHA-TOCOPHEROL; UNILATERAL OCCLUSION; HYDROGEN-PEROXIDE; HYPOBARIC HYPOXIA; MYOCARDIAL-CELLS;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
102
Recensione:
Indirizzi per estratti:
Indirizzo: Currie, RJW Ross Breeders Ltd, Newbridge EH28 8SZ, Midlothian, Scotland Ross Breeders Ltd Newbridge Midlothian Scotland EH28 8SZ land
Citazione:
R.J.W. Currie, "Ascites in poultry: recent investigations", AVIAN PATH, 28(4), 1999, pp. 313-326

Abstract

In recent years, ascites research has centred on gaining an increased understanding of pulmonary hypertension syndrome together with the potential role of primary cardiac pathologies. The impact at a cellular level of factors which trigger ascites;and substances that protect against it has also been documented. Primary pulmonary hypertension has been induced when birds are exposed to hypoxia during incubation. The conditions experienced during this phase of development may impact on the ability of the bird to regulate its basal metabolic rate through endocrine signals controlled by thyroid activity. The extent of ventilation in the lung influences the ability of thebird to oxygenate haemoglobin. Ventilation/perfusion mismatches may occur prior to or post-hatching. This factor has been studied extensively using the pulmonary artery/bronchus clamp model. At high altitude, a decreased ventilation/perfusion ratio may occur following the effective increase in physiological dead space due to the lowered oxygen tension at the level of the parabronchi. This explains the mechanism by which ascites is triggered by hypoxia in this particular situation. The effects of ascites are amelioratedby the use of beta(2) agonists and dietary arginine, which act by increasing ventilation and blood how in the lungs and thus correcting a ventilation/perfusion mismatch. Transient bacterial and viral infections may also influence the induction of pulmonary hypertension. The increases in blood viscosity associated with ascites are most probably a consequence of the condition rather than a cause. A bird may alleviate the effects of pulmonary hypertension by decreasing blood viscosity through inhibition of platelet function, increased erythrocyte deformability and the production of coronary relaxants. Evidence is accumulating that primary cardiac pathology may be associated with a number of ascites cases. Broilers that subsequently develop ascites, exhibit lower heart rates than their normal flock mates. Furthermore, during ascites, hypoxic broilers exhibit bradycardia as opposed to the expected tachycardia. In these cases, a tachycardia induced by feed restriction may protect the bird by raising its cardiac output. Right atrio-ventricular regurgitant flow velocities in chickens are relatively slow compared with similar regurgitant hows induced by pulmonary hypertension in other species. The conduction system in the avian heart is specialized and contains arecurrent bundle branch that innervates the right atrio-ventricular valve,thus initiating active valve closure before right ventricular systole. This predisposes the heart to right ventricular volume overload through a valvular incompetance following a failure of valvular innervation. The resultant elevated diastolic wall stress can trigger the production of angiotensin II and its converting enzyme, which mediate ventricular hypertrophy. Subclinical myocardial damage, irrespective of its cause, can be detected by the presence of troponin T in the blood. Reactive oxygen species may damage cell membranes compromising cellular function in a number of body systems. A positive correlation exists between oxidized glutathione concentrations and right ventricular weight ratio. This indicates a failure to cope with oxidative stress at the level of the respiratory membrane. It is not known if itis possible to modulate levels of antioxidants at this location and hence protect the bird. The final description of the ascites aetiology may lie inthe concept of a circuit of events between the cardiac, pulmonary and vascular systems that satisfy the metabolic requirements of the bird. A deficit in one of these systems, at a level that prevents adequate compensation from other components, triggers the pathological cascade that results in the lend point of clinical ascites.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 00:09:11