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1.
The influence of flow limitation on the magnitude of the cardiorespiratory response to arousal from sleep is of interest in older people, because they experience considerable flow limitation and frequent arousals from sleep. We studied older flow‐limiting subjects, testing the hypothesis that the cardiorespiratory activation response would be larger when arousal occurred during flow limitation, compared to no flow limitation, and chemical stimuli were controlled. In 11 older adults [mean ± standard deviation (SD) age: 68 ± 5 years] ventilation was stabilized using continuous positive airway pressure, and flow limitation was induced by dialling down the pressure. Partial pressure of end‐tidal carbon dioxide (PetCO2) was maintained by titration of the inspired CO2 and hyperoxia was maintained using 40% O2 balanced with nitrogen. Flow limitation at the time of arousal did not augment cardiovascular activation response (heart rate P = 0.7; systolic blood pressure P = 0.6; diastolic blood pressure P = 0.3), whereas ventilation was greater following arousals during flow limitation compared to no flow limitation (P < 0.001). The pre–post‐arousal differences in ventilation reflected significant pre‐arousal suppression (due to flow limitation) plus post‐arousal activation. In summary, the cardiovascular response to arousal from sleep is not influenced by flow limitation at the time of arousal, when chemical stimuli are controlled in older adults. This finding may contribute to the decreased cardiovascular burden associated with sleep‐disordered breathing reported in older adults, although our data do not exclude the possibility that flow limitation in the presence of mild hypoxic hypercapnia could increase the cardiovascular response to arousal.  相似文献   

2.
We have studied diurnal changes in mean arterial pressure (MAP), heart rate (HR) and body temperature (Tb) during wake (W), non-rapid eye movement sleep (NREMS) and REM sleep (REMS) in the rat. Although HR and Tb show a similar sinusoidal diurnal variation during all vigilance states, the diurnal profile for the MAP is vigilance-state dependent. During W, MAP values are higher during the dark phase, during NREMS, no significant diurnal change is seen, and during REMS, the MAP exhibits a reversed diurnal change, being higher during the light phase. The low frequency component (0.25–0.725 Hz) in the power spectral density of the blood pressure, an index of sympathetic activity, is also higher during the light phase than the dark phase in REMS. The present findings suggest that diurnal changes in MAP in the rat result from the wake rhythm, and that the mechanism for the diurnal control of MAP may be different from that for HR or Tb.  相似文献   

3.
Heart rate (HR), blood pressure (BP) and autonomic nervous system (ANS) activity vary diurnally, with a reduction in HR and BP, and a shift to vagal dominance during the dark phase. However, the cause of these changes, particularly the relative influence of sleep and circadian mechanisms, remains uncertain. The present study assessed the effect of sleep onset on HR, BP, high frequency (HF) component of heart rate variability (HRV), low frequency/high frequency (LF/HF) ratio and pre-ejection period (PEP). Sleep onset was dissociated from circadian influences by having subjects go to sleep at two different circadian phases, their normal time of sleep onset (normal sleep onset, NSO), and after a delay of 3 h (delayed sleep onset, DSO). The assumption was that changes caused by sleep onset would occur in association with sleep onset, irrespective of its timing, while circadian effects would have a consistent circadian phase and be independent of when sleep onset occurred. Thirteen and 17 subjects were run in the NSO and DSO conditions, respectively. Following a 1-h adaptation period, data collection began 2 h before subjects' normal time of sleep onset and continued until morning awakening. The lights were turned out after 2 h in the NSO condition and 5 h in the DSO condition. Subjects were required to maintain a supine position throughout the experimental sessions. The night-time decrease in HR was found to be due to both sleep onset and a circadian influence, with the circadian component being more prominent. In contrast, the fall in BP was largely due to a sleep onset effect. Increased vagal activity, as reflected in the HF component and a shift to vagal dominance in the LF/HF ratio, appeared to be primarily a function of the sleep system, while sympathetic activity, as assessed by PEP, reflected a circadian influence.  相似文献   

4.
PURPOSE: The purpose of this study was to investigate the activation of the respiratory centers during insufflation of the larynx with CO2 at different flow rates and concentrations. MATERIALS AND METHODS: The experiments were carried out in spontaneous air breathing rabbits, anesthetized with thiopental sodium (25 mg kg(-1) i.v.). The larynx was separated from the oropharyngeal cavity and the trachea. The tidal volume (VT) and respiratory frequency (f min(-1)) were recorded from the lower tracheal cannula. The respiratory minute volume (VE) was calculated, the action potentials from the right phrenic nerve were recorded and the inspiratory (TI) and expiratory (TE) periods and the mean inspiratory flow rate (VT/TI) were calculated. The larynx was insufflated at flow rates of 500 mL min(-1) and 750 mL min(-1), with 7 and 12% CO2-Air by means of a respiratory pump. RESULTS: Insufflation of the larynx, with both gas mixtures, decreased the f and VT significantly. The TI and TE were found to increase significantly due to the decreasing in f. There was a significant decrease in VT/TI ratio. Following bilateral midcervical vagotomy, on the passing of both gas mixtures, significant decreases were observed in the VT, and the responses of f, TI and TE were abolished. After cutting the superior laryngeal nerve, the responses of the VT to both gas mixtures were abolished. CONCLUSION: In conclusion, the results of this study purpose that the stimulation of the laryngeal mechanoreceptors by the effect of hypercapnia decreases the activation of the respiratory center.  相似文献   

5.
The aim of this study was to investigate the extent of sympathetic nervous system activation during parturition in four unrestrained goats. Chronically implanted radiotelemetry devices registered heart rate and arterial blood pressure around the clock and blood was sampled for determination of plasma adrenaline and noradrenaline concentrations before, during and after labour. Two goats delivered two kids after moderately intensive abdominal contractions. A third goat had dystocia, and was treated with prostaglandin F2α. One normal kid and one mummified foetus were delivered manually. After milking, a third kid was born spontaneously. The fourth goat experienced severe abdominal contractions and delivered one kid. Mean blood pressure was 69 ± 2 mmHg the day before parturition, increased gradually during the labour pains, and reached a maximal value of 120 ± 7 mmHg when the head of the first kid was visible (P ≤ 0.05). Heart rate was 134 ± 4 beats min?1 the day before parturition and peaked when the first kid was born (159 ± 6 beats min?1, P ≤ 0.05), as did plasma adrenaline concentration (from 0.4 ± 0.2 nmol L?1 to 2.7 ± 1.2 nmol L?1, P ≤ 0.05). The concentration of noradrenaline increased from 4.8 ± 2.3 nmol L?1 to 12.2 ± 8.4 nmol L?1 (P ≤ 0.05), when the head of the first kid was visible. Expulsion of the second and third kids caused relatively smaller increases in blood pressure, heart rate and catecholamines than those seen with the first born kid. It is concluded that changes in pressure, heart rate and catecholamines during parturition are related to the different phases of labour and not to its duration or severity.  相似文献   

6.
7.
Obstructive sleep apnea is associated with hypertension, and short‐term studies have demonstrated a modest reduction in blood pressure with continuous positive airway pressure therapy. We evaluated the effects of continuous positive airway pressure versus sham continuous positive airway pressure on blood pressure in 1,101 participants with obstructive sleep apnea from the Apnea Positive Pressure Long‐term Efficacy Study, a randomized, sham‐controlled double‐blinded study designed to assess the impact of continuous positive airway pressure on neurocognition. Participants with apnea?hypopnea index ≥ 10 were randomly assigned to continuous positive airway pressure or sham continuous positive airway pressure. Blood pressures measured in the morning and evening at baseline, 2 months and 6 months were analysed post hoc using a mixed‐model repeated‐measures analysis of variance. The largest magnitude reduction was approximately 2.4 mmHg in morning systolic pressure that occurred at 2 months in the continuous positive airway pressure arm as compared with an approximate 0.5 mmHg reduction in the sham group (continuous positive airway pressure effect ?1.9 mmHg, p = .008). At 6 months, the difference between groups was diminished and no longer statistically significant (continuous positive airway pressure effect ?0.9 mmHg, p = .12). Sensitivity analysis with use of multiple imputation approaches to account for missing data did not change the results. Treatment with continuous positive airway pressure for obstructive sleep apnea reduces morning but not evening blood pressure in a population with well‐controlled blood pressure. The effect was greater after 2 than after 6 months of treatment.  相似文献   

8.
SUMMARY  Eight subjects were studied on an irregular sleep/wake schedule which was designed so that prior wake time and the time of day when 4-h sleep periods were taken were both balanced. Rectal temperature and the sleep EEG were measured throughout the 8-d protocol. A purification method was used to estimate the depression of rectal temperature (masking) caused by the first and second halves of each 4-h sleep period. On average this was 0.187 ± 0.015°C during the first 2h and 0.262 ± 0.017°C during the second 2h. Masking increases beyond the first 2 h of sleep, but any effects due to the phase of the rectal temperature when sleep is taken are very weak. However, masking did increase (that is, the temperature was depressed more) when the amount of prior wake time was greater than 4 h. When the effects of sleep content variables were considered also, masking was still greater in the second half of sleep and tended to increase with the amount of slow-wave sleep, but it decreased with increasing amounts of time awake during a sleep period (sleep latency or sleep discontinuity). Some implications of these results for the mechanism of sleep-induced masking are considered.  相似文献   

9.
The cortisol awakening response (CAR) is presumed critically important for healthy adaptation. The current literature, however, is hampered by systematic measurement difficulties relative to awakening, especially with young children. While reports suggest the CAR is smaller in children than adults, well‐controlled research in early childhood is scarce. We examined whether robust CARs exist in 2‐ to 4‐year‐old children and if sleep restriction, wake timing, and napping influence the CAR (n = 7). During a 25‐day in‐home protocol, researchers collected four salivary cortisol samples (0, 15, 30, 45 min post‐wake) following five polysomnographic sleep recordings on nonconsecutive days after 4 hr (morning nap), 7 hr (afternoon nap), 10 hr (evening nap), 13 hr (baseline night), and 16 hr (sleep restriction night) of wakefulness (20 samples/child). The CAR was robust after nighttime sleep, diminished after sleep restriction, and smaller but distinct after morning and afternoon (not evening) naps. Cortisol remained elevated 45 min after morning and afternoon naps. © 2011 Wiley Periodicals, Inc. Dev Psychobiol 54:412–422, 2012.  相似文献   

10.
We have studied a normal restriction fragment length polymorphism at the renin locus, detected with the restriction enzyme BgII in healthy Norwegians. No association with blood pressure level or variability was found. Thus, the normal genes detected by examination of this restriction fragment length polymorphism at the renin locus have neither "level gene" nor "variability gene" effects on normal blood pressure.  相似文献   

11.
We have examined healthy Norwegians with respect to two restriction fragment length polymorphisms at the locus for atrial natriuretic factor, detectable with the restriction enzymes XhoI and BglI, respectively. No association with systolic or diastolic blood pressure level or variability was found. Thus, the normal genes detected by examination of these restriction fragment length polymorphisms have neither "level gene" nor "variability gene" effects on normal blood pressure.  相似文献   

12.
13.
The effects of two different doses of thyrotropin-releasing hormone on regional blood flows were studied in urethane-anaesthetized rabbits pretreated with the α2 adrenergic antagonists yohimbine and idazoxan. The effects of yohimbine were also studied using unanaesthetized rabbits. Blood flow measurements were performed using the tracer microsphere method. Thyrotropin-releasing hormone was injected i. v. at a dose of either 0.1 mg kg-1 or 2.0 mg kg-1. Yohimbine and idazoxan did not modify the effect of thyrotropin-releasing hormone on mean arterial blood pressure. In the anaesthetized animals, blockade of the α2 adrenoceptors resulted in a vasoconstriction in several peripheral organs and the vasoconstriction increased after thyrotropin-releasing hormone administration. Pretreatment with yohimbine reduced total cerebral blood flow moderately and in such animals thyrotropin-releasing hormone elicited only minor cerebral blood flow effects. Pretreatment with idazoxan did not reduce the total cerebral blood flow and in such animals it increased from 53± 1 to 75±4 g min-1 100 g-1 (P < 0.01) after the administration of the lower dose of thyrotropin-releasing hormone and from 64±5 to 112±17 g min-1 100 g-1 (P < 0.01) after the higher dose. In the conscious animals, yohimbine caused an increase in mean arterial blood pressure and heart rate. Vascular resistance increased in several organs. The cerebral blood flow decreased in white matter (P <0.05) and the caudate nucleus (P < 0.05). The results indicate that there is a yohimbine-sensitive mechanism involved in the cerebrovasodilating effect of thyrotropin-releasing hormone in anaesthetized rabbits. There is also an activation of the sympathetic nervous system by thyrotropin-releasing hormone which results in increased vascular resistance and mean arterial blood pressure. Its effect on the vascular resistance may be enhanced by α2 adrenoceptor blockade. In conscious animals, there seems to be a yohimbine-sensitive mechanism involved in the control of cerebral blood flow.  相似文献   

14.
Berge KE, Berg K. No effect of TaqI polymorphism at the human renal kallikrein (KLK1) locus on normal blood pressure level or variability.
Clin Genet 1993: 44: 196–202. © Munksgaard, 1993
Renal kallikrein is a component of the kallikrein-kinin-system (KKS). Kallikrein has been shown to cleave the precursor kininogen to release small kinins, which cause vasodilatation, increased diuresis and natriures-is. We have studied a normal restriction fragment length polymorphism (RFLP) at the renal kallikrein locus (KLK1), detectable with the restriction enzyme TaqI. In one series of 167 unrelated individuals we found a trend towards an association between genotypes in this polymorphism and level of diastolic blood pressure (DBP), but in two other series comprising 123 and 213 unrelated individuals, respectively, we found no suggestion of an association. Since the three series did not exhibit a consistent pattern of association between DBP levels and genotypes in this RFLP, we conclude that the association that appeared in one of the series was probably a chance event. There was no difference between genotypes in any of the three series, with respect to systolic blood pressure (SBP). In two series of, respectively, 157 and 120 complete monozygotic (MZ) twin pairs, there was no difference between genotypes with respect to within-pair variation in SBP or DBP. This indicates that normal KLK1 genes, expressed as variants in this RFLP, do not participate in the determination of the limits within which life-style factors may cause blood pressure (BP) changes. We conclude that neither "level gene" effects nor "variability gene" effects at the KLK1 locus are detectable with the polymorphism analyzed, in the Norwegian population.  相似文献   

15.
BACKGROUND: Hypersensitivity reactions to non-steroidal anti-inflammatory drugs (NSAIDs), manifested by cutaneous symptoms and/or airway manifestations represent 20-25% of all hypersensitivity reactions to drugs. Today, it is still claimed that no in vitro diagnostic tests exist for that condition and that the only way to confirm the diagnosis is a provocation challenge. OBJECTIVE: The objective of this study was to assess whether NSAIDs may provoke blood basophil activation in vitro in such patients, as detected by a flowcytometric technique. METHODS: Sixty NSAID hypersensitive patients (38 with cutaneous, 20 with airway and two with cutaneous and airway symptoms) and 30 control patients (15 asthmatics) were selected. Their hypersensitivity was confirmed by documented history indicating at least two clinical episodes to two or more different NSAIDs or by positive oral provocation challenge. Isolated buffy coat leukocytes were stimulated in vitro with aspirin, paracetamol, metamizol, diclofenac, and naproxen. The percentage of activated basophils was evaluated by an anti-CD63. RESULTS: Aspirin showed a sensitivity of 43.3%, a specificity of 100%, a positive predictive value of 100% and a negative predictive value of 99.4%. For the other NSAIDs, the sensitivity and specificity values were: for paracetamol 11.7% and 100%, for metamizol 15% and 100%, for diclofenac 43.3% and 93.3% and for naproxen 54.8% and 74.1%. When considering the first four NSAIDs, the global sensitivity raised to 63.3% and specificity to 93.3%. If the number of tests is to be limited for practical reasons, the combination of acetylsalicylic acid and diclofenac at two concentrations yields a sensitivity of 58.3% and a specificity of 93.3%. CONCLUSIONS: Flowcytometric determinations of basophil activation following stimulation with NSAIDs show a high sensitivity (60-70%) with specificity above 90%. So this test may help avoiding some cumbersome and dangerous provocation challenges.  相似文献   

16.
Endothelin is a peptide reported to be one of the most potent vasoconstrictors known. Presumably, endothelin could play a role in the physiological regulation of blood pressure in healthy or hypertensive people. We have studied a normal restriction fragment length polymorphism (RFLP) at the endothelin-I (EDN1) locus detected with the restriction enzyme TaqI. In three different series comprising 166, 120 and 207 unrelated individuals, we found no evidence for association between genotype in this polymorphism and level of systolic or diastolic blood pressure. In two series of 156 and 117 monozygotic (MZ) twin pairs, respectively, there was no difference between genotypes in within-pair variation in systolic or diastolic blood pressure. Thus neither "level gene" nor "variability gene" effects of normal genes at the EDN1 locus could be detected with the polymorphism analyzed, in healthy population samples.  相似文献   

17.
18.
4,4′-Methylene-bis-(2-chlorobenzeneamine) (MbOCA) is a commercially important industrial chemical that is carcinogenic in three animal species and mutagenic in the Ames test. The ability of hepatic postmitochondrial supernatant from humans, dogs, mice, and rats to activate MbOCA to a bacterial mutagen has been investigated using the Ames plate incorporation test and a bacterial fluctuation test. In the Ames plate test, hepatic S9 preparations from mice and Aroclor 1254-induced rats only were sufficiently active to produce a significant mutagenic response. Preincubation of MbOCA with S9 from human liver produced a slight increase in the number of revertants but not a doubling as compared to controls. However, using the more sensitive bacterial fluctuation test, liver S9 from all species activated MbOCA to a bacterial mutagen. The responses produced were dose-related and, for at least part of the dose range, were double the background levels observed in controls. The increases in the mutagenicity of MbOCA produced by liver S9 from humans, dogs, and rats were significant at the 0.1% level of probability. Liver S9 preparations from all species in which MbOCA is carcinogenic have now been demonstrated to be capable of activating this compound to a bacterial mutagen. The finding that S9 from human liver can also activate MbOCA to a mutagen increases the concern that it may be a human carcinogen.  相似文献   

19.
A series of 33 cases of Hodgkin's disease was investigated for the presence of the EBV encoded latent gene product LMP-1 and of CD23 using immunohistochemical techniques. The expression of bcl-2 was examined in a subset of cases. LMP-1 was detected in the Reed-Sternberg cells in 15 cases. Although LMP-1 is known to upregulate CD23 and bcl-2, there was no correlation between the expression of LMP-1 and the detection of CD23 and bcl-2 in Reed-Sternberg cells.  相似文献   

20.
Type 2 diabetes mellitus (T2DM) is a group of multifactorial disorders due to either defective insulin secretion or action. Despite the fact that numerous genetic researches of T2DM have been pursued, the pathogenic mechanisms remain obscure. We encountered a T2DM family associated with a balanced reciprocal translocation, t(3;9)(p21.31;q33.1). To isolate a candidate gene susceptible to T2DM, we constructed physical maps covering both the 3p and 9q breakpoints of the translocation in the family. Consequently, the inositol hexaphosphate kinase 1 gene (IHPK1) (OMIM *606991) was found to be disrupted at the 3p21.31 breakpoint. We then carried out sequence analysis for all coding regions of IHPK1 in 405 unrelated T2DM patients in order to validate whether aberrations of the gene are common in T2DM patients, but we failed to detect any pathogenic changes. The disruption of IHPK1 or another predisposing gene affected by position effect of the translocation may explain the T2DM phenotype at least in this family. Alternatively, the IHPK1 disruption in the family is a chance association.  相似文献   

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