Atenuación de la temperatura y radiación UV de la vegetación en entornos urbanos de ciudades ribereñas y su demanda hídrica / Attenuation of temperature and UV radiation of vegetation in urban environments of riverside cities and their water demand

Introducción. Este trabajo de investigación se realizó en la Ciudad de Honda, Colombia. Identificó el efecto de la sombra de los árboles en la atenuación de la temperatura, humedad relativa, temperatura de superficie del suelo, radiación solar y ultravioleta (UV) y determinó requerimientos de agua para la vegetación arbórea. Metodología. Se tomaron datos de temperatura del aire y de superficie de suelo, humedad relativa del aire, radiaciones solares y UV bajo la sombra de árboles y a plena exposición. Resultados. Se encontró que la temperatura del aire osciló entre 50ºC a plena exposición solar y 41ºC bajo sombra. La temperatura de superficie presentó a plena exposición solar valores de 66.8ºC y 42.6ºC bajo sombra. La variación de la radiación solar registrada ofreció un valor de 17.13 mW/cm2 a plena exposición solar y 1.69 mW/cm2 bajo sombra. La radiación UV presentó valores de 8 a plena exposición solar y 5 bajo sombra. La demanda hídrica por planta/día varió entre 5 y más de 500 litros, siendo la demanda diaria cercana a 2500 m3 . Conclusiones. En la ciudad no se realiza riego a los árboles, lo que conduce a que se produzca un déficit hídrico evidenciado por la pérdida de follaje ocasionando mínimas atenuaciones a la radiación UV. Las especies más relevantes respecto a la sombra son almendro (Terminalia cattapa), Pallandé (Pitecellobium dulce), naranjuelo (Capparis odoratissima), guayacán carrapo (Bulnesia carrapo), chirlobirlo (Tecoma stands), cumulá (Aspidosperma polyneuron) y mango (Manguifera indica). Los árboles pueden generar un buen servicio ecosistémico por la sombra, este servicio está mediado por la selección de la especie y el manejo de que son objeto los árboles.

Introduction: This research work was carried out in the city of Honda, Colombia. It identified the effect of tree shade on temperature attenuation, relative humidity, soil surface temperature, solar and ultraviolet (UV) radiation, and determined water requirements for arboreal vegetation. Methodology: Data on air and soil surface temperature, relative air humidity, solar and UV radiation were taken under the shade of trees and at full exposure. Results: It was found that the air temperature ranged from 50ºC at full sun exposure to 41ºC under shade. The surface temperature was 66.8ºC and 42.6ºC under shade. The variation of the registered solar radiation offered a value of 17.13 mW/cm2 at full solar exposure and 1.69 mW/cm2 under shade. The UV radiation presented values of 8 at full solar exposure and 5 under shade. The water demand per plant/day varied between 5 and more than 500 liters, being the daily demand close to 2500 m3. Conclusions: There is no irrigation of trees in the city which leads to a water deficit evidenced by the loss of foliage causing minimal attenuations to UV radiation. The most relevant species regarding shade are almond (Terminalia cattapa), Pallandé (Pitecellobium dulce), orange (Capparis odoratissima), guayacán carrapo (Bulnesia carrapo), chirlobirlo (Tecoma stands), cumula (Aspidosperma polyneuron) and mango (Manguifera indica). Trees can generate a good ecosystem service by shade which is mediated by the selection of the species and the management of the trees.

In vitro antifungal evaluation and structure-activity relationships of a new series of chalcone derivatives and synthetic analogues, with inhibitory properties against polymers of the fungal cell wall.

Here we report the synthesis, in vitro antifungal evaluation and SAR study of 41 chalcones and analogues. In addition, all active structures were tested for their capacity of inhibiting Saccharomyces cerevisiae beta(1,3)-glucan synthase and chitin synthase, enzymes that catalyze the synthesis of the major polymers of the fungal cell wall.

Inductance plethysmography: an alternative signal to servocontrol the airway pressure during proportional assist ventilation in small animals.

During proportional assist ventilation (PAV), the ventilator pressure is servocontrolled throughout each spontaneous inspiration such that it instantaneously increases in proportion to the airflow (resistive unloading mode), or inspired volume (elastic unloading mode), or both (combined unloading mode). The PAV pressure changes are generated in a closed-loop feedback circuitry commonly using a pneumotachographic signal. In neonates, however, a pneumotachograph increases dead space ventilation, and its signal may include a substantial endotracheal tube leak component. We hypothesized that respiratory inductive plethysmography (RIP) can replace pneumotachography to drive the ventilator during PAV without untoward effects on ventilation or respiratory gas exchange. Ten piglets and five rabbits were supported for 10-min (normal lungs) or 20-min (meconium injured lungs) periods by each of the three PAV modes. In each mode, three test periods were applied in random order with the ventilator driven by the pneumotachograph signal, or the RIP abdominal band signal, or the RIP sum signal of rib cage and abdomen. Interchanging the three input signals did not affect the regularity of spontaneous breathing, and gas exchange was achieved with similar peak and mean airway pressures (ANOVA). However, the RIP sum signal worked adequately only when the relative gains of rib cage and abdominal band signal were calibrated. We conclude that an RIP abdominal band signal can be used to generate PAV, avoiding increased dead space and endotracheal tube leak problems.

Effects of GABA receptor blockade on the ventilatory response to hypoxia in hypothermic newborn piglets.

Hypothermic newborn piglets have a depressed ventilatory response to hypoxia, and this may be due to an increase in CNS gamma-aminobutyric acid (GABA) levels. To evaluate the effects of GABA(A) receptor blockade on the ventilatory response to hypoxia in hypothermic piglets, 31 anesthetized paralyzed mechanically ventilated newborn piglets (2-7 d) were studied at a brain temperature of 38.5 +/- 0.5 degrees C [normothermia (NT), n = 15] or 34 +/- 0.5 degrees C [hypothermia (HT), n = 16]. The central respiratory output was evaluated by measuring burst frequency and moving time average area of phrenic nerve activity. Measurements of minute phrenic output (MPO), arterial blood pressure, heart rate, oxygen consumption, and arterial blood gases were obtained at room air and during 20 min of isocapnic hypoxia [fraction of expired oxygen (FiO2) = 0.10]. After 10 min of hypoxia, a bolus injection of 20 microL of bicuculline methiodide (BM; 10 microg) or Ringer's solution was administered into the cisterna magna over a 1-min period, and the piglets remained in hypoxia for an additional 10 min. There was an initial increase of 50 +/- 6% in MPO during the first minute of hypoxia followed by a decrease to values 24 +/- 8% above baseline at 10 min in the NT group. In contrast, in the HT group, the initial increase in MPO with hypoxia was eliminated, and, at 10 min, there was a decrease to a mean value 35 +/- 4% below baseline level (NT versus HT, p < 0.03). After administration of BM, a significant increase in MPO with hypoxia was observed in both groups compared with their placebo groups (p < 0.002 in NT-BM group, p < 0.0001 in HT-BM group). However, the magnitude of the increase in MPO during hypoxia was significantly greater in the HT group after administration of BM (NT versus HT, p < 0.0001). Changes in oxygen consumption, arterial blood pressure, heart rate, pH, partial pressure of oxygen (PaO2), and base excess with hypoxia were not different between NT and HT groups before and after the administration of BM. The cardiorespiratory response to hypoxia was not modified after administration of Ringer's solution to NT and HT placebo groups. These data suggest that the depression in hypoxic ventilatory response produced by HT is in part modulated by an increased CNS GABA concentration.

Depressed ventilatory response to hypoxia in hypothermic newborn piglets: role of glutamate.

To evaluate whether changes in extracellular glutamate (Glu) levels in the central nervous system could explain the depressed hypoxic ventilatory response in hypothermic neonates, 12 anesthetized, paralyzed, and mechanically ventilated piglets <7 days old were studied. The Glu levels in the nucleus tractus solitarius obtained by microdialysis, minute phrenic output (MPO), O2 consumption, arterial blood pressure, heart rate, and arterial blood gases were measured in room air and during 15 min of isocapnic hypoxia (inspired O2 fraction = 0.10) at brain temperatures of 39.0 +/- 0.5 degrees C [normothermia (NT)] and 35.0 +/- 0.5 degrees C [hypothermia (HT)]. During NT, MPO increased significantly during hypoxia and remained above baseline. However, during HT, there was a marked decrease in MPO during hypoxia (NT vs. HT, P < 0.03). Glu levels increased significantly in hypoxia during NT; however, this increase was eliminated during HT (P < 0.02). A significant linear correlation was observed between the changes in MPO and Glu levels during hypoxia (r = 0.61, P < 0.0001). Changes in pH, arterial PO2, O2 consumption, arterial blood pressure, and heart rate during hypoxia were not different between the NT and HT groups. These results suggest that the depressed ventilatory response to hypoxia observed during HT is centrally mediated and in part related to a decrease in Glu concentration in the nucleus tractus solitarius.

Effect of N-methyl-D-aspartate-receptor blockade on hypoxic ventilatory response in unanesthetized piglets.

The central excitatory amino acid (EAA) neurotransmitter glutamate has been shown to mediate the ventilatory response to hypoxia through N-methyl-D-aspartate (NMDA) receptors in anesthetized adult animals. To determine the role of the EAA glutamate in the neonatal ventilatory response to hypoxia, 19 unanesthetized chronically instrumented piglets were studied. Minute ventilation (VE), oxygen consumption (VO2), arterial blood pressure (ABP), heart rate (HR), and blood gases were measured in room air (RA) and after 1, 5, and 10 min of hypoxia (inspired oxygen fraction = 0.10) before and after an infusion of saline or CGS-19755, a competitive NMDA-receptor blocker (10 mg/kg i.v.). Nine control piglets [age 6 +/- 1 (SD) days; weight 2.02 +/- 0.40 kg] and 10 CGS-19755-treated animals (age 6 +/- 1 days; weight 1.90 +/- 0.66 kg) were studied during quiet sleep and in a thermoneutral environment. There was a marked decrease in the VE response to hypoxia after the administration of CGS-19755. The ventilatory response to hypoxia was not modified by saline infusion. Changes in ABP and arterial PO2 during hypoxia were similar between groups, whereas the decrease in arterial PCO2 was significantly less after CGS-19755 administration. The increase in HR with hypoxia was eliminated by the NMDA-receptor blocker administration. VO2 decreased with hypoxia in both groups, but this decrease was more marked after the NMDA-receptor blockade. These results suggest that the central EAA glutamate mediates, at least in part, the hypoxic hyperventilation in unanesthetized newborn piglets.

Decreased ventilatory response to hypoxia in sedated newborn piglets prenatally exposed to cocaine.

OBJECTIVE: Infants exposed to cocaine in utero have been reported to have a higher incidence of apnea and altered ventilatory response to carbon dioxide and hypoxia. We investigated whether in utero cocaine exposure results in greater ventilatory depression during hypoxia in piglets. METHODS: Cocaine hydrochloride, 1.0 or 2.0 mg/kg given intramuscularly, or saline solution was administered daily to pair-fed pregnant sows during the last month of gestation. Thirteen cocaine-exposed piglets (mean +/- SD: age, 4.4 +/- 1.3 days; weight, 2.10 +/- 0.10 kg) and 15 saline solution-exposed piglets (age, 4.6 +/- 1.1 days; weight, 2.32 +/- 0.42 kg) were studied under chloral hydrate sedation. Minute ventilation (VE), arterial blood pressure (BP), heart rate (HR), oxygen consumption (VO2), and arterial blood gases were measured in room air. During hypoxia (fraction of inspired oxygen = 0.10), the values for VE, BP, and HR were obtained at 1, 5, and 10 minutes, VO2 was calculated during the last 5 minutes, and arterial blood gas samples taken after 10 minutes. RESULTS: Basal VE did not differ between saline solution- and cocaine-exposed animals. The increase in VE at 1 minute of hypoxia was also similar. However, at 5 and 10 minutes of hypoxia, VE was significantly lower in the cocaine group than in the saline group (6% +/- 9% and 4% +/- 10% vs 15% +/- 13% and 21% +/- 14%; p < 0.02). Mean baseline BP and the initial increase in BP during hypoxia were not different between groups. However, BP remained increased throughout hypoxia only in the saline solution-exposed animals (p < 0.05). Changes in HR, VO2, arterial oxygen tension, and base excess during hypoxia were similar between groups. CONCLUSIONS: These results show a decrease in the ventilatory response to hypoxia in newborn piglets prenatally exposed to cocaine. This change is most likely to be centrally mediated because the initial hypoxic hyperventilation was not modified by the intrauterine cocaine exposure. This decrease in ventilation cannot be explained by changes in metabolic rate or in cardiovascular or acid-base status.

Differential antagonism by naltrexone of the effects of opioids on a fixed-ratio discrimination in rats.

In the presence of a stimulus above the center lever, rats were required to complete one of two fixed-ratios (FRs) on the center lever (FR 8 or FR 16). Completion of the ratio turned off the center-lever stimulus and produced a stimulus above each of the two side levers. If the completed ratio was high (e.g., FR 16), a response on the left lever produced a food pellet. If the ratio was low (e.g., FR 8) a response on the right lever produced food. Errors produced a brief timeout. When administered alone, morphine, cyclazocine, pentazocine, dl-N-allylnormetazocine (NANM), d-NANM, I-NANM and phencyclidine each produced dose-related decreases in accuracy and response rate. Ketocyclazocine decreased response rate in a dose-related manner but had little or no effect on accuracy. Naltrexone (0.1 mg/kg) shifted to the right by approximately 0.75 log unit the morphine dose-effect curves. This same dose of naltrexone tended to produce greater antagonism of the effects of pentazocine on accuracy than on rate which was shifted by only 0.25 log unit. Naltrexone (0.1 mg/kg) produced little or no antagonism of the effects of cyclazocine, whereas naltrexone (1 mg/kg) shifted the dose-effect curves to the right by about 0.25 log unit. Naltrexone (0.1 and 1 mg/kg) shifted the ketocyclazocine dose-effect curves to the right by approximately 0.5 and 1 log unit, respectively. Although variable among subjects, across a range of doses (0.1-10 mg/kg), naltrexone failed to antagonize the effects of dl-NANM, d-NANM, l-NANM and phencyclidine. Rather, in some subjects naltrexone tended to shift the dose-effect curves to the left. Fluphenazine (0.1 mg/kg) also failed to antagonize the effects of d-, l-NANM and phencyclidine. In summary, whereas mu and sigma agonists produce qualitatively similar effects on the performance of a discrimination in the rat, they do so through different mechanisms of action.

Effects of kappa agonists and dexoxadrol on the acquisition of conditional discriminations in monkeys.

In each of two components of a multiple schedule, patas monkeys were required to respond on a right or left lever depending upon the stimulus combination (a color and a geometric form) presented. Reinforcement of a response in the presence of one stimulus (the form) was conditional upon the other stimulus (the color). The completion of a two-member chain of discriminations produced a food pellet. Errors produced a brief timeout. One component of the multiple schedule was a repeated-acquisition task in which the discriminative stimuli for left- and right-lever responses changed each session (learning). In the other component, the discriminative stimuli were the same each session (performance). Dose-effect curves were determined for the kappa agonists bremazocine, tifluadom, ethylketocyclazocine and U50488H. Each drug produced dose-related decreases in overall response rate but had little or no effect on accuracy in either learning or performance. The rate-decreasing effects of ethylketocyclazocine and tifluadom were due to a dose-related pause at the start of the session, whereas those of bremazocine and U50488 were due largely to sporadic pausing throughout the session. Naltrexone blocked the effects of each drug whereas quaternary naltrexone had no effect. In contrast to the kappa agonists, dexoxadrol produced a dose-related disruption in accuracy of responding in learning. Dexoxadrol also decreased response rate in both acquisition and performance in a dose-related manner. Naltrexone attenuated the effects of low doses of dexoxadrol on accuracy, but failed to block the disruptive effects of higher doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of mixed agonist-antagonist opioids on the acquisition of conditional discriminations in monkeys.

Responding in patas monkeys was maintained under a multiple schedule of food presentation. One component of the multiple schedule was a repeated-acquisition task in which the discriminative stimuli for left- and right-key responses changed each session (learning). In the other component, the discriminative stimuli were the same each session (performance). The mixed agonist-antagonists dezocine, GPA 1657 and nalbuphine each produced dose-related decreases in the overall rate of responding in each component of the multiple schedule. In general each drug produced greater rate-decreasing effects in the learning than in the performance component, although this differential effect between components was less apparent with dezocine. In the learning component low doses of nalbuphine and GPA 1657 produced small increases in percentage of errors but had little or no effect on response rate. A similar effect was obtained with dezocine in only one of four subjects tested. At doses which produced comparable rate-decreasing effects dezocine also exerted the least disruptive effect on the within-session pattern of acquisition. High doses of each drug disrupted accuracy in each component of the multiple schedule. In contrast to the other drugs tested, buprenorphine had virtually no effect on response rate or percentage of errors in either component of the multiple schedule across a wide range of doses (0.01-3.2 mg/kg). The results suggest that, among the mixed agonist-antagonist, buprenorphine is unique in that it does not disrupt the acquisition or performance of complex discrimination in patas monkeys.

Effect of reserpine on relaxant responses of canine femoral arterial strips.

1. We studied relaxant responses to adenosine, glyceryl trinitrate, and hydralazine in control (n=5) and reserpine pretreated (1 mg/kg i.m., 24 h prior; n=5) canine femoral arterial strips contracted with noradrenaline. 2. Reserpine did not alter contractile responses to noradrenaline. 3. Reserpine pretreated tissues were supersensitive to glyceryl trinitrate, but not to adenosine or hydralazine.

Effects of 6-hydroxydopamine pretreatment on in vivo femoral arterial responses to vasodilator agents.

Reserpine has been previously shown to generally enhance femoral arterial vasodilator responses as indicated by increased slopes of regression lines relating decreases in resistance produced by injections of vasodilator agents to resistance prior to the injections. We have examined the same parameters in dogs pretreated with 6-hydroxydopamine. In contrast, 6-hydroxydopamine either decreased (nitroglycerin, adenosine) or had no effect (isoproterenol, acetylcholine) on femoral arterial vasodilator responses. In a second set of animals, reserpine was administered after pretreatment with 6-hydroxydopamine, and reserpine again tended to augment responses to vasodilator agents. These data suggest that reserpine's effects on vasodilator responses may be a direct effect on vascular smooth muscle and was not dependent on its effects on sympathetic innervation of the femoral bed. The decreased vasodilator responses to certain agents induced by 6-hydroxydopamine, in contrast, may have been attributable to loss of a presynaptic component of their mechanism(s) of vasodilator action.

Effect of reserpine pretreatment on in vivo femoral arterial responses to vasodilator agents.

This study determined the effects of reserpine pretreatment (1 mg/kg i.m., 24 hr before) on in vivo femoral arterial responses in the dog to the vasodilator agents acetylcholine, isoproterenol, dibutyryl cyclic AMP, adenosine, nitroglycerin and hydralazine. Femoral blood flow was monitored from the right femoral artery into which i.a. injections of the vasodilator agents were given just distal to the flow probe. Femoral vascular resistance was calculated as the ratio of mean systemic blood pressure to femoral blood flow. The response to each dose of vasodilator agent was evaluated by the magnitude of the slope of the regression line relating the resultant decrease in resistance to the resistance before the injection. Reserpine pretreatment increased slopes of these regression lines for adenosine, nitroglycerin, acetylcholine and isoproterenol, suggesting a general enhancement of vasodilator responses by reserpine. Both hydralazine pretreatment (1 mg/kg i.v., 1 hr before testing) and partial aortic occlusion during testing decreased femoral perfusion pressure without increasing vasodilator responses of the femoral arterial bed to adenosine, nitroglycerin, acetylcholine or isoproterenol. Therefore, the enhancement of vasodilator responses by reserpine was apparently not a result of decreased femoral perfusion pressure due to reserpine.