Hypoxia-induced changes in neuronal network properties

Because of their high energetic demand, neurons within the mammalian central nervous system are extremely sensitive to changes in partial pressure of oxygen. Faced with acute hypoxic conditions, an organism must follow a complex and highly dynamic emergency plan to secure survival. Behavioral functions that are not immediately essential for survival are turned off, and critical behaviors (such as breathing) undergo a biphasic response. An augmentation of breathing is initially adaptive, whereas prolonged hypoxic conditions are better served by an energy-saving mode. However, the hypoxic response of an organism depends on many additional factors. Environmental conditions, the animal's age and health, and the pattern (continuous vs intermittent) and duration (chronic vs acute) of hypoxia greatly determine the specific course of a hypoxic response. Different forms of hypoxia can cause pathology or be used as therapy. Therefore, it is not surprising that the hypoxic response of an organism results from widespread and highly diverse reconfigurations of neuronal network functions in different brain areas that are accomplished by diverse hypoxic changes at all levels of the nervous system (i.e., molecular, cellular, synaptic, neuronal, network). Hypoxia-induced changes in synaptic transmission are generally depressive and result primarily from presynaptic mechanisms, whereas changes in intrinsic properties involve excitatory and inhibitory alterations involving the majority of K+, Na+, and Ca2+ channels. This article reviews the response of the nervous system to hypoxia, accounting for all levels of integration from the cellular to the network level, and postulates that a better understanding of the diversity of cellular events is only possible if cellular and network events are considered in a functional and organismal context.     

Ambient temperature modulates hypoxic-induced changes in rat body temperature and activity differentially

When rats, acclimated to an ambient temperature (T(a)) of 29 degrees C, are exposed to 10% O(2) for 63 h, the circadian rhythms of body temperature (T(b)) and level of activity (L(a)) are abolished, T(b) falls to a hypothermic nadir followed by a climb to a hyperthermic peak, L(a) remains depressed (Bishop B, Silva G, Krasney J, Salloum A, Roberts A, Nakano H, Shucard D, Rifkin D, and Farkas G. Am J Physiol Regulatory Integrative Comp Physiol 279: R1378-R1389, 2000), and overt brain pathology is detected (Krasney JA, Farkas G, Shucard DW, Salloum AC, Silva G, Roberts A, Rifkin D, Bishop B, and Rubio A. Soc Neurosci Abstr 25: 581, 1999). To determine the role of T(a) in these hypoxic-induced responses, T(b) and L(a) data were detected by telemetry every 15 min for 48 h on air, followed by 63 h on 10% O(2) from rats acclimated to 25 or 21 degrees C. Magnitudes and rates of decline in T(b) after onset of hypoxia were inversely proportional to T(a), whereas magnitudes and rates of T(b) climb after the hypothermic nadir were directly proportional to T(a). No hyperthermia, so prominent at 29 degrees C, occurred at 25 or 21 degrees C. The hypoxic depression of L(a) was least at 21 degrees C and persisted throughout the hypoxia. In contrast, T(a) was a strong determinant of the magnitudes and time courses of the initial fall and subsequent rise in T(b). We propose that the absence of hyperthermia at 21 and 25 degrees C as well as a persisting hypothermia may protect the brain from overt pathology.     

Adrenal and body temperature changes in rabbits exposed to varying effective temperatures

Eight adult New Zealand White rabbits were exposed individually, in series, to each of 23 effective temperatures (t(eff)) until body temperature (tb) increased 1.1 degrees C or for a period of 2 hours. Body temperature was measured to the nearest 0.1 degree C using FM radio transmitters in the pre-test (baseline) condition and at 2 minute intervals during the test conditions where t(eff) ranged between 21.7 and 34.7 degrees C. The frequency at which the rabbits displayed a 1.1 degree C rise in tb was related to the magnitude of the t(eff), with 100% of the rabbits manifesting this change at t(eff) greater than 30.2 degrees C. At t(eff) of 28.4 through 30.2 degrees C, some, but not all, of the rabbits showed a 1.1 degree C rise in tb whereas none displayed the 1.1 degree C rise in tb at t(eff) below 28.4 degrees C. The mean time necessary for the 1.1 degree C rise in tb was negatively correlated (P less than 0.01) to the magnitude of the t(eff). The significantly (P less than 0.01) elevated plasma corticosterone in rabbits exhibiting 0.6 degree C and 1.1 degree C rise in tb suggests that those animals were stressed physiologically by the experimental procedure. It is concluded that the conditions associated with increased tb induce physiological changes commonly associated with stressors and that the techniques reported herein should be useful in establishing upper environmental temperature limits for housing rabbits.     

Alcohol and respiratory and body temperature changes during tepid water immersion

Resting subjects were immersed for 30 min in water at 22 and 30 degrees C after drinking alcohol. Total ventilation, end-tidal PCO2, rectal temperature, aural temperature, mean skin temperature, heart rate, and oxygen consumption were recorded during the experiments. Blood samples taken before the immersion period were analyzed by gas-liquid chromatography. The mean blood alcohol levels were 82.50 +/- 9.93 mg.(100 ml)-1 and 100.6 +/- 12.64 mg (100 ml)-1 for the immersions at 22 and 30 degrees C, respectively. There was no significant change in body temperature measured aurally or rectally, mean surface skin temperature, or heart rate at either water temperature tested. Total expired ventilation was significantly attenuated for the last 15 min of the immersion at 22 degrees C, after alcohol consumption as compared to the ventilation change in water at 22 degrees C without ethanol. This response was not consistently significantly altered during immersion in water at 30 degrees C. It is evident that during a 30-min immersion in tepid water with a high blood alcohol level, body heat loss is not affected but some changes in ventilation do occur.     

The temperature and temperature gradient distribution in the thermophysical model of the rabbit body subjected internal and external changes of temperature

In a laboratory heat-physical model of the rabbit reflecting basic heat-physical parameters of animal body (weight, heat absorption and heat production, size of a relative surface, capacity heat-production etc.), the changes of radial distribution of temperature and size of a cross superficial temperature gradient of the body were investigated with various parities (ratio) of environmental temperature and size of capacity heat production imitated by an electrical heater. Superficial layer of the body dependent from capacity heat production and environmental temperature can serve for definition of general heat content changes in the body for maintaining its thermal balance within the environment.     

去甲肾上腺素介导低氧引起家兔颈动脉体神经电活动增加

在30只家兔颈动脉体-窦神经(CSN)标本上, 记录了窦神经中39个对低氧反应敏感的化学感受性单位由去甲肾上腺素(NA)及其拮抗剂引起的反应。结果如下 (1)以低氧的改良台氏液(MTS)灌流标本时, 19个单位放电频率由0.13±0.06增至0.25±0.12 imp/s (P<0.001); (2)在灌流液中加入去甲肾上腺素(10