scholarly journals The response of the vestibulosympathetic reflex to linear acceleration in the rat

2016 ◽  
Vol 116 (6) ◽  
pp. 2752-2764 ◽  
Author(s):  
S. B. Yakushin ◽  
G. P. Martinelli ◽  
T. Raphan ◽  
B. Cohen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Three Dimensional ◽  
Linear Acceleration ◽  
Peripheral Vascular ◽  
Alert Rat ◽  
Vestibulosympathetic Reflex ◽  
Long Evans ◽  
The Brain ◽  
Linear Regressions

The vestibulosympathetic reflex (VSR) increases blood pressure (BP) upon arising to maintain blood flow to the brain. The optimal directions of VSR activation and whether changes in heart rate (HR) are associated with changes in BP are still not clear. We used manually activated pulses and oscillatory linear accelerations of 0.2–2.5 g along the naso-occipital, interaural, and dorsoventral axes in isoflurane-anesthetized, male Long-Evans rats. BP and HR were recorded with an intra-aortic sensor and acceleration with a three-dimensional accelerometer. Linear regressions of BP changes in accelerations along the upward, downward, and forward axes had slopes of ≈3–6 mmHg · g−1 ( P < 0.05). Lateral and backward accelerations did not produce consistent changes in BP. Thus upward, downward, and forward translations were the directions that significantly altered BP. HR was unaffected by these translations. The VSR sensitivity to oscillatory forward-backward translations was ≈6–10 mmHg · g−1 at frequencies of ≈0.1 Hz (0.2 g), decreasing to zero at frequencies above 2 Hz (1.8 g). Upward, 70° tilts of an alert rat increased BP by 9 mmHg · g−1 without changes in HR, indicating that anesthesia had not reduced the VSR sensitivity. The similarity in BP induced in alert and anesthetized rats indicates that the VSR is relatively insensitive to levels of alertness and that the VSR is likely to cause changes in BP through modification of peripheral vascular resistance. Thus the VSR, which is directed toward the cardiovascular system, is in contrast to the responses in the alert state that can produce sweating, alterations in BP and HR, and motion sickness.

Alterations in Blood Pressure and Heart Rate Variabililty in Transgenic Rats with Low Brain Angiotensinogen

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 727-727
Author(s):  
Ovidiu Baltatu ◽  
Ben J Janssen ◽  
Ralph Plehm ◽  
Detlev Ganten ◽  
Michael Bader
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Baroreflex Sensitivity ◽  
Circadian Variation ◽  
Ang Ii ◽  
Transgenic Rats ◽  
Short Term ◽  
Baroreflex Control ◽  
Sd Rats ◽  
The Brain

P191 The brain renin-angiotensin system (RAS) system may play a functional role in the long-term and short-term control of blood pressure (BPV) and heart rate variability (HRV). To study this we recorded in transgenic rats TGR(ASrAOGEN) with low brain angiotensinogen levels the 24-h variation of BP and HR during basal and hypertensive conditions, induced by a low-dose s.c. infusion of angiotensin II (Ang II, 100 ng/kg/min) for 7 days. Cardiovascular parameters were monitored by telemetry. Short-term BPV and HRV were evaluated by spectral analysis and as a measure of baroreflex sensitivity the transfer gain between the pressure and heart rate variations was calculated. During the Ang II infusion, in SD but not TGR(ASrAOGEN) rats, the 24-h rhythm of BP was inverted (5.8 ± 2 vs. -0.4 ± 1.8 mm Hg/group of day-night differences of BP, p< 0.05, respectively). In contrast, in both the SD and TGR(ASrAOGEN) rats, the 24-h HR rhythms remained unaltered and paralleled those of locomotor activity. The increase of systolic BP was significantly reduced in TGR(ASrAOGEN) in comparison to SD rats as previously described, while the HR was not altered in TGR(ASrAOGEN) nor in SD rats. The spectral index of baroreflex sensitivity (FFT gain between 0.3-0.6 Hz) was significantly higher in TGR(ASrAOGEN) than SD rats during control (0.71 ± 0.1 vs. 0.35 ± 0.06, p<0.05), but not during Ang II infusion (0.6 ± 0.07 vs. 0.4 ± 0.1, p>0.05). These results demonstrate that the brain RAS plays an important role in mediating the effects of Ang II on the circadian variation of BP. Furthermore these data are consistent with the view that the brain RAS modulates baroreflex control of HR in rats, with AII having an inhibitory role.

scholarly journals FLUORESCEIN CIRCULATION TIME AS A PROGNOSTIC SIGN IN EXPERIMENTAL TRAUMATIC SHOCK

1946 ◽  
Vol 84 (6) ◽  
pp. 549-558 ◽  
Author(s):  
S. C. Wang ◽  
E. E. Painter ◽  
R. R. Overman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vascular System ◽  
Peripheral Circulation ◽  
Traumatic Shock ◽  
Systemic Circulation ◽  
The Other ◽  
Circulation Time ◽  
Peripheral Vascular ◽  
Made In

Repeated determinations of the circulation time by the fluorescein method were made in normal and shocked dogs. In normal animals the circulation time ranges from 9 to 16 seconds with an average of 12.6 seconds. In traumatic shock the circulation time is invariably prolonged. For prognosis in the traumatized animal two determinations of fluorescein circulation time separated by an interval of 1 hour are essential. If the second circulation time is longer than the first and both are over 30 seconds, the animal will not survive without therapy. On the other hand, if the second circulation time is below 25 seconds or is considerably shorter than the first, the prognosis is good. In many of these experiments the change in circulation time appeared to be the earliest index of eventual recovery or death. It gave a clue to the fate of the animal when no decisive judgment could be made from the blood pressure and heart rate. In three dogs the cyanide and fluorescein circulation times were compared during shock. It was found that the cyanide circulation time, though increased in shock, remained at a fairly constant value while over the same period the fluorescein circulation time showed progressive changes. This discrepancy between the cyanide and fluorescein methods may be explained by the fact that the former does not include the minute peripheral systemic circulation. Since the study of shock is concerned with tissue anoxia and is primarily a phenomenon of the failure of the peripheral circulation, it is important to choose procedures such as the fluorescein method as a measure of the condition of the peripheral vascular system.

Contrasting neurovascular findings in chronic orthostatic intolerance and neurocardiogenic syncope

2003 ◽  
Vol 104 (4) ◽  
pp. 329-340 ◽  
Author(s):  
Julian M. STEWART ◽  
Amy WELDON
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Orthostatic Intolerance ◽  
Peripheral Vascular ◽  
Neurocardiogenic Syncope ◽  
Control Subjects ◽  
Arterial Resistance ◽  
Vascular Physiology ◽  
Venous Resistance

Simple faint (neurocardiogenic syncope) and postural tachycardia syndrome (POTS) characterize acute and chronic orthostatic intolerance respectively. We explored the hypothesis that vascular function is similar in the two conditions. We studied 29 patients with POTS and compared them with 20 patients with neurocardiogenic syncope who were otherwise well, and with 15 healthy control subjects. We measured continuous heart rate, respiration and blood pressure, and used venous occlusion strain gauge plethysmography to measure calf and forearm blood flow, peripheral arterial resistance, peripheral venous resistance and venous pressure (Pv). Upright tilt was performed to 70° for 10min, during which calf blood flow and volume were measured. Calf Pv was increased (to 27.2±2.0mmHg) in a subgroup of POTS patients, who also had increased arterial resistance (57±6mmHg·ml-1·min-1·100ml-1 tissue), increased venous resistance (2.4±0.3mmHg·ml-1·min-1·100ml-1 tissue), and decreased peripheral flow (1.0±0.2ml·min-1·100ml-1 tissue) in the calf; other POTS patients with a normal Pv had decreased arterial resistance (18±2mmHg·ml-1·min-1·100ml-1 tissue) and increased blood flow (3.8±0.3ml·min-1·100ml-1 tissue). Syncope patients were not different from controls (Pv = 11.4±0.5mmHg; calf flow = 3.1±0.2ml·min-1·100ml-1 tissue; arterial resistance = 27±2mmHg·ml-1·min-1·100ml-1 tissue; venous resistance = 1.2±0.3mmHg·ml-1·min-1·100ml-1 tissue). When upright, syncope patients and control subjects had similar increases in heart rate and calf volume, stable blood pressure, and decreases in blood flow. POTS patients had markedly increased heart rate and calf blood flow, unstable blood pressure, and pooling in the lower extremities, regardless of subgroup. We conclude that peripheral vascular physiology in patients with POTS is abnormal, in contrast with normal peripheral vascular physiology in neurocardiogenic syncope.

scholarly journals Vascular resistance arm of the baroreflex: methodology and comparison with the cardiac chronotropic arm

2020 ◽  
Vol 128 (5) ◽  
pp. 1310-1320
Author(s):  
J. Krohova ◽  
L. Faes ◽  
B. Czippelova ◽  
R. Pernice ◽  
Z. Turianikova ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vascular Resistance ◽  
Vascular Tone ◽  
Heart Rate Response ◽  
Peripheral Vascular Resistance ◽  
Noninvasive Measurement ◽  
Peripheral Vascular ◽  
Pressure Changes

Baroreflex response consists of several arms, but the cardiac chronotropic arm (blood pressure changes evoking heart rate response) is usually analyzed. This study introduces a method to assess the vascular baroreflex arm with the continuous noninvasive measurement of peripheral vascular resistance as an output considering causality in the interaction between oscillations and slower dynamics of vascular tone changes. We conclude that although vascular baroreflex arm involvement becomes dominant during orthostasis, gain of this interaction is relatively stable.

scholarly journals Mathematical modeling of the cardiovascular autonomic control in healthy subjects during a passive head-up tilt test

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yurii M. Ishbulatov ◽  
Anatoly S. Karavaev ◽  
Anton R. Kiselev ◽  
Margarita A. Simonyan ◽  
Mikhail D. Prokhorov ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiovascular System ◽  
Healthy Subjects ◽  
Low Frequency ◽  
Tilt Test ◽  
Peripheral Vascular ◽  
Control Loops ◽  
Head Up Tilt ◽  
Head Up Tilt Test

Abstract A mathematical model is proposed for the autonomic control of cardiovascular system, which takes into account two separated self-exciting sympathetic control loops of heart rate and peripheral vascular tone. The control loops are represented by self-exciting time-delay systems and their tone depends on activity of the aortic, carotid, and lower-body baroreceptors. The model is used to study the dynamics of the adaptive processes that manifest in a healthy cardiovascular system during the passive head-up tilt test. Computer simulation provides continuous observation of the dynamics of the indexes and variables that cannot be measured in the direct experiment, including the noradrenaline concentration in vessel wall and heart muscle, tone of the sympathetic and parasympathetic control, peripheral vascular resistance, and blood pressure. In the supine and upright positions, we estimated the spectral characteristics of the model variables, especially in the low-frequency band, and the original index of total percent of phase synchronization between the low-frequency oscillations in heart rate and blood pressure signals. The model demonstrates good quantitative agreement with the dynamics of the experimentally observed indexes of cardiovascular system that were averaged for 50 healthy subjects.

Thromboxane A2 acts on the brain to mediate hemodynamic, adrenocorticotropin, and cortisol responses

1998 ◽  
Vol 274 (5) ◽  
pp. R1353-R1360 ◽  
Author(s):  
Timothy A. Cudd
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
De Novo ◽  
Blood Pressure Response ◽  
Protective Function ◽  
Prostaglandin Synthase ◽  
Artificial Cerebrospinal Fluid ◽  
Cortisol Responses ◽  
Blood Pressure Responses ◽  
The Brain

Conditions that increase the formation of thromboxane A2(TxA2) also result in activation of hemodynamic and adrenocortical responses. The purpose of this study was to test the hypothesis that TxA2 acts directly on the brain to mediate these responses. Adult sheep were chronically instrumented with vascular and intracerebroventricular catheters. The TxA2 analog U-46619 (0, 100, or 1,000 ng ⋅ kg−1 ⋅ min−1) and artificial cerebrospinal fluid (CSF) were infused intracerebroventricularly for 30 min. Heart rate increased in response to 100 ng ⋅ kg−1 ⋅ min−1U-46619 infusions. Heart rate did not change over preinfusion values in response to the highest infusion rate, but values were elevated compared with the postinfusion period. Mean arterial pressure, ACTH, cortisol, hematocrit, and arterial pH (pHa) increased, and arterial partial CO2 pressure ([Formula: see text]) fell in response to 1,000 ng ⋅ kg−1 ⋅ min−1infusions of U-46619. Plasma vasopressin concentrations and arterial partial O2 pressure did not change. In a second study, U-46619 or artificial CSF was infused intracerebroventricularly during prostaglandin synthase blockade. Blockade reduced but did not prevent blood pressure responses to U-46619 infusion, suggesting that the U-46619 infusions increased prostaglandin synthase metabolism to contribute de novo TxA2 or a second metabolite to augment the blood pressure response. Heart rate, pHa,[Formula: see text], ACTH, and cortisol responses to U-46619 were not different with blockade. We conclude that TxA2 acts on the brain to mediate blood pressure, heart rate, pHa,[Formula: see text], hematocrit, ACTH, and cortisol responses. These findings support the hypothesis that TxA2 acts directly on the brain to promote cardiovascular and hormonal responses that may serve a protective function during conditions when TxA2 formation is increased.

Abstract 13: Relations of Midlife Exercise Blood Pressure, Heart Rate and Fitness to Late Life Brain Structure and Function

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Nicole L Spartano ◽  
Jayandra J Himali ◽  
Alexa S Beiser ◽  
Charles DeCarli ◽  
Ramachandran S Vasan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Frontal Lobe ◽  
Cognitive Performance ◽  
Brain Aging ◽  
Later Life ◽  
Older Age ◽  
Vascular Stiffness ◽  
Response To Exercise ◽  
The Brain

Background: Exaggerated blood pressure (BP) and vascular stiffness have been associated with lower cognitive performance and brain atrophy in older age. The brain is a high-flow, low impedance organ that is susceptible to fluctuation in BP. Poor cardiovascular (CV) fitness is also emerging as a factor associated with cognitive decline in older age. The BP and heart rate (HR) response to exercise are impacted by CV fitness; and exercise BP is also highly determined by vascular stiffness. The objective of this investigation was to examine whether poor fitness and exaggerated BP and HR response to exercise in midlife are associated with worse brain morphology in later life. Methods: A subset of Framingham Offspring Study participants (n=1340, 54.5% F) free from dementia and CV disease underwent an exercise treadmill test (the modified Bruce protocol) in midlife [mean age of 41±9 y] and continued until exhaustion or until 85% HR maximum (age- and sex- predicted) was reached. Exercise test duration was used to estimate VO2max. BP and HR were measured during stage 2. MRI scans of the brain and neurocognitive tests (Trail Making Tests [Trails] B-A) were administered in later life [mean age of 59±9 y]. Results: A greater exercise systolic (S)BP and HR response at midlife was associated with smaller total cerebral brain volume (TCBV) in later life (β=-0.09 ±0.04, p=0.042; β=-0.10 ±0.05, p=0.033) after adjustment models including resting SBP and HR; an effect equal to approximately 0.5 y brain aging for every 11.1 mm Hg increase in SBP or 10 beats per min increase in HR. Higher estimated VO2max at midlife was associated with larger TCBV in later life (β=0.03 ±0.01, p=0.014). Additionally, greater exercise HR response at midlife was associated with smaller frontal lobe volume in later life (β=-0.012 ±0.05, p=0.002). Exercise diastolic (D)BP at midlife was associated with poorer performance on Trails B-A in later life (β=-0.009 ±0.004, p=0.017) and the achievement of target HR during exercise was associated with better performance on Trails B-A in later life (β=0.03 ±0.01, p=0.044). Resting SBP at midlife was associated with greater white matter hyperintensity volume in later life (β=0.05 ±0.02, p=0.031); and resting SBP and DBP at midlife were also associated with smaller frontal lobe volume in later life (β=-0.17 ±0.07, p=0.011; β=-0.21 ±0.10, p=0.030). Conclusion: Our investigation provides new evidence that lower midlife fitness and worse exercise BP and HR responses are associated with smaller brain volumes and poorer cognitive performance nearly two decades later. Promotion of midlife physical fitness may be an important step towards ensuring healthy brain aging in the population.

Atrial natriuretic factor-induced vasodepression occurs through central nervous system

1988 ◽  
Vol 255 (3) ◽  
pp. H616-H622 ◽  
Author(s):  
E. R. Levin ◽  
M. A. Weber ◽  
S. Mills
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Nervous System ◽  
Fourth Ventricle ◽  
Saline Control ◽  
Arterial Blood ◽  
Adrenergic Antagonist ◽  
Adrenergic Nervous System ◽  
The Brain ◽  
Atrial Natriuretic

To characterize the blood pressure and heart rate effects of atrial natriuretic peptide (ANP) in the brain, we administered 20 micrograms/kg of atriopeptin III in 5 microliters of 0.9 normal saline into the fourth ventricle of awake, freely moving, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. ANP produced a 13 +/- 1 mmHg decrease in mean arterial blood pressure (MAP) in the SHR (P less than 0.001 vs. base line or saline control, n = 10) and a 9 +/- 2 mmHg decrease in the WKY (P less than 0.02). Heart rate did not change significantly in response to ANP. To determine whether an interaction with the adrenergic nervous system played a role in the effects of ANP, we administered 100 ng yohimbine HCL, an alpha 2-antagonist, by intracerebroventricular injection, 45 min before ANP and completely prevented the ANP-induced decrease in MAP. In contrast, 100 ng intracerebroventricular prazosin, an alpha 1-adrenergic antagonist, had no significant influence on the MAP effect induced by ANP. A third group of SHR was pretreated with intracerebroventricular 6-OH dopamine to deplete central catecholamines or with saline. The rats pretreated with 6-OH dopamine (n = 6) had no significant response to ANP, which was administered 9 days later. This was significantly different from the saline-pretreated control group (n = 6), which responded with a 19 +/- 3 mmHg decrease in MAP (P less than 0.025). These studies indicate that the administration of ANP into the fourth ventricle of the brain decreases the MAP of rats through an interaction with the central alpha 2-adrenergic nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)

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