Non‐invasive determination of heart rate in newly hatched chicks

Tazawa, Hiroshi; Takami, Masashi; Kobayashi, Kazusuke; Hasegawa, J; Ar, Amos

doi:10.1080/00071669208417553

Cited by 17 publications

(7 citation statements)

References 14 publications

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“…3, 4). This is exactly the opposite of the pattern observed in birds (Tazawa et al 1991b(Tazawa et al , 1992, but is similar to that of the direct developing frog, Eleutherodactylus coqui (Burggren et al 1990). The pattern differences likely reflect the differences between species in the magnitude of the post-hatching O2 consumption increase and the change in 02 transport efficiency resulting from the gas exchanger being in parallel (chorioallantoic membrane) with the tissues being in series (lung).…”

Section: Heart Ratesupporting

confidence: 53%

Heart rate during development in the turtle embryo: effect of temperature

Birchard

Reiber

1996

J Comp Physiol B

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Growth and development can occur over a wide range of physical conditions in reptiles. Cardiovascular function must be critical to this ability. However, information on cardiovascular function in developing reptiles is lacking. Previous work indicated that in reptiles the effects of temperature on growth and metabolism are largely restricted to early development. This study examined whether the previously observed effects of temperature and different perinatal patterns of metabolism observed in amniotic vertebrates are correlated with cardiovascular function. Embryonic and hatchling carcass mass, heart mass and heart rate (HR) were compared for snapping turtle eggs (Chelydra serpentina) incubated at 24 degrees and 29 degrees C. Incubation time was shorter at 29 degrees C (56.2 days) than at 24 degrees C (71.1 days). Carcass and heart growth showed a sigmoidal pattern at both temperatures. However, cardiac growth showed a relative decrease as incubation proceeded. Incubation temperature significantly affected the HR pattern during development. The HR of embryos incubated at 24 degrees C was constant for most of incubation (51.8 +/- 4.8 min-1). A small decrease was observed just prior to and a large decrease immediately following hatching (posthatch, 22.3 +/- 4.1 min-1). At 29 degrees C embryonic HR was greater than at 24 degrees C early in development (72.3 +/- 3 min-1). The HR steadily decreased to values equivalent to those at 24 degrees C. The HRs of 24 degrees C and 29 degrees C hatchlings were not different. Cardiac output (estimated as the product of heart mass and HR) increased rapidly during early development and then slowed dramatically at both temperatures. These data are consistent with the suggestion that temperature exerts its effects primarily early in development. Furthermore, the changes in cardiovascular function are correlated with metabolic changes in hatching vertebrates.

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Section: Heart Ratesupporting

confidence: 53%

Heart rate during development in the turtle embryo: effect of temperature

Birchard

Reiber

1996

J Comp Physiol B

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“…This pattern is observed in mammals including humans (Davignon et al, 1979). In normal (White Leghorn) chickens the increase in HR begins shortly after hatching, peaks at approximately 2 to 4 weeks of age, plateaus and slowly declines until maturity (Ringer et al, 1957;Flick, 1967;Tazawa et al, 1992). The progressive increase in HR with age is likely to be the most important means whereby CO is increased to meet the metabolic demands of rapid growth.…”

Section: Introductionmentioning

confidence: 85%

Progressive bradycardia, a possible factor in the pathogenesis of ascites in fast growing broiler chickens raised at low altitude

Olkowski

Classen²

1998

British Poultry Science

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1. The first objective was to evaluate baseline heart rate (HR) responses in fast growing broilers fed ad libitum from 1 to 45d or subjected to a food restriction (85%, 70% and 55% of ad libitum from 7 to 21d) and a refeeding (22 to 45d) regimen in a normal thermal environment. The second was to evaluate HR and haematocrit responses in fast growing broilers reared at a low environmental temperature and fed ad libitum (A-L) from 1 to 42d, subjected to food restriction (70% ad libitum) between 7 to 21d and refed thereafter (R-R), or subjected to food restriction between 7 to 42d (R), and to follow the changes in normal birds and those prone to ascites. 2. The baseline HR in the normal thermal environment at 21 and 45d in birds fed ad libitum was lower (P < 0.001) than at 7d. The food-restricted groups had higher HRs at 21d than at 7d, with the differences significant (P < 0.01) for the 70% and 55% treatments. At 21d the HRs in restricted groups were significantly higher (P < 0.01) than in ad libitum-fed birds. After returning to ad libitum feeding the HRs in these birds tended to decline, with the differences significant (P < 0.05) for the 70% and 55% treatments. 3. In the birds exposed to cold, each feeding regimen produced distinct patterns of change in HR and haematocrit. Both feeding regimen and age had significant (P < 0.001) effects on the changes of both variables. Relative to 7d, on 14d and 21d the HRs decreased and haematocrits increased in all groups, but the rates of change were highest in the A-L and R-R birds. The first fulminant cases of ascites were observed during the third week in the A-L group and during the fourth week in the R-R group. None of the chickens from the R group developed ascites. Altogether, the incidence of ascites was 48% in the A-L group and 28% in the R-R group. 4. Among the birds exposed to cold, the ascitic birds had significantly (P < 0.001) lower HRs and higher haematocrits than normal birds from the same feeding regimen group. The time trends in the rates of change in HR and haematocrit were distinctly different (P < 0.001) for ascitic and normal birds. The change in feeding regimen from restricted to ad libitum in the R-R group resulted in a significant (P < 0.001) decrease in HR and increase in haematocrit. 5. In view of the evidence presented, it appears that hypoxaemia and tissue hypoxia in broiler chickens may be a result of circulatory insufficiency associated with progressive bradycardia rather than, as commonly believed, pulmonary insufficiency. In this situation the pulmonary hypertension may be a secondary symptom.

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“…These results were in agreement with those of Druyan et al [166], who found that generation S3 chicks from their AS-S line had a significantly higher heart rate on day of hatch than that of generation S3 chicks from the AS-R line. It was reported [167] that heart rate began to increase shortly after hatch, and reached a peak close to 4 wk of age; thereafter, it declined slowly [168]. The AS-S selected line exhibited increased heart rate only between d 1 and d 7, with a decline thereafter toward d 17, while the birds were kept under standard brooding condition [57].…”

Section: The Heartmentioning

confidence: 99%

Ascites Syndrome in Broiler Chickens - A Physiological Syndrome Affected by Red Blood Cell

Druyan¹

2012

Blood Cell - An Overview of Studies in Hematology

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Non‐invasive determination of heart rate in newly hatched chicks

Cited by 17 publications

References 14 publications

Heart rate during development in the turtle embryo: effect of temperature

Heart rate during development in the turtle embryo: effect of temperature

Progressive bradycardia, a possible factor in the pathogenesis of ascites in fast growing broiler chickens raised at low altitude

Ascites Syndrome in Broiler Chickens - A Physiological Syndrome Affected by Red Blood Cell

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