A neurochemical mechanism for hypoxia-induced anapyrexia

Steiner, Alexandre A.; Rocha, Maria José Alves da; Branco, Luiz Guilherme de Siqueira

doi:10.1152/ajpregu.00328.2002

Cited by 41 publications

(21 citation statements)

References 37 publications

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“…Both traits are related since hypoxia elicits an array of compensatory responses, among them is anapyrexia, the regulated drop of body temperature, which is a very efficient way to prevent cellular damage caused by hypoxia . The general importance of anapyrexia resides in the fact that it reduces the consumption of oxygen and increases the affinity of haemoglobin to oxygen (Bicego et al, 2002;Steiner et al, 2002). Variations in temperature tend to affect the entire organism (Odehnalová et al, 2008); the neonate piglets that obtained a low vitality score showed hypercapnia, results in agreement with previous work by Randall (1971) and Herpin et al (1996); whereas more recently, Groenendaal et al (2009) indicated that hypothermia affects PCO 2 diminishing this gas concentration at low temperatures.…”

Section: Vitality: Body Temperature and Blood Gasessupporting

confidence: 83%

Porcine neonates failing vitality score: physio-metabolic profile and latency to the first teat contact

Ortega¹,

Mota-Rojas²,

Juárez³

et al. 2011

Czech J. Anim. Sci.

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Clinical studies by Mota-Rojas et al. (2007) carried out on commercial pig farms showed that out of 1000 newly born piglets between 150 and 200 animals experienced apnoea after birth and it was related to perinatal asphyxia longer than 30 s, affecting the vitality in a negative way and delaying the latency of connecting to the dam's teat, which represents an economic impact for the producer. In another study where 11 324 farrowings were analysed from 5000 breeding Mexican pig farms, MotaRojas and Ramírez (1996) ABSTRACT:The objective of this study was to compare the metabolic and electrolytic profile as well as the morphological appearance of the umbilical cord and newly born piglets' weight that failed the vitality test scale compared to those who passed. Newborn piglets were divided into three groups according to the vitality with a modified Apgar score at birth: Group 1, failing with a score < 5 (G 1 : n = 218), Group 2 had a score of 6 to 7 (G 2 : n = 439) and Group 3 had scores > 8 (G 3 : n = 464). Results showed significant differences among groups (P < 0.05) in the physio-metabolic pH, PCO 2 , PO 2 , Na + , Ca 2+ , glucose, lactate and bicarbonate values. Regarding weight, temperature and latency to connect the maternal teat, there were also significant differences (P < 0.05) among groups; it took 23.38 min for G 3 while neonatal piglets from G 1 took 30 min longer (P < 0.05) to make the first teat contact. The neonates from the latter group had a higher percentage (75.68%) of broken umbilical cords, with higher birth weight (+200 g, P < 0.05), showed higher than normal blood glucose concentrations, and had lower body temperature at birth (-0.7°C, P < 0.05) and PO 2 in comparison with the other groups of neonates that passed the vitality score. A novel point of this study is the profile characterization of piglets that failed and passed the vitality score; we expect that the data provided may be applicable as reference values of metabolic and electrolyte blood profiles in newborn piglets according to their vitality. In conclusion, this study demonstrates that low vitality newborn piglets had clearly undergone through perinatal asphyxia. Potential indicators increasing this condition are: high birth weight, low body temperature, vitality score ≤ 5, and the presence of the broken umbilical cord at birth.

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Section: Vitality: Body Temperature and Blood Gasessupporting

confidence: 83%

Porcine neonates failing vitality score: physio-metabolic profile and latency to the first teat contact

Ortega¹,

Mota-Rojas²,

Juárez³

et al. 2011

Czech J. Anim. Sci.

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“…A role for NO in N 2 Oaugmented heat dissipation seems plausible in part because Quock and colleagues (7,26,28) have implicated NO in other N 2 O effects, specifically its antinociceptive and anxiolytic effects. Additionally, because hypoxia-induced hypothermia is attenuated by microinjection of a NO synthesis inhibitor in the preoptic hypothalamus (65), it is possible that central as well as peripheral NO release could participate in mediating the hypothermic effect of N 2 O.…”

Section: Discussionmentioning

confidence: 99%

Assessment of heat production, heat loss, and core temperature during nitrous oxide exposure: a new paradigm for studying drug effects and opponent responses

Kaiyala¹,

Ramsay²

2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Kaiyala, Karl J., and Douglas S. Ramsay. Assessment of heat production, heat loss, and core temperature during nitrous oxide exposure: a new paradigm for studying drug effects and opponent responses. Am J Physiol Regul Integr Comp Physiol 288: R692-R701, 2005. First published November 24, 2004; doi:10.1152/ajpregu. 00412.2004.-Studies using core temperature (T c) have contributed greatly to theoretical explanations of drug tolerance and its relationship to key features of addiction, including dependence, withdrawal, and relapse. Many theoretical accounts of tolerance propose that a given drug-induced psychobiological disturbance elicits opponent responses that contribute to tolerance development. This proposal and its theoretical extensions (e.g., conditioning as a mechanism of chronic tolerance) have been inferred from dependent variables, such as T c, which represent the summation of multiple underlying determinants. Direct measurements of determinants could increase the understanding of opponent processes in tolerance, dependence, and withdrawal. The proximal determinants of T c are metabolic heat production (HP) and heat loss (HL). We developed a novel system for simultaneously quantifying HP (indirect calorimetry), HL (direct gradient layer calorimetry), and T c (telemetry) during steady-state administrations of nitrous oxide (N 2O), an inhalant with abuse potential that has been previously used to study acute and chronic tolerance development to its hypothermia-inducing property. Rats were administered 60% N 2O (n ϭ 18) or placebo gas (n ϭ 16) for 5 h after a 2-h placebo baseline exposure. On average, N 2O rapidly but transiently lowered HP and increased HL, each by ϳ16% (P Ͻ 0.001). On average, rats reestablished and maintained thermal equilibrium (HP ϭ HL) at a hypothermic T c (Ϫ1.6°C). However, some rats entered positive heat balance (HP Ͼ HL) after becoming hypothermic such that acute tolerance developed, i.e., T c rose despite continued drug administration. This work is the first to directly quantify the thermal determinants of T c during administration of a drug of abuse and establishes a new paradigm for studying opponent processes involved in acute and chronic hypothermic tolerance development. addiction; drug tolerance; acute tolerance; drug dependence; gradient layer calorimetry; indirect calorimetry IN AN INFLUENTIAL 1971 REVIEW, Kalant et al. (32) made a convincing case for measuring drug tolerance using outcome variables that are continuously scaled, reliable, dose responsive, and amenable to analysis at the component level. An additional, desirable attribute is mediation by central regulatory mechanisms, reflecting the concept that drug use activates neuronal regulatory systems in ways that contribute to acute tolerance, chronic tolerance, withdrawal, drug dependence, and the potential for relapse in abstinent individuals (25,35,48,49,51,55,63). Core body temperature (T c ) epitomizes each of these attributes and has a long (59) and extensive history as an outcome variable in studies focus...

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“…This response is typically seen as being protective and contributes to the preservation of arterial oxygen pressure in hypoxia. This is an active process resulting from a reduction of the thermoregulatory set point, regulated within the preoptic hypothalamic nucleus (Barros et al, 2001;Steiner et al, 2002). It is possible to ask whether the drop in rectal temperature accounted for the fall in metabolic rate or whether is there evidence of metabolic suppression beyond that due to a resetting of the body temperature set point (Barros et al, 2001).…”

Section: Respiratory and Metabolic Responses To Hypoxia In High Altitmentioning

confidence: 99%

Divergent physiological responses in laboratory rats and mice raised at high altitude

Jochmans-Lemoine

Villalpando

Gonzales

et al. 2015

Journal of Experimental Biology

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Ecological studies show that mice can be found at high altitude (HAup to 4000 m) while rats are absent at these altitudes, and there are no data to explain this discrepancy. We used adult laboratory rats and mice that have been raised for more than 30 generations in La Paz, Bolivia (3600 m), and compared their hematocrit levels, right ventricular hypertrophy (index of pulmonary hypertension) and alveolar surface area in the lungs. We also used whole-body plethysmography, indirect calorimetry and pulse oxymetry to measure ventilation, metabolic rate (O 2 consumption and CO 2 production), heart rate and pulse oxymetry oxygen saturation (p O2,sat ) under ambient conditions, and in response to exposure to sea level P O2 (32% O 2 =160 mmHg for 10 min) and hypoxia (18% and 15% O 2 =90 and 75 mmHg for 10 min each). The variables used for comparisons between species were corrected for body mass using standard allometric equations, and are termed mass-corrected variables. Under baseline, compared with rats, adult mice had similar levels of p O2,sat , but lower hematocrit and hemoglobin levels, reduced right ventricular hypertrophy and higher mass-corrected alveolar surface area, tidal volume and metabolic rate. In response to sea level P O2 and hypoxia, mice and rats had similar changes of ventilation, but metabolic rate decreased much more in hypoxia in mice, while p O2,sat remained higher in mice. We conclude that laboratory mice and rats that have been raised at HA for >30 generations have different physiological responses to altitude. These differences might explain the different altitude distribution observed in wild rats and mice.

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A neurochemical mechanism for hypoxia-induced anapyrexia

Cited by 41 publications

References 37 publications

Porcine neonates failing vitality score: physio-metabolic profile and latency to the first teat contact

Porcine neonates failing vitality score: physio-metabolic profile and latency to the first teat contact

Assessment of heat production, heat loss, and core temperature during nitrous oxide exposure: a new paradigm for studying drug effects and opponent responses

Divergent physiological responses in laboratory rats and mice raised at high altitude

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