scholarly journals Effects of allergic airway inflammation and chronic intermittent hypoxia on systemic blood pressure

2020 ◽  
Vol 319 (5) ◽  
pp. R566-R574
Author(s):  
Ashish Chaddha ◽  
Oleg Broytman ◽  
Mihaela Teodorescu

Asthma and obstructive sleep apnea (OSA) are highly prevalent chronic conditions, and both are associated with systemic hypertension. Additionally, asthma and OSA reciprocally interact, mutually exacerbating each other. In this study, we tested the effect of allergen-induced lower airway inflammation and concurrent chronic intermittent hypoxia (CIH) on systemic blood pressure (BP), pulmonary function, and proinflammatory cytokines, in a rat model. Brown Norway rats were exposed to 43 days of normoxia (NORM) or CIH, concurrent with weekly house dust mite (HDM) challenges. BP was measured 1 day after the last HDM challenge. On day 44, pulmonary function was tested, and blood for Th-2 and Th-1 cytokine levels was collected. HDM significantly increased mean ( P = 0.002), systolic ( P = 0.003), and diastolic ( P = 0.004) BP compared with saline-challenged controls. Higher mean BP significantly correlated to increased total respiratory system resistance ( R2 = 0.266, P = 0.002), driven by an association with parenchymal tissue dampening ( R2 = 0.166, P = 0.016). HDM relative to saline-challenged controls increased the expression of serum IL-6 ( P = 0.008), but no relationships of systemic BP with IL-6 or any other cytokines were found. CIH did not alter the allergen-induced responses on BP, although it tended to increase the expression of serum IL-6 ( P = 0.06) and monocyte chemoattractant protein-1 (MCP-1, P = 0.09), regardless of HDM challenge. Chronic allergen-induced airway inflammation results in systemic hypertension that is correlated to the degree of distal airway obstruction induced by the allergen. These effects do not appear to be explained by the associated systemic inflammation.

BMJ Open ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. e039342
Author(s):  
Sara Rodriguez-Lopez ◽  
Stefan Palkowski ◽  
Christopher Gerdung ◽  
Diana Keto-Lambert ◽  
Meghan Sebastianski ◽  
...  

IntroductionChildhood obstructive sleep apnoea (OSA) is a highly prevalent disorder that may directly contribute to the development of obesity, hypertension and renal injury. Although those associations seem to be clearer in adults, studies in children have revealed conflicting results and updated synthesis of the evidence is lacking. The aim of this systematic review is to summarise the available evidence on the effect of OSA on obesity, systemic blood pressure and kidney function, to help to elucidate whether respiratory interventions to correct OSA would have the potential to improve those outcomes.Methods and analysisA systematic literature review search was created by a medical librarian and peer-reviewed by a second librarian prior to running. Ovid Medline, Ovid Embase, CINAHL via EbscoHOST, Wiley Cochrane Library and ProQuest Dissertations and Theses Global were searched on 25 February 2020. Titles and abstracts will be screened by two independent reviewers for inclusion, followed by full-text screening of relevant articles. Studies in children will be included if they report data on OSA and weight, systemic blood pressure or kidney parameters. The extracted data will be combined for analysis and the information subcategorised in groups based on outcome. Risk of bias will be determined using tools specific to study methodology and certainty of the evidence using the Grading of Recommendations, Assessment, Development and Evaluations approach.Ethics and disseminationThis study will provide essential information for healthcare professionals to better understand the relationship between childhood OSA and changes in body mass index, systemic blood pressure and kidney function indicators. Our findings will be disseminated through conferences and publications. The results of this review may guide the initiation of new strategies and the development of future research studies. This research did not involve human subjects and therefore did not undergo research ethical review.PROSPERO registration numberCRD42020171186.


Thorax ◽  
2006 ◽  
Vol 61 (12) ◽  
pp. 1083-1090 ◽  
Author(s):  
D S Hui ◽  
K W To ◽  
F W Ko ◽  
J P Fok ◽  
M C Chan ◽  
...  

2001 ◽  
Vol 90 (4) ◽  
pp. 1600-1605 ◽  
Author(s):  
Eugene C. Fletcher

One of the major manifestations of obstructive sleep apnea is profound and repeated hypoxia during sleep. Acute hypoxia leads to stimulation of the peripheral chemoreceptors, which in turn increases sympathetic outflow, acutely increasing blood pressure. The chronic effect of these repeated episodic or intermittent periods of hypoxia in humans is difficult to study because chronic cardiovascular changes may take many years to manifest. Rodents have been a tremendous source of information in short- and long-term studies of hypertension and other cardiovascular diseases. Recurrent short cycles of normoxia-hypoxia, when administered to rats for 35 days, allows examination of the chronic cardiovascular response to intermittent hypoxia patterned after the episodic desaturation seen in humans with sleep apnea. The result of this type of intermittent hypoxia in rats is a 10- to 14-mmHg increase in resting (unstimulated) mean blood pressure that lasts for several weeks after cessation of the daily cyclic hypoxia. Carotid body denervation, sympathetic nerve ablation, renal sympathectomy, adrenal medullectomy, and angiotensin II receptor blockade block the blood pressure increase. It appears that adrenergic and renin-angiotensin system overactivity contributes to the early chronic elevated blood pressure in rat intermittent hypoxia and perhaps to human hypertension associated with obstructive sleep apnea.


Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3169-3169 ◽  
Author(s):  
Victor R. Gordeuk ◽  
Mark T. Gladwin ◽  
Gregory Kato ◽  
Oswaldo Castro

Abstract In an emerging paradigm of sickle cell disease (SCD) vasculopathy, the risk for pulmonary and systemic hypertension, renal dysfunction, proteinuria, stroke and early death may be related to the degree of hemolysis, nitric oxide scavenging and resultant damage to the vasculature (JAMA2005;293:1653). The systemic blood pressure (BP) in sickle cell anemia (SS) is lower than in normal subjects. Yet, the concept of relative systemic hypertension has been proposed because SS pts. Have higher BP than subjects with other forms of congenital anemias (Am J Med Sci 1993). Furthermore, apparently minor BP increases in SS are associated with stroke risk (Am J Med Sci1993;305:150, Am J Med1997;102:171). We hypothesized that in contrast to otherwise healthy individuals without SCD, systolic blood pressures (sBP) of 120 to 139 mm Hg define relative hypertension in SCD and identify patients at increased risk for vasculopathy and its complications. We analyzed entry data from 195 adult patients enrolled in the prospective Sickle Cell Pulmonary Hypertension Screening Study (NEJM2004;350:886), and stratified their ECHO-determined tricuspid regurgitant jet velocity (TRV) and serum creatinine concentration according to sBP categories. As shown in Figure 1, among Hb SS and S beta thal patients, the prevalence of pulmonary hypertension (PHTN, TRV 2.5 m/sec or greater) was 26% with sBP <120 mm Hg, 36% with sBP 120–139 mm Hg and 89% with sBP 140 mm Hg or higher (P <0.0005 for trend). Similarly, the prevalence of a serum creatinine concentration of 1.0 mg/dL or higher was 7% with sBP <120 mm Hg, 13% with sBP 120–139 mm Hg and 30% with sBP 140 mm Hg or higher (P = 0.002 for trend, Figure 2). The increasing prevalences of PHTN and renal dysfunction with the three progressively higher sBP categories are consistent with our hypothesis that sBP 120–139 represents relative hypertension and increased risk for vascular complications in patients with SCD. Whether treatment of relative hypertension in sickle patients would improve vasculopathy and lower their risk for PHTN, renal impairment or other complications such as stroke, is unknown. Consideration should be given to clinical trials to answer this important question. Figure Figure Figure Figure


Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 54
Author(s):  
Jesus Prieto-Lloret ◽  
Elena Olea ◽  
Ana Gordillo-Cano ◽  
Inmaculada Docio ◽  
Ana Obeso ◽  
...  

Chronic sustained hypoxia (CSH), as found in individuals living at a high altitude or in patients suffering respiratory disorders, initiates physiological adaptations such as carotid body stimulation to maintain oxygen levels, but has deleterious effects such as pulmonary hypertension (PH). Obstructive sleep apnea (OSA), a respiratory disorder of increasing prevalence, is characterized by a situation of chronic intermittent hypoxia (CIH). OSA is associated with the development of systemic hypertension and cardiovascular pathologies, due to carotid body and sympathetic overactivation. There is growing evidence that CIH can also compromise the pulmonary circulation, causing pulmonary hypertension in OSA patients and animal models. The aim of this work was to compare hemodynamics, vascular contractility, and L-arginine-NO metabolism in two models of PH in rats, associated with CSH and CIH exposure. We demonstrate that whereas CSH and CIH cause several common effects such as an increased hematocrit, weight loss, and an increase in pulmonary artery pressure (PAP), compared to CIH, CSH seems to have more of an effect on the pulmonary circulation, whereas the effects of CIH are apparently more targeted on the systemic circulation. The results suggest that the endothelial dysfunction evident in pulmonary arteries with both hypoxia protocols are not due to an increase in methylated arginines in these arteries, although an increase in plasma SDMA could contribute to the apparent loss of basal NO-dependent vasodilation and, therefore, the increase in PAP that results from CIH.


2011 ◽  
Vol 70 (3) ◽  
Author(s):  
J. A. Ebeigbe ◽  
P. N. Ebeigbe ◽  
A. D. A Ighoroje

Background: Mean intraocular pressure (IOP) in postmenopausal women has been reported higher than that in menstruating women. Also, intraocular pressure is said to be positively correlated with systemic blood pressure. No previous study in Nigeria has compared intraocular pressure in postmenopausal women with and without systemic hypertension. Purpose: To investigate the effects of menopause on intraocular pressure in subjects with and without high blood pressure. Methods: Normotensive and hypertensive premenopausal and postmenopausal subjects in the   same agerange of 45 to 55 years were studied. Intraocular pressure was measured with the hand-held Kowa applanation tonometer.  Blood pressure was taken in the sitting position at the right upper arm using a manual mercury sphygmomanometer with the right cuff size. The average of two readings was recorded. Results: Mean IOP for premenopausal normotensive women was 14.58 ± 2.56 mmHg whilethat of postmenopausal normotensive women was16.15 ± 1.80 mmHg (p<0.05).  Also, the difference in mean IOP between premenopausal hypertensive (16.58 ± 3.23 mmHg) and postmenopausal hypertensive women (18.24 ± 3.89 mmHg)was statistically significant (p<0.05). A statistically significant and positive correlation was observed between IOP and systemic blood pressure in postmenopausal hypertensive women, p<0.05.Conclusion: Menopause significantly increases intraocular pressure. Mean intraocular pressure of hypertensive postmenopausal women was significantly higher than that of normotensive post-menopausal women, (p<0.05). Knowledge of the normal level of intraocular pressure during various stages of the female reproductive cycle may help during glaucoma screening. (S Afr Optom 2011 70(3) 117-122)


2020 ◽  
Vol 318 (1) ◽  
pp. H34-H48
Author(s):  
Alexandria B. Marciante ◽  
Lei A. Wang ◽  
Joel T. Little ◽  
J. Thomas Cunningham

Obstructive sleep apnea is characterized by interrupted breathing that leads to cardiovascular sequelae including chronic hypertension that can persist into the waking hours. Chronic intermittent hypoxia (CIH), which models the hypoxemia associated with sleep apnea, is sufficient to cause a sustained increase in blood pressure that involves the central nervous system. The median preoptic nucleus (MnPO) is an integrative forebrain region that contributes to blood pressure regulation and neurogenic hypertension. The MnPO projects to the paraventricular nucleus (PVN), a preautonomic region. We hypothesized that pathway-specific lesions of the projection from the MnPO to the PVN would attenuate the sustained component of chronic intermittent hypoxia-induced hypertension. Adult male Sprague-Dawley rats (250–300 g) were anesthetized with isoflurane and stereotaxically injected bilaterally in the PVN with a retrograde Cre-containing adeno-associated virus (AAV; AAV9.CMV.HI.eGFP-Cre.WPRE.SV40) and injected in the MnPO with caspase-3 (AAV5-flex-taCasp3-TEVp) or control virus (AAV5-hSyn-DIO-mCherry). Three weeks after the injections the rats were exposed to a 7-day intermittent hypoxia protocol. During chronic intermittent hypoxia, controls developed a diurnal hypertension that was blunted in rats with caspase lesions. Brain tissue processed for FosB immunohistochemistry showed decreased staining with caspase-induced lesions of MnPO and downstream autonomic-regulating nuclei. Chronic intermittent hypoxia significantly increased plasma levels of advanced oxidative protein products in controls, but this increase was blocked in caspase-lesioned rats. The results indicate that PVN-projecting MnPO neurons play a significant role in blood pressure regulation in the development of persistent chronic intermittent hypoxia hypertension. NEW & NOTEWORTHY Chronic intermittent hypoxia associated with obstructive sleep apnea increases oxidative stress and leads to chronic hypertension. Sustained hypertension may be mediated by angiotensin II-induced neural plasticity of excitatory median preoptic neurons in the forebrain that project to the paraventricular nucleus of the hypothalamus. Selective caspase lesions of these neurons interrupt the drive for sustained hypertension and cause a reduction in circulating oxidative protein products. This indicates that a functional connection between the forebrain and hypothalamus is necessary to drive diurnal hypertension associated with intermittent hypoxia. These results provide new information about central mechanisms that may contribute to neurogenic hypertension.


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