Acute systemic blood pressure elevation in obstructive and nonobstructive breath hold in primates

1995 ◽  
Vol 79 (1) ◽  
pp. 324-330 ◽  
Author(s):  
S. G. White ◽  
E. C. Fletcher ◽  
C. C. Miller
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Intrathoracic Pressure ◽  
Systemic Blood Pressure ◽  
Breath Hold ◽  
Rapid Rise ◽  
Systemic Blood ◽  
Blood Pressure Elevation ◽  
Human Sleep ◽  
Incremental Increase

Phasic blood pressure (BP) response during obstructive apnea (OA) in human sleep has been previously described as consisting of a slow incremental increase in BP to the point of apnea termination followed by a rapid rise and then fall in BP at the resumption of respiration. This rise in BP has been attributed to postapneic augmentation of cardiac output resulting after release of the marked negative intrathoracic pressure (NIP) of obstructed inspiration. Via an endotracheal tube, we created obstructed and nonobstructed breath hold (apnea) in chloralose-anesthesized baboons consisting of fixed-duration (30, 45, and 60 s) single OAs (mechanical obstruction) and nonobstructive (paralysis, ventilator cessation) apneas of matched duration and arterial desaturation. Systemic BP was measured before apnea (T0), during the last 5 s of apnea (T1), and during the first 5 s after resumption of respiration (T2). Despite wide fluctuations in NIP and BP during the T0 to T1 phase of OA, BP elevation in OA and nonobstructive apnea at T0, T1, or T2 did not differ for any duration apnea. At the release of obstruction, when resolution of NIP changes could theoretically increase cardiac output and accentuate BP, there was no difference in T1 and T2 pressures between the two conditions. We conclude that in this anesthesized animal model, mechanical (NIP) changes do not play a major role in overall maximum BP response to OA. Because of physiological differences between natural sleep in humans and the anesthetized state in animals, care must be taken in extrapolating these results to human sleep apnea.

Control of Blood Pressure and the Distribution of Blood Flow

1991 ◽  
Vol 7 (S1) ◽  
pp. 79-84 ◽  
Author(s):  
Hans T. Versmold
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Systemic Blood Pressure ◽  
Adrenergic Innervation ◽  
Systemic Blood ◽  
Low Cardiac Output ◽  
Neurohumoral Control ◽  
The Brain

Systemic blood pressure (BP) is the product of cardiac output and total peripheral resistance. Cardiac output is controlled by the heart rate, myocardial contractility, preload, and afterload. Vascular resistance (vascular hindrance × viscosity) is under local autoregulation and general neurohumoral control through sympathetic adrenergic innervation and circulating catecholamines. Sympathetic innovation predominates in organs receivingflowin excess of their metabolic demands (skin, splanchnic organs, kidney), while innervation is poor and autoregulation predominates in the brain and heart. The distribution of blood flow depends on the relative resistances of the organ circulations. During stress (hypoxia, low cardiac output), a raise in adrenergic tone and in circulating catecholamines leads to preferential vasoconstriction in highly innervated organs, so that blood flow is directed to the brain and heart. Catecholamines also control the levels of the vasoconstrictors renin, angiotensin II, and vasopressin. These general principles also apply to the neonate.

scholarly journals THE USE OF GENERIC MOXONIDINE IN SYSTEMIC BLOOD PRESSURE ELEVATION

2015 ◽  
Vol 14 (4) ◽  
pp. 13
Author(s):  
B. B. Ruksin ◽  
O. B. Grishin ◽  
S. V. Yashchenkova ◽  
М. В. Onuchin
Keyword(s):  
Blood Pressure ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Blood Pressure Elevation ◽  
Pressure Elevation

Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea

1992 ◽  
Vol 72 (5) ◽  
pp. 1978-1984 ◽  
Author(s):  
E. C. Fletcher ◽  
J. Lesske ◽  
R. Behm ◽  
C. C. Miller ◽  
H. Stauss ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intermittent Hypoxia ◽  
Ventricular Hypertrophy ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Systemic Blood ◽  
Blood Pressure Elevation ◽  
Group 4 ◽  
Episodic Hypoxia ◽  
Group 3

We have described a rat model that responds to repetitive episodic hypoxia (12-s infusions of nitrogen into daytime sleeping chambers every 30 s, 7 h/day for 35 days) with an increase in diurnal systemic blood pressure. We hypothesized that afferent information from the peripheral chemoreceptors may be necessary to produce diurnal blood pressure elevation in this hypoxia model. Carotid body denervation (CBD) was accomplished by severing both carotid sinus nerves in two groups of male Wistar rats (250–375 g). Group 4 CBD rats were subjected to intermittent hypoxia for 35 days (3–5% nadir ambient O2) as described above, whereas group 5 CBD rats remained unhandled in their usual cages. Additional sham-operated controls included group 2 sham-“hypoxia” rats, which were housed in chambers identical to the hypoxia rats but supplied with compressed air instead of nitrogen, group 1 (not denervated) rats, which remained unhandled in their usual cages, and group 3 sham-operated rats, which were subjected to 35 days of intermittent hypoxia identical to group 4 CBD rats. Femoral arterial baseline and end-of-study blood pressures were measured in conscious rats. The group 3 rats exposed to episodic hypoxia displayed a 13-mmHg increase in mean blood pressure, whereas the other groups showed no significant change from baseline. Left ventricular hypertrophy was evident in all rats exposed to episodic hypoxia, but right ventricular hypertrophy was evident only in the group 4 rats. All CBD rats developed increased hematocrit and hemoglobin, while the group 3 rats (non-CBD, episodic hypoxia) did not. The baroreceptor reflex at baseline was not depressed in the CBD rats.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

2020 ◽  
Vol 319 (1) ◽  
pp. H162-H170 ◽  
Author(s):  
Jacqueline K. Limberg ◽  
James A. Smith ◽  
Rogerio N. Soares ◽  
Jennifer L. Harper ◽  
Keeley N. Houghton ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Systemic Blood Pressure ◽  
Experimental Protocol ◽  
Systemic Blood ◽  
Peripheral Vasodilation ◽  
Experimental Protocols ◽  
Isolated Arteries ◽  
Principal Contributor

We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.

Effect of recurrent episodic hypocapnic, eucapnic, and hypercapnic hypoxia on systemic blood pressure

1995 ◽  
Vol 78 (4) ◽  
pp. 1516-1521 ◽  
Author(s):  
E. C. Fletcher ◽  
G. Bao ◽  
C. C. Miller
Keyword(s):  
Blood Pressure ◽  
Rat Model ◽  
Blood Pressure Response ◽  
Systemic Blood Pressure ◽  
Protective Mechanism ◽  
Systemic Blood ◽  
Blood Pressure Elevation ◽  
Arterial Blood ◽  
Episodic Hypoxia ◽  
Hypoxic Group

We have described a rat model that responds to chronic (8 h/day, 35 days) repetitive nonapneic episodic (cycled every 30 s) hypocapnic hypoxia with sustained increase in systemic blood pressure. Because the usual blood gas change of apnea is mildly increased CO2, we hypothesized that episodic hypoxia ranging from eucapnea to hypercapnia might cause a greater chronic increase in blood pressure than hypocapnic hypoxia in this model. Five groups of male Sprague-Dawley rats were studied: unhandled group received no treatment, sham group received compressed air in their chambers, hypocapnic hypoxic group received episodic hypoxia for 35 days, eucapnic hypoxic group received the same level of hypoxia but with 7–10% inspired fraction of CO2, and hybercarbic hypoxic group received hypoxia with 11–14% inspired fraction of CO2. Mean arterial blood pressure was measured in unrestrained conscious animals at baseline and after 35 days under their respective study conditions. Neither episodic eucapnic nor hypercarbic hypoxia had any additional effect on the changes in chronic diurnal blood pressure compared with hypocapnic hypoxia. These results suggest that the sympathetic nervous system or other neurohumoral systems contributing to chronic diurnal blood pressure elevation may be maximally stimulated by hypoxia or there may be some protective mechanism limiting the blood pressure response to asphyxia in this rat model.

scholarly journals Current understanding of the effects of inspiratory resistance on the interactions between systemic blood pressure, cerebral perfusion, intracranial pressure, and cerebrospinal fluid dynamics

2019 ◽  
Vol 127 (5) ◽  
pp. 1206-1214 ◽  
Author(s):  
Pawel J. Winklewski ◽  
Jacek Wolf ◽  
Marcin Gruszecki ◽  
Magdalena Wszedybyl-Winklewska ◽  
Krzysztof Narkiewicz
Keyword(s):  
Blood Pressure ◽  
Intracranial Pressure ◽  
Clinical Medicine ◽  
Respiratory Muscles ◽  
Intrathoracic Pressure ◽  
Brain Perfusion ◽  
Systemic Blood Pressure ◽  
Systemic Blood ◽  
Obstructive Sleep ◽  
Inspiratory Resistance

Negative intrathoracic pressure (nITP) is generated by the respiratory muscles during inspiration to overcome inspiratory resistance, thus enabling lung ventilation. Recently developed noninvasive techniques have made it possible to assess the effects of nITP in real time in several physiological aspects such as systemic blood pressure (BP), intracranial pressure (ICP), and cerebral blood flow (CBF). It has been shown that nITP from 0 to −20 cmH2O elevates BP and diminishes ICP, which facilitates brain perfusion. The effects of nITP from −20 to −40 cmH2O on BP, ICP, and CBF remain largely unrecognized, yet even nITP at −40 cmH2O may facilitate CBF by diminishing ICP. Importantly, nITP from −20 to −40 cmH2O has been documented in adults in commonly encountered obstructive sleep apnea, which justifies research in this area. Recent revelations about interactions between ICP and BP have opened up new fields of research in physiological regulation and the pathophysiology of common diseases, such as hypertension, brain injury, and respiratory disorders. A better understanding of these interactions may translate directly into new therapies in various fields of clinical medicine.

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