Habitat and roe deer fawn vulnerability to red fox predation.

1. Notwithstanding the growing amount of literature emphasizing the link between habitat, life-history traits and behaviour, few empirical studies investigated the combined effect of these parameters on individual predation risk. We investigated direct and indirect consequences of habitat composition at multiple spatial scales on predation risk by red foxes on 151 radio-monitored roe deer fawns. We hypothesized that the higher resource availability in fragmented agricultural areas increased predation risk because of: (i) shorter prey movements, which may increase predictability; (ii) larger litter size and faster growth rates, which may increase detectability in species adopting a hiding neonatal anti-predator strategy. The sharing of risky habitat among littermates was expected to promote whole-litter losses as a result of predation. 2. The landscape-scale availability of agricultural areas negatively affected pre-weaning movements, but did not influence growth rates or litter size. Predation risk was best described by the interplay between movements and fine-scale habitat fragmentation: a higher mobility increased the encounter rate and predation risk in highly fragmented home ranges, while it reduced predation risk in forest-dominated areas with clumped resources because of decreased predictability. This is one of the first demonstrations that movement patterns can be an efficient anti-predator strategy when adjusted to local conditions. 3. In accordance with previous studies documenting the existence of family effects (i.e. non-independence among siblings) in survival, littermates survived or died together more often than expected by chance. In addition, our study specifically demonstrated the occurrence of behaviourally mediated family effects in predation risk: after a fox killed one fawn the probability of a sibling being killed within a few days rose from 20% to 47%, likely because of the win-stay strategy (i.e. return to a previously rewarding site) adopted by the predator. Hence, the predator's hunting strategy has the potential to raise fawn mortality disproportionately to predator abundance. 4. There is increasing evidence that fawns inhabiting highly productive predator-free habitats are granted lifetime fitness benefits; these potential advantages, however, can be cancelled out when predation risk increases in the very same high-productivity areas, which might thus turn into attractive sinks.

Cerebral blood flow and evoked potentials during reoxygenation with 21 or 100% O2 in newborn pigs.

The effects of resuscitation with 21 or 100% O2 on cerebral blood flow (CBF) and somatosensory evoked potentials (SEPs) were studied in 19 newborn pigs anesthetized with pentobarbital sodium. They were ventilated with 8% O2 until base excess reached -20 mmol/l and then were randomly reoxygenated with 21% O2 (n = 10) or 100% O2 (n = 9) for 25 min followed by 21% O2. Mean duration of hypoxemia in the two groups was 57 +/- 6 (SE) and 59 +/- 6 min, respectively. CBF determined by radioactive microspheres was significantly increased in all areas in both groups after 5 and 20 min of reoxygenation. At 5 min of reoxygenation forebrain O2 uptake (CMRo2) had increased significantly compared with baseline values in the 21% O2 group (2.5 +/- 0.1 to 3.2 +/- 0.2 ml.100 g-1.min-1) but not in the 100% O2 group. There were, however, no significant differences between the two groups in CBF or CMRo2 at any time, and by 60 min of reoxygenation both had returned to baseline levels. SEPs were not significantly different in the two groups. We conclude that, as judged by CBF, CMRo2, and SEP, 21% O2 is not inferior to 100% O2 when hypoxemic newborn pigs are reoxygenated.

Effects of hyperoxia on entry of bilirubin and albumin into rat brain.

The effects of hyperoxia on the entry of bilirubin and albumin into the brain were studied in five to six-week-old male Sprague-Dawley rats. Bilirubin was infused at 20 mg/kg/hour for three hours through a carotid catheter, resulting in serum bilirubin levels of 200-220 microM at 180 minutes. Group 1 (n = 8) was normoxic at all times. Group 2 (n = 8) was given oxygen (FiO2 = 0.75 -0.80) for the last hour of the three-hour bilirubin infusion. Group 3 (n = 10) was given oxygen (FiO2 = 0.75 -0.80) for 24-27 hours prior to, as well as during the bilirubin infusion. No significant differences were found in brain bilirubin (as measured by chloroform extraction) or brain albumin (as measured by 125I-albumin uptake) between the groups. Under these experimental conditions, hyperoxia does not increase bilirubin deposition in rat brain nor does it cause opening of the blood-brain barrier as measured by albumin entry into the brain.

[Neonatal asphyxia in full-term infants]. / Neonatal asfyksi hos fullbårne.

This study includes 57 children born at term with asphyxia and admitted to Children's Department, Rikshospitalet, during the period 1981-85. The mortality in this study was 14% which proves that asphyxia represents a serious illness in newborn infants. The results of this investigation confirm that Apgar score is not a very precise parameter and offers limited information when estimating prognosis after birth. 17% of the newborn infants suffered from neonatal seizures during their first day in the neonatal period, and this symptom appears to indicate a high risk of subsequent mortality and morbidity. Nearly 44% of the newborns needed mechanical ventilation.

Effect of intraventricular hemorrhage on pulmonary function in newborn piglets.

Intracranial hemorrhage in the premature infant is often associated with respiratory failure and need for mechanical ventilation. We therefore addressed the question of possible interactions with and pulmonary consequences of intraventricular hemorrhage. Newborn piglets were studied during intraventricular hemorrhage simulated by intraventricular blood infusion. Infusion volume amounted to 8% of estimated brain weight. Respiratory rate, minute ventilation, lung resistance and dynamic lung compliance, as well as arterial blood gases, arterial and intraventricular pressures were measured. The piglets were mechanically ventilated with a low basal rate of 20 breaths per minute throughout the study. All piglets experienced significant rise in intraventricular pressure and respiratory failure during the study. Respiratory failure was mainly a result of a reduction in respiratory frequency and minute ventilation until apnea. However, a rise in lung resistance was also noted while lung compliance did not change. We conclude that increased need for mechanical ventilation during intracranial hemorrhage is primarilty a consequence of hypoventilation. The increase seen in lung resistance could also suggest that intraventricular hemorrhage causes an element of bronchiolar constriction. Furthermore, these effects are not only a result of the increase in intraventricular pressure, but specific effects of blood components within the central nervous system must be considered.

Effect of hypoxemia and hypovolemia on retinal and choroidal blood flow in the newborn piglet.

The effect of hypoxemia and/or hypovolemia on ocular blood flow was studied in paralyzed and mechanically ventilated newborn piglets with the isotope-labelled microsphere method. Twenty-six piglets were studied in four different groups. One group of piglets (n = 6) was made hypoxemic by breathing 10% O2, a second group (n = 7) and a third group (n = 7) were studied during hypoxemia (10% O2), followed by hypovolemia (bleeding 20 and 30% of estimated blood volume, respectively). A fourth group of piglets (n = 6) was made hypovolemic by bleeding 20% of estimated blood volume. Hypoxemia resulted in a 2- to 3-fold increase in retinal blood flow (RBF), while hypovolemia did not change RBF, not even when preceded by a period of hypoxemia. In the case of choroidal blood flow (ChBF), the increase caused by hypoxemia was only 10-40%. Although ChBF decreased significantly during hypovolemia, no significant correlation between mean arterial blood pressure and ChBF was found. The results indicate that autoregulation is normally seen in RBF, but probably not in ChBF. However, during hypoxemia autoregulation was found neither in RBF nor in ChBF.

The effect of arterial PCO2-variations on ocular and cerebral blood flow in the newborn piglet.

The response of ocular and cerebral blood flow to different arterial PCO2 levels was studied in ventilated paralyzed newborn piglets with the radionuclide-labeled microsphere method. The retina and the choroid have different blood flow responses to variations in arterial PCO2 levels. Retinal blood flow (ml/g/min) was increased during hypercarbia, from 0.26 +/- 0.03 at baseline to 0.51 +/- 0.07 (PaCO2 8.7 +/- 0.2 kPa) and 0.62 +/- 0.07 (PaCO2 11.0 +/- 0.2 kPa). However, no significant change was found in choroidal blood flow during hypercarbia. Cerebral blood flow was more responsive to PaCO2 than retinal blood flow, increasing from 0.71 +/- 0.03 at baseline to 2.25 +/- 0.25 (PaCO2 8.7 +/- 0.2) and 1.77 +/- 0.13 (PaCO2 11.0 +/- 0.2). Hypocarbia did not influence either retinal or choroidal blood flow.

Effect of light and hyperoxia on ocular blood flow in the newborn piglet.

Ocular blood flow was studied in newborn piglets during light exposure and light combined with hyperoxia. Light caused a significant increase in ocular blood flow which returned to values not significantly different from baseline levels during superimposed hyperoxia. None of these experimental conditions changed total cerebral blood flow or cardiac output. The findings indicate that light might be a regulator of ocular blood flow. This influence of light on ocular blood flow may be of importance in the pathophysiology of retinopathy of prematurity.

Cerebral blood flow during experimental hypoxaemia and ischaemia in the newborn piglet.

The effect of selective hypoxaemia or ischaemia on cerebral blood flow was studied in 14 newborn piglets with the microsphere method. Surgery and experiments were performed under general anesthesia with 70% nitrous oxide. The spontaneously breathing piglet was then exposed to either low (zero) oxygen in the inspired air (hypoxaemia), or a graded tourniquet (3-5 kg string weight) of the neck above the level of the tracheostomy (ischaemia). Cerebral blood flow was measured at baseline, during the hypoxaemic/ischaemic insult, and 30 and 60 min thereafter. Brainstem blood flow was remarkably stable during both ischaemia and hypoxaemia. The reduction in blood flow to the cerebrum and to the cerebellum was greater during ischaemia than during hypoxaemia. Reactive hyperaemia followed hypoxaemia but was not obvious after selective ischaemia. Ischaemia and hypoxaemia thus seem to have different effects on cerebral blood flow.

Effect of nimodipine on cerebral and organ blood flow in normal and posthypoxemic newborn piglets.

Using the isotope-labelled microsphere method, blood flow to the brain, the heart and the kidneys were studied in newborn piglets during nimodipine infusion. Twenty piglets were studied in two different groups. Group 1 (n = 8) was kept normoxic and given a continuous nimodipine infusion (15 micrograms/kg/min). Group 2 (n = 12) was made hypoxemic by breathing 10% O2 for 10 min followed by an identical nimodipine infusion as group 1. In spite of a significant systemic hypotension, nimodipine infusion alone significantly increased blood flow in the brain stem and right cardiac ventricle at 30-60 min of infusion, while blood flow to cerebellum, cerebrum and the left cardiac ventricle did not change. Blood flow to the kidneys decreased significantly. In posthypoxemic piglets nimodipine infusion gave almost similar flow patterns, however, the changes appeared at an earlier time. We conclude that in spite of a significant reduction in blood pressure, cerebral and cardiac blood flow is preserved both in normal and posthypoxemic animals even at high doses of nimodipine. However, because of the decreased blood flow to the kidneys further dose-response studies are needed before clinical use in asphyctic newborns.

Cerebral blood flow autoregulation after moderate hypoxemia in the newborn piglet.

The isotope-labelled microsphere method was used to study blood flow autoregulation in the brainstem (BS), cerebellum (CBL), cerebrum (CBR) and choroid plexus (ChPl) in 21 newborn piglets exposed to hypoxemia and/or hypovolemia. One group of piglets (n = 7) was made hypoxemic by breathing 10% O2 for 10 min, a second group (n = 8) was studied during hypoxemia (10% O2, 10 min), followed by hypovolemia (bleeding 20% of estimated blood volume). A third group of piglets (n = 6) was made hypovolemic by bleeding 20%. Hypoxemia significantly impaired the autoregulatory capacity in CBL and CBR resulting in a pressure-passive flow pattern. Hypovolemia alone did not produce any significant cerebral vascular response in BS, CBL and CBR, not even when hypovolemia was preceded by hypoxemia, indicating a rapid restoration of the autoregulatory capacity of the cerebral vasculature after hypoxemia of moderate duration. The hypotension seen both during hypoxemia and hypovolemia was gradually compensated for and normalized within 60 min. However, animals exposed to both hypoxemia and hypovolemia were still hypotensive 60 min after the hypoxemic insult. Cardiac output (CO) was not affected by hypoxemia, but was consistently reduced in hypovolemia. We therefore speculate that in the newborn a reduced CO might be a more specific parameter for hypovolemia than a low blood pressure.

Regional blood flow during severe hypoxemia and resuscitation with 21% or 100% O2 in newborn pigs.

Our aim was to determine whether the use of room air or 100% oxygen has different effects on the peripheral circulation during resuscitation from severe hypoxemia. Twenty-four piglets, 2-to 5-days old, were anesthetized with pentobarbital and randomized to control (n = 5, surgery only) or hypoxemia. Hypoxemia (FiO2 = 0.08) was continued until base excess reached - 20 mml/L. Resuscitation was then performed with 21% (n = 10) or 100% O2 (n = 9) for 25 min followed by 21% O2 in both groups. Regional blood flow was measured with radioactive microspheres. Both hypoxic groups showed marked hyperemia during resuscitation in cardiac and skeletal muscle, a moderate hyperemia in intestine and pancreas while kidneys, liver, spleen and skin showed no hyperemic response. There were no significant differences between the two treatment groups in blood flow to any organ. Arterial oxygen content was significantly higher in the 100% O2 group than in the 21% O2 at 5 and 20 min after onset of resuscitation (11.6 +/- 0.7 and 11.2 +/- 0.6 vs 8.6 +/- 0.3 and 8.7 +/- 0.3 ml/100 ml, p < 0.01). Oxygen delivery was, however, significantly higher in the 100% O2 group than in the 21% O2 group only to the intestine and pancreas at 5 min of resuscitation. We conclude that resuscitation with 21% or 100% oxygen produces similar changes in peripheral blood flow in this porcine model of neonatal hypoxemia.

Retinal and choroidal blood flow response to hyperoxemia after severe hypoxemia in the newborn piglet.

To investigate the effect of hyperoxemia on the ocular circulation after a severe hypoxemic insult (8% O2 until base excess reached -20 mmol/l), we randomly reoxygenated newborn piglets with 100% (study group, n = 8) or 21% O2 (control group, n = 10). Retinal (RBF) and choroidal blood flow (ChBF) were measured with radioactive microspheres. The hypoxemic insult did not change RBF, while ChBF significantly decreased. However, a marked reduction in both retinal (RDO2) and choroidal oxygen delivery (ChDO2) was observed, probably resulting in hypoxia both in the inner and outer retina. At 5 and 20 min of reoxygenation a similar hyperemic response in the retina was seen in both groups. RDO2 also increased significantly and no significant differences between the 2 groups could be demonstrated. We found no indication of retinal vasoconstriction during hyperoxemia. We speculate that the vasodilating effect of the preceding hypoxemia overrules the vasoconstrictive effect of the retinal vessels normally found during hyperoxemia.

Home range size and choice of management strategy for lynx in Scandinavia.

Annual and seasonal home ranges were calculated for 47 Eurasian lynx in four Scandinavian study sites (two in Sweden and two in Norway). The observed home ranges were the largest reported for the species, with study site averages ranging from 600 to 1,400 km2 for resident males and from 300 to 800 km2 for resident females. When home range sizes were compared to the size of protected areas (national parks and nature reserves) in Scandinavia, it was concluded that very few protected areas contained sufficient forest to provide space for more than a few individuals. As a direct consequence of this, most lynx need to be conserved in the multiuse semi-natural forest habitats that cover large areas in Scandinavia. This conservation strategy leads to a number of conflicts with some land uses (sheep and semidomestic reindeer herding, and roe deer hunters), but not all (forestry and moose harvest). Accordingly research must be aimed at understanding the ecology of these conflicts, and finding solutions.