Comparison of Physiological Indicators of Chronic Stress in Confined and Nonconfined Gilts1

Rampacek, George B.; Kraeling, Robert R.; Fonda, Edward S.; Barb, C. R.

doi:10.2527/jas1984.582401x

Cited by 27 publications

(7 citation statements)

References 24 publications

(29 reference statements)

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“…This in turn could result in an increased MCR [45]. Such caveats notwithstanding, the MCRs measured in this study are quite comparable to those measured in nonsurgically stressed, nonpregnant gilts (2.31 liters/min) [56]. Similar studies for other species with mothers maintained under halothane and nitrous oxide (rhesus monkeys) [13], sodium pentobarbitone with atropine (guinea pigs) [11], and ketamine-HC (baboons) [14] have been reported.…”

Section: Discussionsupporting

confidence: 76%

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Placental Metabolism of Cortisol at Mid- and Late Gestation in Swine1

Klemcke

1995

Biology of Reproduction

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An experiment was conducted in pigs to determine the source of fetal cortisol at 50 (n = 5) or 100 days (n = 4) of gestation (term = 114 days). Equilibrium concentrations of tritiated cortisol were achieved, and all hormonal measures were made at 110, 130, 140, and 150 min in anesthetized pigs. Maternal plasma cortisol did not differ (p = 0.48) between 50 (70.2 +/- 7.4 ng/ml; mean +/- SEM) and 100 days (62.4 +/- 5.8 ng/ml). Conversely, fetal cortisol increased (p = 0.048) between 50 (8.5 +/- 2.5 ng/ml) and 100 days (24.2 +/- 4.2 ng/ml), and, at each gestational age, values were lower (p = 0.001) than those in maternal plasma. Plasma cortisone (15.1 +/- 2.3 ng/ml) did not change with gestational age (p = 0.42) in either compartment (maternal or fetal), nor did it differ between compartments (p = 0.08). Maternal cortisol accounted for 22.8 +/- 2.0% of fetal cortisol at 50 days of gestation, and this contribution decreased (p < 0.001) to 5.87 +/- 0.8% at 100 days. At both ages, maternal cortisol accounted for almost 50% of fetal cortisone. Metabolism of maternal cortisol by the entire uterofetoplacental unit was 8.4 +/- 1.7% at 50 days and 7.5 +/- 2.4% at 100 days (p = 0.76). The maternal metabolic clearance rate of cortisol increased 44% (p = 0.003) between 50 and 100 days (1.49 +/- 0.4 vs. 2.15 +/- 0.2 L/min). Hence at these gestational ages, the fetus--presumably the fetal adrenal--is the primary source of fetal plasma cortisol. The major contribution of maternal cortisol to fetal cortisone strongly suggests the presence of porcine placental 11 beta-hydroxysteroid dehydrogenase activity. Further, factors constituting the placental "barrier" that metabolize maternal cortisol to cortisone and other products may be major regulators of porcine fetal plasma cortisol and cortisone.

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Section: Discussionsupporting

confidence: 76%

“…Thus, if the MCR estimates are reduced because of the blood sampling procedure, such a reduction is undoubtedly minimal. Previous investigations have also determined MCR using both infusion and blood sample removal from peripheral veins [5,14,56].…”

Section: Discussionmentioning

confidence: 99%

Placental Metabolism of Cortisol at Mid- and Late Gestation in Swine1

Klemcke

1995

Biology of Reproduction

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“…We also interpret in rodent models of HI injury that stress due to restraint nullifies the neuroprotective effects of HT, 22,23 and that tolerance to anoxia during hypothermia is increased if the animals are anesthetized. 24 It is known that cortisol in piglets is a good marker of stress, 25,26 and it has been suggested that corticosteroids released during stress lead to energy depletion in the brain, making it more vulnerable to excitotoxicity. 27 A causal link between stress and the failure of hypothermic neuroprotection needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

Head cooling with mild systemic hypothermia in anesthetized piglets is neuroprotective

Tooley

Šatas

Porter

et al. 2002

Annals of Neurology

164

140

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Hypothermia is potentially therapeutic in the management of neonatal hypoxic-ischemic brain injury. However, not all studies have shown a neuroprotective effect. It is suggested that the stress of unsedated hypothermia may interfere with neuroprotection. We propose that selective head cooling (SHC) combined with mild total-body hypothermia during anesthesia enhances local neuroprotection while minimizing the occurrence of systemic side effects and stress associated with unsedated whole-body cooling. Our objective was to determine whether SHC combined with mild total-body hypothermia while anesthetized for a period of 24 hours reduces cerebral damage in our piglet survival model of global hypoxia-ischemia. Eighteen anesthetized piglets received a 45-minute global hypoxic-ischemic insult. The pigs were randomized either to remain normothermic or to receive SHC. We found that the severity of the hypoxic-ischemic insult was similar in the SHC versus the normothermic group, and that the mean neurology scores at 30 and 48 hours and neuropathology scores were significantly better in the SHC group versus the normothermic group. We conclude that selective head cooling combined with mild systemic hypothermia and anesthesia is neuroprotective when started immediately after the insult in our piglet model of hypoxic-ischemic encephalopathy.

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“…The main evidence is the steady increase in cortisol levels during HT, which fell immediately to normal levels on rewarming. Cortisol in piglets is a good marker of stress (44,45). The lack of the expected reduction in HR during HT is an indirect marker of increased metabolic stress.…”

Section: Stress Ht and Neuroprotectionmentioning

confidence: 99%

Twenty-Four Hours of Mild Hypothermia in Unsedated Newborn Pigs Starting after a Severe Global Hypoxic-Ischemic Insult Is Not Neuroprotective

et al. 2001

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Three to 12 h of mild hypothermia (HT) starting after hypoxiaischemia is neuroprotective in piglets that are anesthetized during HT. Newborn infants suffering from neonatal encephalopathy often ventilate spontaneously and are not necessarily sedated. We aimed to test whether mild posthypoxic HT lasting 24 h was neuroprotective if the animals were not sedated. Thirty-nine piglets (median weight 1.6 kg, range 0.8 -2.2 kg; median age 24 h, range 7-48 h) were anesthetized and ventilated and subjected to a 45-min hypoxic (FiO 2~6 %) global insult (n ϭ 36) or sham hypoxia (n ϭ 3). On reoxygenation, 18 were maintained normothermic (NT, 39.0°C) for 72 h, and 21 were cooled from 39 (NT) to 35°C (HT) for the first 24 h before NT was resumed (18 experimental, three sham hypoxia). Cardiovascular parameters and intermittent EEG were documented throughout. The brain was perfusion fixed for neuropathology and five main areas examined using light microscopy. The insult severity (duration in minutes of EEG amplitude Ͻ 7V) was similar in the NT and HT groups, mean Ϯ SD (28 Ϯ 7.2 versus 27 Ϯ 8.6 min), as was the mean FiO 2 (5.9 Ϯ 0.7 versus 5.8 Ϯ 0.8%) during the insult. Six NT and seven HT piglets developed posthypoxic seizures that lasted 29 and 30% of the time, respectively. The distribution and degree of injury (0.0 -4.0, normal-maximal damage) within the brain (hippocampus, cortex/white matter, cerebellum, basal ganglia, thalamus) were similar in the NT and HT groups (overall score, mean Ϯ SD, 2.3 Ϯ 1.5 versus 2.4 Ϯ 1.3) as was the EEG background amplitude at 3 h (13 Ϯ 3.5 versus 10 Ϯ 3.3 V).The HT animals shivered and were more active. The sham control group (n ϭ 3) shivered but had normal physiology and neuropathology. Plasma cortisol was significantly higher in the HT group during the HT period, 766 Ϯ 277 versus 244 Ϯ 144 M at 24 h. Mild postinsult HT for 24 h was not neuroprotective in unsedated piglets and did not reduce the number of animals that developed posthypoxic seizures. Cortisol reached 3 times the NT value at the end of HT. We speculate that the stress of shivering and feeling cold interfered with the previously shown neuroprotective effect of HT. Many studies on newborn animal models show that mild HT, which starts after an HI insult, is neuroprotective (1-5). The duration of HT in these studies varies from 3 to 72 h, and the reduction in body temperature varies between 3.5 and 6°C. Some studies, however, show only a minor beneficial effect (6), or the neuroprotection is temporary and not maintained (7).

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Comparison of Physiological Indicators of Chronic Stress in Confined and Nonconfined Gilts1

Cited by 27 publications

References 24 publications

Placental Metabolism of Cortisol at Mid- and Late Gestation in Swine1

Placental Metabolism of Cortisol at Mid- and Late Gestation in Swine1

Head cooling with mild systemic hypothermia in anesthetized piglets is neuroprotective

Twenty-Four Hours of Mild Hypothermia in Unsedated Newborn Pigs Starting after a Severe Global Hypoxic-Ischemic Insult Is Not Neuroprotective

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