Fastigial nucleus cardiovascular response and brain stem lesions in the beagle

1986 ◽  
Vol 250 (2) ◽  
pp. H231-H239 ◽  
Author(s):  
K. J. Dormer ◽  
J. A. Andrezik ◽  
R. J. Person ◽  
J. T. Braggio ◽  
R. D. Foreman

Changes in the excitatory cardiovascular response (heart rate, arterial blood pressure, left ventricular pressure, and LV dP/dt as an index of myocardial contractility) resulting from electrical stimulation of the cerebellar fastigial nucleus (FN) were recorded after placement of DC or radio-frequency lesions or after microinjections of kainic acid into brain stem areas that receive FN projections and have been shown to be involved in central cardiovascular control. FN-induced increases in heart rate, blood pressure, and contractility were reduced or abolished by lesions made in the restiform body or the A5 area, which is homologous to the catecholamine-containing region in cats and rats. Lesions in the paramedian reticular nucleus, rostral and caudal to obex, failed to reduce the FN cardiovascular response. Nucleus of the solitary tract lesions augmented the FN pressor response and tachycardia. Kainic acid (1 microliter of 100 mM solution) caused profound depression of heart rate, blood pressure, and contractility and reduced or eliminated the FN-induced cardiovascular response when injected into the A5 area, previously identified by the pressor response following electrical stimulation. We concluded from these observations that a descending fastigiobulbar sympathoexcitatory pathway courses through a previously identified A5 pressor area that is also capable of a depressor response when the cell bodies alone are activated.

1989 ◽  
Vol 257 (6) ◽  
pp. R1436-R1440
Author(s):  
R. T. Henry ◽  
J. D. Connor

Bilateral destruction of perikarya in the fastigial nucleus (FN) of the rat with the cytotoxic agent kainic acid (0.5 mg) did not alter the blood pressure (BP) increases observed during monopolar electrical stimulation (100 microA, 50 Hz, 0.5-ms pulse width) of this region. BP increases in control animals were 30 +/- 8 mm Hg, whereas BP increased 30 +/- 7 mmHg in kainic acid-lesioned rats. Furthermore, picrotoxin (100 ng) and muscimol (25 ng) microinjected unilaterally into the FN of conscious, unrestrained rats produced postural asymmetry but no change in BP or heart rate. These data suggest that the FN pressor response may be due, at least in part, to stimulation of axons of passage.


1984 ◽  
Vol 246 (5) ◽  
pp. R811-R816 ◽  
Author(s):  
R. Casto ◽  
M. I. Phillips

The blood pressure and heart rate responses to microinjection of angiotensin II (ANG II) into the brain stem of urethan-anesthetized rats were studied. Microinjection of ANG II into the area postrema (AP) resulted in significant elevation of blood pressure and significant reduction of heart rate. Microinjection into the region of the nucleus tractus solitarius (NTS) yielded a significant dose-dependent elevation in blood pressure and consistent increases in heart rate. The response to microinjection of ANG II into the region of the NTS was not due to leakage into the peripheral circulation, since intravenous administration of the ANG II antagonist, saralasin, did not attenuate the response. In fact, the cardiovascular response was increased after peripheral ANG II blockade, and the heart rate, which was consistently but not significantly elevated by NTS injection alone, was significantly elevated after saralasin pretreatment. Thermal ablation of the AP did not change the heart rate or the pressor response to microinjection of ANG II into the region of the NTS, indicating that the response was not mediated through the AP.


1981 ◽  
Vol 60 (2) ◽  
pp. 139-143 ◽  
Author(s):  
S. J. Watt ◽  
R. D. Thomas ◽  
P. W. Belfield ◽  
P. W. Goldstraw ◽  
S. H. Taylor

1. The effects of single oral doses of various sympatholytic drugs on the heart rate and blood pressure increases during isometric handgrip contraction were studied in six healthy subjects. 2. Bethanidine reduced both the systolic and diastolic increases in pressure. Clonidine reduced the systolic but not the diastolic increase. Oxprenolol alone or in combination with phentolamine or phenyoxybenzamine failed to influence the pressor response. 3. The increase in systemic blood pressure associated with sustained contraction of voluntary muscle appears to be relatively resistant to acute sympathetic adrenoreceptor blockade in man.


2004 ◽  
Vol 286 (5) ◽  
pp. R851-R856 ◽  
Author(s):  
Christoph Schroeder ◽  
Frauke Adams ◽  
Michael Boschmann ◽  
Jens Tank ◽  
Sebastian Haertter ◽  
...  

Norepinephrine transporter (NET) function has a central role in the regulation of synaptic norepinephrine concentrations. Clinical observations in orthostatic intolerance patients suggest a gender difference in NET function. We compared the cardiovascular response to selective NET inhibition with reboxetine between 12 healthy men and 12 age-matched women. Finger blood pressure, brachial blood pressure, and heart rate were measured. The subjects underwent cardiovascular autonomic reflex testing and a graded head-up tilt test. In a separate study, we applied incremental concentrations of tyramine and isoproterenol through subcutaneous microdialysis catheters in eight men and in eight women. NET inhibition elicited a threefold greater increase in supine blood pressure in men than women ( P < 0.05). The pressor response was driven by an increased cardiac output. The orthostatic heart rate increase during NET inhibition was greater in men than women (56 ± 5 beats/min in men, 42 ± 4 beats/min in women, P < 0.001). In contrast, NET inhibition resulted in a similar suppression in the cold pressor and handgrip response, low-frequency blood pressure oscillations, and venous norepinephrine in the supine position. Men and women were similarly sensitive to the lipolytic effect of isoproterenol and tyramine. We conclude that NET inhibition results in more pronounced changes in cardiac regulation in men than women. Our observations suggest that the NET contribution to cardiac norepinephrine turnover may be decreased in women. The gender difference in NET function may not be expressed in tissues that are less NET dependent than the heart.


1997 ◽  
Vol 272 (5) ◽  
pp. R1588-R1594 ◽  
Author(s):  
D. C. Hatton ◽  
V. Brooks ◽  
Y. Qi ◽  
D. A. McCarron

Borderline hypertensive rats (BHR) were used to test the hypothesis that baroreflex resetting prevents a fall in blood pressure (BP) when cardiac output (CO) is reduced during air-jet stress. Eight-week-old BHR were instrumented with flow probes around the ascending aorta for measuring CO, femoral and jugular catheters were inserted for measurement of arterial pressure and infusion of drugs, and sinoaortic baroreceptors were either denervated (SAD) or left intact. Alternating bolus injections of phenylephrine and sodium nitroprusside were given at baseline and during air-jet stress to assess the baroreflex. Air-jet stress immediately shifted the midpoint of the baroreflex curve for heart rate (HR) to a higher BP levels. When metoprolol was administered during air-jet stress, HR was reduced and CO reverted to prestress levels, but the stress-induced pressor response was not changed. In SAD BHR, air-jet stress caused an elevation of BP that was not different from intact rats. Administration of metoprolol to SAD rats during air-jet stress resulted in a further elevation rather than a reduction in BP. We conclude that the sinoaortic cardiac baroreflex is reset during air-jet stress and that it integrates reflex changes in BP during stress. The arterial baroreflex is not, however, necessary for the initiation or maintenance of the pressor response during stress, nor does it prevent a fall in BP when CO is compromised during stress.


Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 524-531 ◽  
Author(s):  
John D. O’Connor ◽  
Matthew D. L. O’Connell ◽  
Hugh Nolan ◽  
Louise Newman ◽  
Silvin P. Knight ◽  
...  

Assessment of the cerebrovascular and cardiovascular response to standing has prognostic value for a range of outcomes in the older adult population. Studies generally attempt to control for standing speed differences by asking participants to stand in a specified time but little is known about the range of transition times observed. This study aimed to characterize how standing speed associates with cardiovascular and cerebrovascular measures following transition from supine to standing. Continuous cerebral oxygenation, heart rate, systolic and diastolic blood pressure were monitored for 3 minutes after transitioning from supine to standing. An algorithm was used to calculate the time taken to transition from existing Finometer data (from the height correction unit). Linear mixed-effects models were used to assess the influence of transition time on each of the signals while adjusting for covariates. Transition time ranged from 2 to 27 s with 17% of participants taking >10 s to stand. Faster transition was associated with a more extreme decrease 10 s after standing but improved recovery at 20 s for cerebral oxygenation and blood pressure. Standing faster was associated with an elevated heart rate on initiation of stand and a quicker recovery 10 to 20 s after standing. The speed of transitioning from supine to standing position is associated with cardiovascular and cerebrovascular response in the early period after standing (<40 s). Care should be taken in the interpretation of findings which may be confounded by standing speed and statistical adjustment for standing time should be applied where appropriate.


1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


Entropy ◽  
2018 ◽  
Vol 20 (11) ◽  
pp. 860 ◽  
Author(s):  
Marcos Hortelano ◽  
Richard Reilly ◽  
Francisco Castells ◽  
Raquel Cervigón

Orthostatic intolerance syndrome occurs when the autonomic nervous system is incapacitated and fails to respond to the demands associated with the upright position. Assessing this syndrome among the elderly population is important in order to prevent falls. However, this problem is still challenging. The goal of this work was to determine the relationship between orthostatic intolerance (OI) and the cardiovascular response to exercise from the analysis of heart rate and blood pressure. More specifically, the behavior of these cardiovascular variables was evaluated in terms of refined composite multiscale fuzzy entropy (RCMFE), measured at different scales. The dataset was composed by 65 older subjects, 44.6% (n = 29) were OI symptomatic and 55.4% (n = 36) were not. Insignificant differences were found in age and gender between symptomatic and asymptomatic OI participants. When heart rate was evaluated, higher differences between groups were observed during the recovery period immediately after exercise. With respect to the blood pressure and other hemodynamic parameters, most significant results were obtained in the post-exercise stage. In any case, the symptomatic OI group exhibited higher irregularity in the measured parameters, as higher RCMFE levels in all time scales were obtained. This information could be very helpful for a better understanding of cardiovascular instability, as well as to recognize risk factors for falls and impairment of functional status.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Ke-Vin Chang ◽  
Wen-Shiang Chen ◽  
Ruey-Meei Wu ◽  
Ssu-Yuan Chen ◽  
Hsiu-Yu Shen ◽  
...  

The study aim was to assess sympathetic vasomotor response (SVR) by using pulsed wave Doppler (PWD) ultrasound in patients with multiple system atrophy (MSA) and correlate with the tilt table study. We recruited 18 male patients and 10 healthy men as controls. The SVR of the radial artery was evaluated by PWD, using inspiratory cough as a provocative maneuver. The response to head-up tilt was studied by a tilt table with simultaneous heart rate and blood pressure recording. The hemodynamic variables were compared between groups, and were examined by correlation analysis. Regarding SVR, MSA patients exhibited a prolonged latency and less heart rate acceleration following inspiratory cough. Compared with the tilt table test, the elevation of heart rate upon SVR was positively correlated to the increase of heart rate after head-up tilt. The correlation analysis indicated that the magnitude of blood pressure drop from supine to upright was positively associated with the SVR latency but negatively correlated with the heart rate changes upon SVR. The present study demonstrated that blunted heart rate response might explain MSA's vulnerability to postural challenge. PWD may be used to predict cardiovascular response to orthostatic stress upon head-up tilt in MSA patients.


1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.


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