Cardiovascular responses to three simple, provocative tests of autonomic activity in sleeping infants

2001 ◽  
Vol 91 (2) ◽  
pp. 561-568 ◽  
Author(s):  
C. Harrington ◽  
T. Kirjavainen ◽  
A. Teng ◽  
C. E. Sullivan
Keyword(s):  
Blood Pressure ◽  
Slow Wave Sleep ◽  
Blood Pressure Response ◽  
Cardiovascular Responses ◽  
Sudden Infant Death ◽  
Autonomic Control ◽  
Sudden Infant ◽  
Measure Blood Pressure ◽  
Cold Face Test ◽  
Postural Challenge

Whereas defective cardiovascular autonomic control has been implicated in the sudden infant death syndrome, relatively little is known about the normal development of autonomic control, due to the inability to measure blood pressure in infants noninvasively. We studied 12 normal infants [age: 13 ± 2 (SD) wk] using a noninvasive method of continuous blood pressure recording and examined the cardiovascular responses to 45° head-up tilting, a modified cold face test, and a loud noise. In head-up tilting, in both slow-wave sleep and rapid eye movement sleep, all infants displayed a rapid biphasic heart rate response (mean increase of 16% and mean decrease of 21%) and blood pressure response (mean increase of 16% and mean decrease of 16%), with a return to pretest values within 20 s. Both ice and noise caused a less pronounced biphasic response. In conclusion, at 3 mo, infants show the adult pattern of response to postural challenge. The short latency of the response suggests that neural inputs, apart from baroreceptors, are involved in the initial phase of the response.

Abstract 15839: Effect of Serotonin Neuron Depletion on Arterial Blood Pressure Regulation in Young Rats

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Jennifer Magnusson ◽  
Kevin Cummings
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Recovery Period ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Hypoxic Conditions ◽  
Arterial Blood

Infants dying of Sudden Infant Death Syndrome (SIDS) have reduced brainstem serotonin (5-hydroxytryptamine, 5-HT) where some cases die following episodes of severe bradycardia and hypoxemia. The specific role of central 5-HT in resting arterial blood pressure (BP) and on baroreflex sensitivity during neonatal life has not been studied. In adult animals, systemic depletion of 5-HT increases BP with no effect on heart rate (HR) and reduces the sensitivity of the baroreflex. Other studies have also shown that a loss of central 5-HT beginning in embryogenesis reduces resting BP and HR in adulthood. Based on these reports, we hypothesized that loss of brainstem 5-HT neurons in the neonatal period would reduce baseline BP and HR as well as reduce baroreflex gain. To test this, we utilized 3-week old Sprague Dawley rats treated centrally with 5,7-dihydroxytryptamine (5,7-DHT, n=4; ~120 ug in saline, i.c.v.), a chemical that is toxic to serotonergic neurons. Littermate controls were injected with saline (CTRL, n=5, ~3ul, i.c.v.). We measured BP with a femoral artery catheter. HR was derived from BP. Following a recovery period, we measured resting variables for 15 minutes and then injected phenylephrine (PE; 3mg/kg s.c.) followed by sodium nitroprusside (SNP; 2.5mg/kg s.c.), separated by 15 minutes, to induce pressor or depressor responses, respectively. For both responses, baroreflex gain was calculated as the [[Unable to Display Character: &#8710;]]HR at the maximum [[Unable to Display Character: &#8710;]]BP following drug injection. We found that a loss of 5-HT neurons did not alter baseline BP (p>0.05) but did reduce baseline HR when compared to control littermates (p<0.02). 5-HT neuron deficiency tended to reduce baroreflex gain in response to PE (CTRL: -2.756 ± 0.483 beats/mmHg; 5,7-DHT: -1.499 ± 0.348 beats/mmHg; p=0.058), but not SNP (CTRL: -2.408 ± 0.351 beats/mmHg; 5,7-DHT: -3.316 ± 1.214 beats/mmHg; p>0.05). Our data indicate that brainstem 5-HT maintains resting HR, and is involved in baroreflex control of HR in response to hypertensive stimuli. Reduced brainstem 5-HT may predispose an infant to SIDS via altered autonomic control of BP and HR. The role of 5-HT in BP regulation during hypoxic conditions remains to be elucidated.

scholarly journals A reversal of fate : unravelling the role of central 5-HT in cardiorespiratory control in neonatal and adult rodents

2018 ◽  
Author(s):  
◽  
Jennifer Magnusson
Keyword(s):  
Blood Pressure ◽  
Physiological Role ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
Autonomic Tone ◽  
Neurogenic Hypertension ◽  
Cardiorespiratory Control ◽  
Arterial Blood ◽  
Lower Blood

We seek to address the extent to which a specific loss of 5-hydroxytryptamine (5-HT) affects the control of respiration, arterial blood pressure (ABP) and heart rate (HR) across vigilance-states based on existing evidence suggesting that 5-HT defects increase the risk for Sudden Infant Death Syndrome (SIDS) and neurogenic hypertension. SIDS is the leading cause of infant mortality between 1 month and 1 year of age, occurs during sleep, and up to 70% of all SIDS cases have at least one 5-HT system abnormality. Neonatal rodents lacking central 5-HT exhibit severe apneas, and a reduced ABP and HR. Central 5-HT has been implicated in the etiology of neurogenic hypertension, presumably due to projections of 5-HT neurons within the midline raphe to vagal and presympathetic regions of the brain. However, data from studies examining the specific role of central 5-HT function is conflicting or inconclusive. Neurogenic hypertension accounts for more than 90% of all hypertensive cases and the normal fall in ABP that occurs during non-rapid eye movement sleep is absent in some patients with hypertension. Understanding the mechanisms associated with the development of hypertension is critical not only to lower blood pressure, but to lower its associated cardiovascular events. The purpose of this dissertation is to examine the role of central 5-HT in the control of ABP during sleep and reveal, mechanistically, the physiological role of 5-HT in the autonomic control of ABP in neonatal and adult rodents. The overarching hypothesis for this dissertation is that central 5-HT is required for the maintenance of ABP and autonomic tone at rest in both neonatal and adult rodents.

Enhanced baroreflex-mediated inhibition of respiration after muscimol dialysis in the rostroventral medulla

2002 ◽  
Vol 92 (6) ◽  
pp. 2554-2564 ◽  
Author(s):  
Aidan K. Curran ◽  
Daniel Peraza ◽  
Cheryl A. Elinsky ◽  
J. C. Leiter
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Respiratory Activity ◽  
Sudden Infant Death ◽  
Human Infant ◽  
Sudden Infant ◽  
Facial Nucleus ◽  
Respiratory Inhibition ◽  
Before And After ◽  
Ventral Medullary Surface

The rostral ventral medulla (RVM) may be important in the control of cardiorespiratory interactions. We hypothesized that inhibition of the RVM would enhance inhibition of breathing associated with transient blood pressure elevations. In 25 piglets 3–16 days of age, we studied the effect of acutely increasing blood pressure, by systemic infusion of phenylephrine, on respiratory activity before and after inhibition of neural activity in the RVM by dialysis of 10 mM muscimol, a GABAA-receptor agonist. Muscimol dialysis through probes that were placed along the ventral medullary surface from ∼1 mm rostral to the facial nucleus to ∼0.5 mm caudal to the facial nucleus augmented the respiratory inhibition associated with acute increases in blood pressure. No similar enhancement of respiratory inhibition after phenylephrine treatment was seen in six control animals that did not receive muscimol dialysis. We conclude that the piglet RVM participates in cardiorespiratory interactions and that dysfunction of homologous regions in the human infant could lead to cardiorespiratory instability and may be involved in the pathogenesis of sudden infant death syndrome.

Hypercapnic blood pressure response is greater during the luteal phase of the menstrual cycle

1996 ◽  
Vol 81 (5) ◽  
pp. 2142-2146 ◽  
Author(s):  
N. Edwards ◽  
I. Wilcox ◽  
O. J. Polo ◽  
C. E. Sullivan
Keyword(s):  
Blood Pressure ◽  
Menstrual Cycle ◽  
Luteal Phase ◽  
Blood Pressure Response ◽  
Cardiovascular Responses ◽  
Follicular Phase ◽  
Pressure Response ◽  
Serum Progesterone ◽  
Menstrual Cycles ◽  
Blood Pressure Responses

Edwards, N., I. Wilcox, O. J. Polo, and C. E. Sullivan.Hypercapnic blood pressure response is greater during the luteal phase of the menstrual cycle. J. Appl. Physiol. 81(5): 2142–2146, 1996.—We investigated the cardiovascular responses to acute hypercapnia during the menstrual cycle. Eleven female subjects with regular menstrual cycles performed hypercapnic rebreathing tests during the follicular and luteal phases of their menstrual cycles. Ventilatory and cardiovascular variables were recorded breath by breath. Serum progesterone and estradiol were measured on each occasion. Serum progesterone was higher during the luteal [50.4 ± 9.6 (SE) nmol/l] than during the follicular phase (2.1 ± 0.7 nmol/l; P < 0.001), but serum estradiol did not differ (follicular phase, 324 ± 101 pmol/l; luteal phase, 162 ± 71 pmol/l; P = 0.61). The systolic blood pressure responses during hypercapnia were 2.0 ± 0.3 and 4.0 ± 0.5 mmHg/Torr (1 Torr = 1 mmHg rise in end-tidal [Formula: see text]) during the follicular and luteal phases, respectively, of the menstrual cycle ( P < 0.01). The diastolic blood pressure responses were 1.1 ± 0.2 and 2.1 ± 0.3 mmHg/Torr during the follicular and luteal phases, respectively ( P < 0.002). Heart rate responses did not differ during the luteal (1.7 ± 0.3 beats ⋅ min−1 ⋅ Torr−1) and follicular phases (1.4 ± 0.3 beats ⋅ min−1 ⋅ Torr−1; P = 0.59). These data demonstrate a greater pressor response during the luteal phase of the menstrual cycle that may be related to higher serum progesterone concentrations.

Cardiovascular Responses to Sustained Handgrip in Normal Subjects and in Patients with Diabetes Mellitus: A Test of Autonomic Function

1974 ◽  
Vol 46 (3) ◽  
pp. 295-306 ◽  
Author(s):  
D. J. Ewing ◽  
J. B. Irving ◽  
F. Kerr ◽  
J. A. W. Wildsmith ◽  
B. F. Clarke
Keyword(s):  
Diabetes Mellitus ◽  
Blood Pressure ◽  
Blood Pressure Response ◽  
Muscle Tension ◽  
Maximum Voluntary Contraction ◽  
Pressure Rise ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Simple Method ◽  
Patients With Diabetes

1. The blood pressure and heart rate responses to static muscular exercise were measured in sixty normal subjects and 124 patients with diabetes mellitus, aged 25–54 years, during a standardized sustained handgrip test at 30% maximum voluntary contraction (MVC). 2. The normal range of the response was established. Females had a smaller blood pressure rise than males, and their MVC was lower. In the normal subjects there was a significant correlation between the size of the MVC and the height of the blood pressure response. The absolute muscle tension exerted should be taken into account in addition to the percentage MVC, when comparing responses to sustained exercise in different disease states. 3. The diabetic subjects showed a similar sex difference in their response. The mean diastolic blood pressure rises were smaller than in the control groups, both in males and females, but this was related to a smaller mean MVC. 4. Twenty-two of the diabetic subjects had an abnormally low response to sustained handgrip, which was not related to age, duration of diabetes, treatment or control of the disease. These diabetic subjects probably had damage of the autonomic fibres mediating the response. The findings would suggest that sustained handgrip is a useful and simple method of detecting involvement of the autonomic nervous system in diabetes.

scholarly journals Augmented Hemodynamic Responses in Obese Young Men during Dynamic Exercise: Role of the Muscle Metaboreflex

2020 ◽  
Vol 17 (19) ◽  
pp. 7321
Author(s):  
Byung-Sun Lee ◽  
Kyung-Ae Kim ◽  
Jong-Kyung Kim ◽  
Hosung Nho
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Cardiovascular Responses ◽  
Normal Weight ◽  
Dynamic Exercise ◽  
Handgrip Exercise ◽  
Vascular Conductance ◽  
Post Exercise ◽  
Muscle Metaboreflex

Studies found that cardiovascular responses to exercise are enhanced in individuals with obesity and are associated with a greater cardiac output (CO) response compared to normal weight controls. However, the mechanisms underlying these altered responses during dynamic exercise are not clear. We investigated whether the cardiovascular responses mediated by the muscle metaboreflex (MMR) activation are augmented in obese men during both static and dynamic exercise. Twenty males (10 obese (OG) and 10 non-obese (NOG)) were studied. Changes in CO, mean arterial pressure (MAP), and total vascular conductance (TVC) were compared between the two groups during dynamic handgrip exercise (DHE), post-exercise muscular ischemia (PEMI), and dynamic exercise corresponding to 40%, 60% and 80% workloads. Subjects completed 2 min of DHE at 30% of MVC, followed by 2 min of PEMI. MAP, CO, and TVC responses to DHE and dynamic exercise were significantly higher in OG, whereas there were no differences during PEMI. Increases in CO and MAP during mild to heavy dynamic exercise were seen in both groups, but the changes in these variables were greater in the OG. There were no significant differences in TVC between the two groups. Compared to NOG, the augmented blood pressure response to DHE and dynamic exercise in OG was associated with a greater increase in CO. Thus, the augmented CO and MAP responses were not associated with the activation of the MMR. Consequently, additional factors specific to obesity, such as the mechanoreflex, may have been involved.

Effects of temperature on sleep in the developing rat

1998 ◽  
Vol 274 (4) ◽  
pp. R1087-R1093
Author(s):  
Roger N. Morrissette ◽  
H. Craig Heller
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Sudden Infant Death ◽  
Sudden Infant ◽  
State Structure ◽  
Rat Pups ◽  
The Relationship ◽  
Developing Rat ◽  
Wake State

In altricial species, such as humans and rats, much of the development of autonomic systems occurs postnatally. Consequently, vulnerabilities exist early in postnatal development when immature autonomic functions are challenged by external factors such as variations in ambient temperature (Ta). Ta profoundly influences sleep/wake state structure in adult animals and humans, and exposure to excessive warmth has been implicated as a risk factor in sudden infant death syndrome. To better understand the relationship between temperature and sleep during development, we investigated the effect of Ta variation on sleep/wake state structure and sleep intensity in developing rats. In this experiment, sleep intensity was measured by the intensity of slow-wave activity during slow-wave sleep. Neonatal Long-Evans hooded rat pups were surgically prepared for chronic sleep/wake state and brain temperature (Tbr) recording. Two-hour recordings of sleep/wake state and Tbr were obtained from rats on postnatal day 12( P12), P14, P16, P18, and P20 at a Ta of either 28.0–30.0, 33.0–35.0, or 38.0–40.0°C. Ta significantly influenced sleep/wake state structure but had little, if any, effect on sleep intensity in developing rats.

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