The best of two worlds: ecology and evolution of ambophilous plants.

Ambophily, the mixed mode of wind and insect pollination is still poorly understood, even though it has been known to science for over 130 years. While its presence has been repeatedly inferred, experimental data remain regrettably rare. No specific suite of morphological or ecological characteristics has yet been identified for ambophilous plants and their ecology and evolution remain uncertain. In this review we summarise and evaluate our current understanding of ambophily, primarily based on experimental studies. A total of 128 ambophilous species - including several agriculturally important crops - have been reported from most major habitat types worldwide, but this probably represents only a small subset of ambophilous species. Ambophilous species have evolved both from wind- and insect-pollinated ancestors, with insect-pollinated ancestors mostly representing pollination by small, generalist flower visitors. We compiled floral and reproductive traits for known ambophilous species and compared our results to traits of species pollinated either by wind or by small generalist insects only. Floral traits were found to be heterogeneous and strongly overlap especially with those of species pollinated by small generalist insects, which are also the prominent pollinator group for ambophilous plants. A few ambophilous species are only pollinated by specialised bees or beetles in addition to pollination by wind. The heterogeneity of floral traits and high similarity to generalist small insect-pollinated species lead us to conclude that ambophily is not a separate pollination syndrome but includes species belonging to different insect- as well as wind-pollination syndromes. Ambophily therefore should be regarded as a pollination mode. We found that a number of ecological factors promoted the evolution of ambophily, including avoidance of pollen limitation and self-pollination, spatial flower interference and population density. However, the individual ecological factors favouring the transition to ambophily vary among species depending on species distribution, habitat, population structure and reproductive system. Finally, a number of experimental studies in combination with observations of floral traits of living and fossil species and dated phylogenies may indicate evolutionary stability. In some clades ambophily has likely prevailed for millions of years, for example in the castanoid clade of the Fagaceae.

Prehospital noninvasive pressure support ventilation for acute cardiogenic pulmonary edema.

Severe acute cardiogenic pulmonary edema (ACPE) can successfully be treated with noninvasive pressure support ventilation (NIPSV) in a clinical setting. Whether prehospital NIPSV starting early at patients' home and being continued until hospital arrival is feasible and improves ACPE emergency care is examined in this study. End points of the study were oxygen saturation at hospital admission and clinical outcome. Twenty-three patients suffering from severe cardiac pulmonary edema with severe dyspnea, an oxygen saturation of less than 90% and basal rales were included in this controlled prospective randomized trial. All patients received standard medical treatment and 10 patients were additionally treated with NIPSV (pressure support level, 12 cmH2O; positive endexpiratory pressure, 5 cmH2O; FiO2, 0.6) whereas the other patients received oxygen (8 l/min) via Venturi face mask. Improvement in oxygen saturation was significantly faster in the NIPSV group and oxygen saturation was higher at the time of the hospital admission (NIPSV=97.3+/-0.8%; standard=89.5+/-2.7%, P=0.002). A trend toward higher troponin T levels was seen in the standard treatment group. The need for intensive care treatment did not differ, and one patient of each treatment group died in hospital. No complications were noted during the treatment with NIPSV. Prehospital NIPSV is feasible and able to improve emergency management of ACPE.

To dip or not to dip: on the physiology of blood pressure decrease during nocturnal sleep in healthy humans.

That sleep is accompanied by a blood pressure decrease is well known; however, the underlying physiology deserves further investigation. The present study examines in healthy subjects 2 main questions: is this dipping actively evoked? and what are the consequences of nondipping for daytime blood pressure? Nocturnal blood pressure was extrinsically elevated in 12 sleeping subjects to mean daytime values by continuously infused phenylephrine. This nondipping significantly lowered morning blood pressure during rest and 3 hours after resuming physical activity compared with a control condition (isotonic saline). Neither muscle sympathetic nerve activity nor sensitivity of alpha-adrenoceptors was reduced. However, the set point for initiation of regulatory responses through the baroreflex was clearly shifted toward lower blood pressure levels. Our results support the hypothesis of an actively regulated central mechanism for blood pressure resetting and set point consolidation of the baroreflex during nighttime sleep. This is suggested by the fact that extrinsically induced nondipping induces sustained decrease in blood pressure during the following morning through an actively lowered baroreflex set point.

Effect of facial cooling and cold air inhalation on sympathetic nerve activity in men.

In nine healthy subjects, cold stimuli were administered to the forehead and hand, to the oral and nasal cavities via ice cubes and to the bronchial system via inhalation of cold air (-25 degrees C). Blood pressure, heart rate and muscle sympathetic nerve activity (MSNA) from the peroneal nerve were recorded. MSNA expressed as total activity increased during cold air inhalation, cooling of the forehead (P < 0.001, ANOVA), hand and mouth (P < or = 0.05), paralleled by a rise in blood pressure during cold air inhalation and cooling of the forehead and hand (P < 0.01). Cooling of the forehead provoked a faster increase of MSNA expressed as total activity (P < 0.05) and higher levels of diastolic blood pressure (P = 0.05) compared with cooling of the hand. Bradycardia was observed only during cooling of the nasal cavity (P < 0.001) and the forehead (P < 0.05). It is concluded that cooling of the skin and mucous membranes of the tracheobronchial tract elicits sympathetically mediated hemodynamic adaptations, probably via stimulation of cold-sensitive afferents.

Evidence for lower sympathetic nerve activity in young adults with low birth weight.

OBJECTIVE: A dysfunction of the sympathetic nervous system may contribute to the development of hypertension and obesity in subjects with low birth weight (LBW). The present study examines resting sympathetic nerve traffic and its baroreflex modulation to the muscle vascular bed in healthy LBW subjects. DESIGN: Case-control studies of 13 healthy LBW subjects (< 2500 g at term) aged 20-30 years and 13 normal birth weight subjects (NBW; 3200-3700 g) closely matched for age, gender and body mass index. METHODS: Muscle sympathetic nerve activity (MSNA) recordings from the superficial peroneal nerve, blood pressure and heart rate were obtained at rest, during an inspiratory apnoea and a cold pressor test. Baroreflex function was evaluated by short-term infusion of nitroprusside and phenylephrine, respectively, in nine subjects of each group. RESULTS: During resting conditions burst frequency was significantly lower in LBW subjects (LBW: 24.7 +/- 2.4; NBW: 34.4 +/- 2.1 bursts/min, P < 0.05). When normalized for the different baseline values, baroreflex-mediated changes in MSNA were similar in both groups. Maximal MSNA levels in response to inspiratory apnoea and the cold pressor test did not differ between the groups. Blood pressure and heart rate were similar in LBW and NBW subjects both at rest and during sympatho-excitatory manoeuvres. CONCLUSIONS: Subjects born too small for their gestational age show a significantly lower sympathetic nerve activity under baseline conditions. Given the different baseline values, the sympathetic response to haemodynamic alteration is not affected in LBW subjects, and maximal activation during non-haemodynamic sympatho-excitatory manoeuvres is preserved.

Effects of selective angiotensin II receptor blockade on sympathetic nerve activity in primary hypertensive subjects.

OBJECTIVE: The role of the renin-angiotensin system in the regulation of sympathetic nervous activity in human hypertension was evaluated in patients with moderate primary hypertension. For that purpose, the effects of selective angiotensin II (ANG II) receptor blockade by valsartan on sympathetic outflow to the muscle vascular bed and hemodynamic parameters were examined. Results were compared with the effects of the peripherally acting calcium antagonist amlodipine. DESIGN: Eighteen hypertensive but otherwise healthy subjects were examined in a double-blind, placebo-controlled, cross-over protocol receiving either valsartan or amlodipine or placebo for 7 days in a randomized sequence. Treatment periods were separated by washout periods of 2 weeks. METHODS: At the seventh day of treatment, blood pressure, heart rate, muscle sympathetic nerve activity (MSNA), norepinephrine, renin and angiotensin were measured during resting conditions. Additionally, parameters were measured after administration of negative pressure of -15 mmHg to the lower part of the body and after a cold pressor test. RESULTS: Both antihypertensive drugs significantly decreased oscillometrically measured systolic blood pressure and diastolic blood pressure without any difference in effect. While valsartan did not affect the heart rate at rest, amlodipine increased it significantly. Likewise, MSNA was significantly enhanced by amlodipine but not by valsartan. Only ANG II receptor blockade increased renin and angiotensin levels. CONCLUSIONS: Selective ANG II receptor blockade not only decreases blood pressure, but also shifts the baroreflex set-point for the initiation of counter-regulatory reflex responses of heart rate and blood pressure towards normal blood pressure levels. Thus, data suggest that ANG II plays a pathogenetic role in the elevation of the baroreflex set point in primary hypertensive subjects.