Abstract Since studies suggest that both hypoxia and sleep fragmentation are related to cardiovascular alterations induced by obstructive sleep apnea, the present study was designed to evaluate the ...effects of hypoxia, sleep deprivation, and their combination on biochemical blood parameters in rats. In subchronic experiments (4 days), rats were exposed to intermittent hypoxia (IH) during the light period (2 min room air–2 min 10% O2 for 12 h/day) and/or paradoxical sleep deprivation (PSD, 24 h/day). Consequences of chronic intermittent hypoxia (CIH) exposure were examined after 21 consecutive days of hypoxia protocol from 10:00 to 16:00 followed by a sleep restriction (SR) period of 18 h (16:00–10:00). Rats were randomly assigned to seven treatment groups: (1) control (2) IH (3) PSD (4) IH-PSD (5) SR (6) CIH and (7) CIH-SR. PSD reduced triglycerides and very low-density lipoprotein (VLDL) cholesterol concentrations and increased total cholesterol and high-density lipoprotein (HDL) cholesterol. IH did not alter any of these parameters. The combination of IH-PSD did not modify the values of total cholesterol and HDL compared to control group. In the chronic experiment, the animals exposed to CIH displayed a reduction of Vitamin B6 and an increase of triglycerides and VLDL. Our findings show a duration-dependent effect of hypoxia on triglycerides. Rats in the SR and CIH-SR groups showed a diminished concentration of triglycerides and VLDL. SR rats showed a reduction in the concentration of homocysteine but the animals in the CIH-SR treatment condition did not display any alterations in this parameter. In this latter group, an augmentation of cysteine concentration was observed. These results suggest that sleep deprivation and hypoxia modify biochemical blood parameters in distinct ways.
Abstract The peripheral hyperosmolarity elicited by intravenous infusion of hypertonic saline brings potential benefits to the treatment of hemorrhage. The neural mechanisms involved in these ...beneficial effects remain unknown. The present study examines the role of carotid chemoreceptors in cardiovascular responses induced by hypertonic saline after hypovolemic hemorrhage in rats. Male Wistar rats (300–400 g) were anesthetized with thiopental, and instrumented for recording of mean arterial pressure. Arterial pressure was reduced to 60 mm Hg by withdrawal of arterial blood over 10 min, and maintained at this level for 60 min by withdrawal or infusion of blood. In control rats (n = 8) with intact chemoreceptors, the subsequent intravenous infusion of hypertonic saline (3 M NaCl, 1.8 ml kg − 1 body weight, in 2 min) restored blood pressure (pressure increased from 61 ± 4 to 118 ± 5 mm Hg). In experimental rats (n = 8), the carotid body arteries were tied, 30 min after the beginning of the hypotensive phase, leaving the carotid chemoreceptors ischemic. In these rats, hypertonic saline failed to restore blood pressure (pressure increased from 55 ± 1 to 70 ± 6 mm Hg). These findings suggest that the restoration of blood pressure after hypovolemic hemorrhage induced by hypertonic saline depends on intact carotid chemoreceptors.
A Monte Carlo simulation program for the radio detection of Ultra High Energy (UHE) neutrino interactions in the Antarctic ice as viewed by the Antarctic Impulsive Transient Antenna (ANITA) is ...described in this article. The program, icemc, provides an input spectrum of UHE neutrinos, the parametrization of the Askaryan radiation generated by their interaction in the ice, and the propagation of the radiation through ice and air to a simulated model of the third and fourth ANITA flights. This paper provides an overview of the icemc simulation, descriptions of the physics models used and of the ANITA electronics processing chain, data/simulation comparisons to validate the predicted performance, and a summary of the impact of published results.
•Obstructive sleep apnea (OSA) is associated with SUDEP risk.•No study characterized the acute responses of OSA in the chronic epilepsy model.•The REM OSA was shorter in chronic epilepsy than in ...control rats.•No differences in OSA-induced cardiorespiratory responses between the groups.
OSA is known to increase the risk for SUDEP in persons with epilepsy, but the relationship between these two factors is not clear. Also, there is no study showing the acute responses to obstructive apnea in a chronic epilepsy model. Therefore, this study aimed to characterize cardiorespiratory responses to obstructive apnea and chemoreceptor stimulation in rats. In addition, we analyzed respiratory centers in the brain stem by immunohistochemistry. Epilepsy was induced with pilocarpine. About 30–60 days after the first spontaneous seizure, tracheal and thoracic balloons, and electrodes for recording the electroencephalogram, electromyogram, and electrocardiogram were implanted. Intermittent apneas were made by inflation of the tracheal balloon during wakefulness, NREM sleep, and REM sleep. During apnea, respiratory effort increased, and heart rate fell, especially with apneas made during wakefulness, both in control rats and rats with epilepsy. Latency to awake from apnea was longer with apneas made during REM than NREM, but rats with epilepsy awoke more rapidly than controls with apneas made during REM sleep. Rats with epilepsy also had less REM sleep. Cardiorespiratory responses to stimulation of carotid chemoreceptors with cyanide were similar in rats with epilepsy and controls. Immunohistochemical analysis of Phox2b, tryptophan hydroxylase, and NK1 in brain stem nuclei involved in breathing and sleep (retrotrapezoid nucleus, pre-Bötzinger complex, Bötzinger complex, and caudal raphe nuclei) revealed no differences between control rats and rats with epilepsy. In conclusion, our study showed that rats with epilepsy had a decrease in the latency to awaken from apneas during REM sleep, which may be related to neuroplasticity in some other brain regions related to respiratory control, awakening mechanisms, and autonomic modulation.
1 Departments of Psychology, Pharmacology, and Exercise
Science, and the Cardiovascular Center, University of Iowa, Iowa City,
Iowa 52242-1407; and 2 Department of Physiology and
Pathology, School ...of Dentistry, Paulista State University,
São Paulo 14801-903, Araraquara, Brazil
10.1152/ajpregu.00295.2000. Adult rats deprived of water for 24-30
h were allowed to rehydrate by ingesting only water for 1-2 h.
Rats were then given access to both water and 1.8% NaCl. This
procedure induced a sodium appetite defined by the operational criteria
of a significant increase in 1.8% NaCl intake (3.8 ± 0.8 ml/2 h;
n = 6). Expression of Fos (as assessed by
immunohistochemistry) was increased in the organum vasculosum of the
lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical
organ (SFO), and supraoptic nucleus (SON) after water deprivation.
After rehydration with water but before consumption of 1.8% NaCl, Fos
expression in the SON disappeared and was partially reduced in the OVLT
and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1 ) increased plasma renin activity (PRA),
osmolality, and plasma Na + ; 2 ) decreased blood
volume; and 3 ) reduced total body Na + ; but
4 ) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na +
concentration to revert to euhydrated levels. The changes in Fos
expression and PRA are consistent with a proposed role for ANG II in
the control of the sodium appetite produced by water deprivation
followed by rehydration with only water.
salt intake; hypovolemia; circumventricular organs; dehydration; thirst
Abstract It is thought that cardiovascular changes may contribute to sudden death in patients with epilepsy. To examine cardiovascular alterations that occur during epileptogenesis, we measured the ...heart rate of rats submitted to the electrical amygdala kindling model. Heart rate was recorded before, during, and after the induced seizures. Resting heart rate was increased in stages 1, 3, and 5 as compared with the unstimulated control condition. In the initial one third of the seizures, we observed bradycardia, which increased in intensity with increasing stage and was blocked by injecting methyl atropine. During stage 5 seizures, a rebound tachycardia was observed that also increased in intensity with increasing number of seizures. This study demonstrated the influence of seizure frequency on cardiac autonomic modulation, providing a basis for discussion of potential mechanisms that cause patients with epilepsy to die suddenly.
The nucleus of the solitary tract (NTS) receives primary afferents involved in cardiovascular regulation. We investigated the role of NK(1)-receptor bearing neurons in the NTS on cardiovascular ...reflexes in awake rats fitted with chronic venous and arterial cannulae. These neurons were lesioned selectively with saporin conjugated with substance P (SP-SAP, 2 microM, bilateral injections of 20 nL in the subpostremal NTS, or 200 nL in both the subpostremal and the commissural NTS). Before, and 7 and 14 days after injection of SP-SAP, we measured changes in blood pressure and heart rate induced by i.v. injection of phenylephrine and nitroprusside (baroreceptor reflex), cyanide (arterial chemoreceptor reflex), and phenylbiguanide (Bezold-Jarisch reflex). The smaller injections with SP-SAP completely abolished NK1 receptor staining in the subpostremal NTS. The larger injections abolished NK1 receptor immunoreactivity in an area that extended from the commissural NTS to the rostral end of the subpostremal NTS. The lesions seemed to affect only a limited number of neurons, since neutral red stained sections did not show any obvious reduction in cell number. The smaller lesions reduced the gain of baroreflex bradycardia and the hypotension induced by phenylbiguanide. The larger lesions completely abolished the response to phenylbiguanide, blocked the baroreflex bradycardia induced by phenylephrine, severely blunted the baroreflex tachycardia, and blocked the bradycardia and reduced the hypertension induced by cyanide. Thus, these responses depend critically on NK(1)-receptor bearing neurons in the NTS.
Abstract
Study Objectives
Obstructive sleep apnea can induce hypertension. Apneas in REM may be particularly problematic: they are independently associated with hypertension. We examined the role of ...sleep stage and awakening on acute cardiovascular responses to apnea. In addition, we measured cardiovascular and sympathetic changes induced by chronic sleep apnea in REM sleep.
Methods
We used rats with tracheal balloons and electroencephalogram and electromyogram electrodes to induce obstructive apnea during wakefulness and sleep. We measured the electrocardiogram and arterial pressure by telemetry and breathing effort with a thoracic balloon.
Results
Apneas induced during wakefulness caused a pressor response, intense bradycardia, and breathing effort. On termination of apnea, arterial pressure, heart rate, and breathing effort returned to basal levels within 10 s. Responses to apnea were strongly blunted when apneas were made in sleep. Post-apnea changes were also blunted when rats did not awake from apnea. Chronic sleep apnea (15 days of apnea during REM sleep, 8 h/day, 13.8 ± 2 apneas/h, average duration 12 ± 0.7 s) reduced sleep time, increased awake arterial pressure from 111 ± 6 to 118 ± 5 mmHg (p < 0.05) and increased a marker for sympathetic activity. Chronic apnea failed to change spontaneous baroreceptor sensitivity.
Conclusion
Our results suggest that sleep blunts the diving-like response induced by apnea and that acute post-apnea changes depend on awakening. In addition, our data confirm that 2 weeks of apnea during REM causes sleep disruption and increases blood pressure and sympathetic activity.
We present a study of the expectations for very-high-energy (VHE) to ultra-high-energy (UHE) gamma-ray and neutrino emission from interacting cosmic rays in our Galaxy as well as a comparison to the ...latest results for the Galactic UHE diffuse emission. We demonstrate the importance of properly accounting for both the mixed cosmic-ray composition and the gamma-ray absorption. We adopt the wounded-nucleon model of nucleus interactions and provide parameterisations of the resulting gamma-ray and neutrino production. Nucleon shielding due to clustering inside nuclei is shown to have a measurable effect on the production of gamma rays and is particularly evident close to breaks and cutoffs in mixed-composition particle spectra. The change in composition around the ‘knee’ in the cosmic ray spectrum has a noticeable impact on the diffuse neutrino and gamma-ray emission spectra. We show that current and near-future detectors can probe these differences in the key energy range from 10 TeV to 1 PeV, testing the paradigm of the universality of the cosmic ray spectrum and composition throughout the Galaxy.
Inhibition of the commissural nucleus of the solitary tract (commNTS) induces a fall in sympathetic nerve activity and blood pressure in spontaneously hypertensive rats (SHR), which suggests that ...this subnucleus of the NTS is a source of sympathoexcitation. Exercise training reduces sympathetic activity and arterial pressure. The purpose of the present study was to investigate whether the swimming exercise can modify the regional vascular responses evoked by inhibition of the commNTS neurons in SHR and normotensive Wistar-Kyoto (WKY) rats. Exercise consisted of swimming, 1 h/day, 5 days/wk for 6 wks, with a load of 2% of the body weight. The day after the last exercise session, the rats were anesthetized with intravenous alpha-chloralose, tracheostomized, and artificially ventilated. The femoral artery was cannulated for mean arterial pressure (MAP) and heart rate recordings, and Doppler flow probes were placed around the lower abdominal aorta and superior mesenteric artery. Microinjection of 50 mM GABA into the commNTS caused similar reductions in MAP in swimming and sedentary SHR (-25 +/- 6 and -30 +/- 5 mmHg, respectively), but hindlimb vascular conductance increased twofold in exercised vs. sedentary SHR (54 +/- 8 vs. 24 +/- 5%). GABA into the commNTS caused smaller reductions in MAP in swimming and sedentary WKY rats (-20 +/- 4 and -16 +/- 2 mmHg). Hindlimb conductance increased fourfold in exercised vs. sedentary WKY rats (75 +/- 2% vs. 19 +/- 3%). Therefore, our data suggest that the swimming exercise induced changes in commNTS neurons, as shown by a greater enhancement of hindlimb vasodilatation in WKY vs. SHR rats in response to GABAergic inhibition of these neurons.
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