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The phenology of trees is highly susceptible to changing global temperatures. Leaf budburst advances with increasing spring temperatures, but can also be delayed when warmer winters reduce chilling exposure. Results from long-term observations show that increasing temperatures have triggered advanced budburst in the past decades, but some studies also show that budburst advance has slowed recently. Here, we conducted an experiment with five temperate deciduous tree species (Acer rubrum L., Larix laricina (Du Rois) K. Koch, Populus tremuloides Michx., Quercus ellipsoidalis E. j. Hill, Betula papyrifera Marsh.) and one invasive species (Rhamnus cathartica L.) in Minnesota, USA, to assess the impact of chilling on the timing of leaf budburst. We collected twigs over two winter seasons (2011/2012 and 2012/2013) on a biweekly basis and exposed them to spring-like temperatures of 21 °C/16 °C day and night, long day photoperiod (16 h). We found a significant relationship of advanced budbreak with increased chilling for all species tested (P < 0.001) and significant differences in the timing to budburst among all species (P < 0.001). Acer rubrum responded strongly to chilling, showing a very steep linear decline in days to budburst with increased exposure to chilling. On the other end of the spectrum, L. laricina responded least to increases in chilling. These results suggest that rising global temperatures will likely have diverse impacts on tree species with potential implications for species interactions such as competition.

Background Pulseless electrical activity is an important cause of cardiac arrest. Our purpose was to determine if induction of hypothermia with a cold perfluorocarbon-based total liquid ventilation (TLV) system would improve resuscitation success in a swine model of asphyxial cardiac arrest/PEA. Methods Twenty swine were randomly assigned to control (C, no ventilation, n =11) or TLV with pre-cooled PFC ( n =9) groups. Asphyxia was induced by insertion of a stopper into the endotracheal tube, and continued in both groups until loss of aortic pulsations (LOAP) was reached, defined as a pulse pressure less than 2mmHg. The TLV animals underwent asphyxial arrest for an additional 2min after LOAP, followed by 3min of hypothermia, prior to starting CPR. The C animals underwent 5min of asphyxia beyond LOAP. Both groups then underwent CPR for at least 10min. The endpoint was the resumption of spontaneous circulation maintained for 10min. Results Seven of 9 animals achieved resumption of spontaneous circulation (ROSC) in the TLV group vs. 5 of 11 in the C group ( p =0.2). The mean pulmonary arterial temperature was lower in total liquid ventilation animals starting 4min after induction of hypothermia (TLV 36.3±0.2°C vs. C 38.1±0.2°C, p p O 2 was higher in total liquid ventilation animals at 2.5min of CPR (TLV 76±12mmHg vs. C 44±2mmHg; p =0.03). Conclusion Induction of moderate hypothermia using perfluorocarbon-based total liquid ventilation did not improve ROSC success in this model of asphyxial cardiac arrest.

Rapid intra-arrest induction of hypothermia using total liquid ventilation (TLV) with cold perfluorocarbons improves resuscitation outcome from ventricular fibrillation (VF). Cold saline intravenous infusion during cardiopulmonary resuscitation (CPR) is a simpler method of inducing hypothermia. We compared these 2 methods of rapid hypothermia induction for cardiac resuscitation.Three groups of swine were studied: cold preoxygenated TLV (TLV, n=8), cold intravenous saline infusion (S, n=8), and control (C, n=8). VF was electrically induced. Beginning at 8 min of VF, TLV and S animals received 3 min of cold TLV or rapid cold saline infusion. After 11 min of VF, all groups received standard air ventilation and closed chest massage. Defibrillation was attempted after 3 min of CPR (14 min of VF). The end point was resumption of spontaneous circulation (ROSC).Pulmonary arterial (PA) temperature decreased after 1 min of CPR from 37.2 degrees C to 32.2 degrees C in S and from 37.1 degrees C to 34.8 degrees C in TLV (S or TLV vs. C p0.0001). Coronary perfusion pressure (CPP) was higher in TLV than S animals during the initial 3 min of CPR. Arterial pO(2) was higher in the preoxygenated TLV animals. ROSC was achieved in 7 of 8 TLV, 2 of 8 S, and 1 of 8C (TLV vs. C, p=0.03).Moderate hypothermia was achieved rapidly during VF and CPR using both cold saline infusion and cold TLV, but ROSC was higher than control only in cold TLV animals, probably due to better CPP and pO(2). The method by which hypothermia is achieved influences ROSC.

Induced external hypothermia during ventricular fibrillation (VF) improves resuscitation outcomes. Our objectives were twofold (1) to determine if very rapid hypothermia could be achieved by intrapulmonary administration of cold perfluorocarbons (PFC), thereby using the lungs as a vehicle for targeted cardiopulmonary hypothermia, and (2) to determine if this improved resuscitation success.Part 1: Nine female swine underwent static intrapulmonary instillation of cold perfluorocarbons (PFC) during electrically induced VF. Part 2: Thirty-three female swine in VF were immediately ventilated via total liquid ventilation (TLV) with pre-oxygenated cold PFC (-15 degrees C) or warm PFC (33 degrees C), while control swine received no ventilation during VF. All swine in both Parts 1 and 2 underwent VF arrest for 11 min, then defibrillation, ventilation and closed chest massage until resumption of spontaneous circulation (ROSC). The endpoint was continued spontaneous circulation for 1h without pharmacologic support.Static intrapulmonary instillation of cold PFC achieved rapid cardiopulmonary hypothermia; pulmonary artery (PA) temperature of 33.5+/-0.2 degrees C was achieved by 10 min. Nine of 9 achieved ROSC. Hypothermia was achieved faster using TLV: at 6 min VF, cold TLV temperature was 32.9+/-0.4 degrees C vs. cold static instillation temperature 34.3+/-0.2 degrees C. Nine of 11 cold TLV swine achieved ROSC for 1h vs. 3 of 11 control swine (p=0.03). Warm PFC also appeared to be beneficial, with a trend toward greater achievement of ROSC than control (ROSC; warm PFC 8 of 11 vs. control 3 of 11, p=0.09).Targeted cardiopulmonary intra-arrest moderate hypothermia was achieved rapidly by static intrapulmonary administration of cold PFC and more rapidly by total liquid ventilation with cold PFC; resumption of spontaneous circulation was facilitated. Warm PFC showed a trend toward facilitating ROSC.