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PubMed1990

Development of baroreflex control of heart rate in swine.

The purpose of this study is to describe the developmental course of arterial baroreflex control of heart rate in swine. Tests of baroreflex function were performed with eight conscious piglets serially over their first 2 mo of life. Systemic blood pressure was raised with phenylephrine (pressor test) and lowered with nitroprusside (depressor test), and stimulus-response curves relating heart rate to mean blood pressure were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Baroreflex sensitivity decreased with increasing age. Baroreflex sensitivity was not different between pressor and depressor tests except when the piglets were greater than 52 d old and sensitivity was greater with the depressor test. The heart rates at threshold and saturation, and therefore the heart rate response range, shifted to lower heart rates with increasing age. This shift was more than can be accounted for by the simultaneously decreasing resting heart rate.

Age Factors↗
PubMed1992

Baroreflex control of heart rate in rats with heart failure after myocardial infarction: effects of captopril.

Activation of the renin-angiotensin and sympathetic nervous systems in heart failure may result in altered baroreflex control of heart rate. To determine the specific effects of treatment with captopril on baroreceptor dysfunction in heart failure, baroreflex control of heart rate was measured in conscious rats with heart failure 6 weeks after ligation of the left coronary artery. Plasma norepinephrine was measured as a reflection of sympathetic nervous system activity. After bolus injections of phenylephrine (2-50 micrograms/kg) and nitroprusside (2-50 micrograms/kg), the arterial baroreflex was analyzed by fitting percentage of mean arterial pressure changes and heart rate changes to a logistic regression function. There were no differences in baroreflex function between normal and sham-operated rats. Plasma norepinephrine was increased (P < .05) in the heart-failure rats and did not change with captopril treatment. In untreated rats, heart failure increased (P < .05) the centering point by 900%, threshold by 243% and saturation by 89%, whereas decreasing (P < .05) the operational point by 73%. There was a decrease (P < .05) in the nitroprusside-related gain and an increase (P < .05) in phenylephrine-related gain, but the overall baroreflex gain was not changed. In heart-failure rats, captopril increased (P < .05) threshold, saturation and centering point and decreased (P < .05) operational point and nitroprusside- and phenylephrine-related gain abnormalities. The increase in operational point and decreases in threshold, saturation, centering point and phenylephrine-related gain were the results of a specific interactive effect of captopril in heart failure (P = .0033, .0176, .0509, .0217 and .0567, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Role of renin-angiotensin system in the impairment of baroreflex control of heart rate in renal hypertension.

Studies of the baroreceptor heart rate reflex were performed in two-kidney, one clip (2K1C) hypertensive rats to evaluate the relative importance of two factors--high blood pressure and high angiotensin II circulating levels--on impairment of the baroreflex, present in the acute phase of this model of hypertension. The sensitivity of baroreceptor reflex was determined by the slope of the relationship between changes in mean arterial pressure (MAP) and changes in heart rate in response to injections of phenylephrine and nitroprusside. Bradycardic and tachycardic responses were analyzed separately. In basal conditions, the slope of the MAP-heart rate relationship in 2K1C hypertensive animals was significantly lower than in control animals, both for tachycardic and bradycardic responses. Lowering of blood pressure with captopril to normotensive levels in the 2K1C animals significantly increased baroreflex gain in bradycardic responses to the level found in normotensive rats. Normalization of blood pressure with nitroprusside did not change baroreflex sensitivity. Infusion of angiotensin II at a dose that did not change MAP, previously normalized with captopril, completely reverted the effect of this agent on baroreflex sensitivity. Our data indicate that, in 2K1C hypertensive rats, decreased baroreflex sensitivity is mediated, at least in part, by high angiotensin II circulating levels. Elevated blood pressure per se is of secondary importance.

Angiotensin II↗
PubMed1990

Development of the sympathetic nervous system response to endotoxicosis in the rat: importance of non-baroreflex mechanisms in pre-weanlings and adults.

The sympathetic nervous system response to endotoxicosis was studied in the rat at ages before (11-12 days) and after (19-20 days) maturation of the baroreflex and in adults by recording preganglionic impulses during i.v. infusions of endotoxin (S. enteriditis). At all ages, the discharge rate increased before there was any decrease in arterial blood pressure. The magnitude of the increase (65%) was the same in 11-12 days-old and adult rats while 19-20 days-old rats were hyperactive (278% increase). Subsequently, in the hypotensive phase of the endotoxicosis (diastolic pressure decrease 50-60%) there was an additional increase in discharge in the 19-20 days- old rats (43% and in adults (70%) but not in 11-12 days-old rats. The hypotensive discharge rate of the 11-12 days-old rat reached only 20% of the maximum; it reached 80% in the hyperactive 19-20 days-old rat and 65% in adults. At all ages, the elevated hypotensive discharge rate persisted after steady state blood pressure was raised by infusing dextran. The discharge rate was diminished transiently during pressor responses to accelerated infusion or bolus injections of dextran. The conclusions are: (i) endotoxic stimulation of sympathetic outflow is initiated by a non-baroreflex mechanism in adult as well as in pre-weaning rats; (ii) there is added stimulation during hypotension after the baroreflex is mature, but (iii) the non-baroreflex stimulation continues to excite the preganglionic neurons and obtunds baroreflex feedback inhibition.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1991

Baroreflex responsiveness during hypobaric hypoxia.

Baroreflex responses to graded neck suction during held expiration were studied in five healthy females at sea level and at a simulated altitude of 4,572 m (15,000 ft), with and without oxygen administration. An apparent resetting of the baroreflex was observed during hypobaric hypoxia, but this effect was abolished by oxygen administration. Held expiration alone induced a pulse prolongation in all experimental conditions, however this bradycardiac response was smaller during hypobaric hypoxia than during the two normoxic conditions. When the bradycardic responses of held expiration were subtracted, the baroreflex responses to neck suction were equal in all experimental situations. Similarly, the baroreflex was unaffected by hypobaric hypoxia when the R-R interval prolongations were expressed in percentage of the R-R intervals immediately prior to the neck suction. These data indicate that reduced ambient pressure per se has no influence on the carotid baroreflex control of heart rate.

Adult↗
PubMed1990

Endurance training alters arterial baroreflex function in dogs.

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.

Animals↗
PubMed1989

[Arterial baroreflex in the renal hypertensive rabbits].

In 14 anesthetized male rabbits subjected bilateral renal wrapping 12 weeks before, the baroreflex control of heart rate (HR), hindlimb vascular resistance (HVR) and renal sympathetic nerve activity (RSNA) was examined during arterial baroreceptor loading and unloading by injecting phenylephrine (PE) and nitroprusside (NP). The results were as follows: (1) The mean arterial pressure (131 +/- 9 mmHg) of the kidney-wrapped rabbits was significantly higher than that (95 +/- 10 mmHg) of the control rabbits (P less than 0.001). (2) With the buffer nerves intact, the baroreflex control of HR was obviously impaired in the hypertensive rabbits (P less than 0.01), whereas the reflex control of HVR and RSNA remained unchanged as compared with the normotensive rabbits (P greater than 0.05), indicating a dissociation of baroreflex control of HR from that of peripheral circulation. However, in response to local intraarterial injection of PE and NP, the changes in HVR showed no difference between the hypertensive and normotensive rabbits. (3) After aortic or carotid baroreceptor denervation, the reflex control of HR was further reduced in the hypertensive rabbits, and the reflex control of HVR and RSNA was also significantly reduced (P less than 0.01), suggesting an impairment of potential baroreflex regulation of the circulation. It is likely that the changes of baroreflex in hypertensive rabbits may be attributed to the abnormalities in both baroreceptor and central integrating mechanism.

Animals↗
PubMed1989

Effects of propofol on baroreflex control of heart rate and on plasma noradrenaline levels.

The effects of propofol induction (2.5 mg kg-1) and of two continuous infusion rates of propofol (100 and 200 micrograms kg-1 min-1) on baroreflex control of heart rate and on plasma noradrenaline concentration were investigated in 11 unpremedicated patients. Baroreflex function was assessed using a pressor test (phenylephrine) and a depressor test (sodium nitroprusside). In addition, samples for subsequent determination of plasma noradrenaline levels and blood propofol levels were collected before each test. Baroreflex sensitivity and plasma noradrenaline concentrations were not significantly changed at any time of the study. By contrast, a significant and sustained resetting of baroreflex set point was observed, allowing unchanged heart rate at lower arterial pressure. It is concluded that the effects of propofol on baroreflex function and noradrenaline concentration are moderate.

Adult↗
PubMed1985

Relationship between carotid baroreflex sensitivity, physical fitness and activity in cyclists.

Carotid baroreceptors were stimulated with neck suction in 24 cycling tourists and pulse interval lengthening was measured. Eight intensities of neck chamber suction were applied to select a criterion for computing the RR response that gives a significant linear relationship with the magnitude of the stimuli in the highest number of individuals. The best criterion was the maximal RR prolongation within 5 s after the onset of the stimulus. The slope of this relationship was defined as baroreflex sensitivity. Baroreflex sensitivity averaged 7.3 +/- 0.8 ms/mmHg. The cycling tourists underwent an exercise test on a bicycle ergometer until exhaustion, and oxygen uptake, pulmonary ventilation, peak heart rate and exercise duration were determined. In single and multiple regression analysis, baroreflex sensitivity was not significantly related to basal heart rate, peak oxygen uptake and ventilation, duration of exercise or other training characteristics. The results suggest that in man the so-called sensitivity of the carotid baroreflex control of heart rate is not influenced by the level of physical fitness and therefore the measurement of these characteristics can be neglected in evaluating baroreflex sensitivity.

Adolescent↗
PubMed1988

Fentanyl-diazepam anesthesia with or without N2O does not attenuate cardiopulmonary baroreflex-mediated vasoconstrictor responses to controlled hypovolemia in humans.

Cardiopulmonary baroreceptors located primarily on the low-pressure side of the circulation sense slight reductions in cardiac filling pressures and elicit sustained peripheral vasoconstriction. Because most inhalation and many intravenous anesthetics attenuate arterial baroreflex function, the low-pressure baroreflex may serve a major role in maintaining blood pressure during intraoperative hypovolemia. To activate the low-pressure baroreflex, progressive nonhypotensive reductions in central venous pressure were produced with graded applications of lower body negative pressure (LBNP, -5, -10, -15 mm Hg) in 18 ASA class I patients before elective surgery. This produced linear reductions in stroke volume as determined by impedance cardiography and cardiac output. Cardiopulmonary baroreflex-mediated increases in total and forearm vascular resistance assisted in maintaining stable blood pressure. After ten patients were anesthetized with fentanyl (12.5 micrograms/kg) and diazepam (0.25 mg/kg) and an additional eight received these agents plus supplemental N2O (70%), reflex vasoconstrictor responses to LBNP were not attenuated and, therefore, blood pressure continued to be well maintained despite substantial reductions in cardiac filling pressures. Thus, these anesthetic regimens preserved vasoconstrictor responses mediated by cardiopulmonary baroreflexes. This promoted cardiovascular stability that may be particularly beneficial in patients with cerebral, cardiovascular, or renal disease undergoing surgical procedures with potential for rapid blood loss.

Adult↗
PubMed1985

Subtle cardiac autonomic impairment in Chagas' disease detected by baroreflex sensitivity testing.

The sensitivity of baroreflex bradycardia and tachycardia was determined in fourteen patients with Chagas' disease who seemed to be normal with respect to cardiac autonomic control evaluated in terms of heart rate responses to the conventional atropinization and Valsalva maneuver tests. Eleven normal subjects were studied for comparison. Baroreflex sensitivity was determined by relating the beat-to-beat pulse intervals to systolic pressure values during transient phenylephrine- and amyl nitrite-induced changes in arterial pressure. Chagasic patients showed mean bradycardia sensitivity (10.1 +/- 1.3 ms/mmHg) which was significantly lower than that obtained for the control group (16.7 +/- 2.1 ms/mmHg). When only the subgroup of ten patients with overt disease (cardiac and/or digestive form) was considered, the value fell to 8.6 +/- 1.4 ms/mmHg. The lowest individual values were exhibited by the majority of patients with exclusive cardiac or associated cardiac and digestive disease. Patients with only digestive disease or without overt disease (indeterminate form) had values within the normal range. Tachycardia sensitivity (6.3 +/- 0.8 ms/mmHg) was similar to that obtained for the control group (6.6 +/- 1.0 ms/mmHg). Only one patient with associated disease presented a reduced value. These data show that the estimation of baroreflex sensitivity can be used to identify impaired cardiac autonomic control in chronic Chagas' disease not detectable by conventional tests. The reduced baroreflex sensitivity appears to be due to the subtle impairment of the parasympathetic influence on the heart. Furthermore, there is a relationship between the degree of baroreflex sensitivity and the clinical form of organic involvement in Chagas' disease.

Adult↗
PubMed1985

Acute and chronic effects of the loop diuretic, piretanide, on baroreflex set point and sensitivity in hypertensive man.

Intra-arterial blood pressure (IABP), baroreflex sensitivity and set point were measured in nine patients with essential hypertension during a control period and then after acute (4 h after a 12 mg oral dose) and chronic (after 3 months) treatment with the loop diuretic piretanide, mean dose 10 mg. Acutely, there was a fall in mean systolic IABP (P less than 0.05) associated with a reduction in pulse interval (P less than 0.01). Chronically, mean systolic IABP remained significantly reduced (P less than 0.01) but pulse interval returned to control values. There were no significant changes in baroreflex sensitivity, either acutely or chronically. These results demonstrate acute deactivation of the vagal efferent limb of the baroreflex followed by a chronic resetting of the baroreflex-heart rate mechanism. We conclude that changes in baroreflex sensitivity are not responsible for the hypotensive effects of this drug and that resetting of the reflex arc is likely to be due to physiological adaptation rather than to any direct drug effect.

Adult↗
PubMed1995

Non-invasive ambulatory blood pressure variability and cardiac baroreflex sensitivity.

AIM: The objective of this study was to evaluate the relationship between non-invasive ambulatory blood pressure variability and cardiac baroreflex sensitivity in hypertensive patients. SUBJECTS AND METHODS: Ambulatory blood pressure measurements (15-min intervals for 24 h) and continuous blood pressure measurements (Finapres, 20 min at rest after a 10-min resting period) were performed in 123 untreated hypertensives (resting diastolic blood pressure > or = 90 mmHg; 80 males, 43 females; mean +/- SD age 49 +/- 12 years, range 19-73). Fourier series were used to model 24-h blood pressure profiles (four harmonics). Ambulatory blood pressure variability was assessed by determination of the residuals in each 24-h blood pressure profile (measured minus predicted pressures). Resting blood pressure variability was defined as the SD of the mean Finapres value. Baroreflex sensitivity was evaluated by automatic detection of blood pressure and pulse interval sequences of > or = 3 beats when systolic blood pressure and pulse interval sequences changed in the same direction (increase or decrease: 1 mmHg for systolic blood pressure and 4 ms for RR interval), and was assessed as the slope of the regression line for each sequence. RESULTS: Ambulatory systolic blood pressure variability increased with age (r = 0.28*) and systolic pressure (r = 0.44**). Baroreflex sensitivity (increasing systolic pressure/pulse interval) decreased significantly with age (r = -0.48**) and systolic pressure (r = -0.23**), and was significantly related to increased ambulatory blood pressure variability (r = -0.33**). In a multivariate stepwise analysis the relationship between ambulatory blood pressure variability and baroreflex sensitivity (increasing systolic pressure/pulse interval) was statistically independent of age and systolic pressure (R = 0.55, P<0.001); this relationship was not observed with the corresponding decreasing sequence. CONCLUSIONS: This study shows that in uncomplicated hypertension, ambulatory blood pressure variability is related to baroreflex sensitivity independently of the blood pressure level. This finding has prognostic implications for this non-invasive measurement, which needs to be confirmed by large longitudinal studies.

Adult↗
PubMed1998

Clonidine premedication modifies responses to adrenoceptor agonists and baroreflex sensitivity.

PURPOSE: To evaluate the effects of clonidine on responses to adrenoceptor agonists and baroreflex sensitivity, we examined arterial blood pressure (AP) responses to phenylephrine and heart rate (HR) responses to isoproterenol and baroreflex sensitivity (HR response to AP changes due to phenylephrine or nitroglycerin). METHODS: We studied 60 anaesthetized patients who either did or did not receive 5 micrograms.kg-1 clonidine po before they were anaesthetized. After induction of general anaesthesia, the patients received 3 micrograms.kg-1 phenylephrine, 0.02 microgram.kg-1 isoproterenol, or 2-3 micrograms.kg-1 nitroglycerin, and haemodynamic measurements were taken. Baroreflex sensitivity was expressed as the slope of the linear regression line (msec.mmHg-1; in msec of R-R interval change vs mmHg change in systolic arterial pressure) following the administration of phenylephrine and nitroglycerin. RESULTS: Patients who received clonidine had greater augmented responses in AP to phenylephrine and in HR to isoproterenol (47.2 +/- 15.6% vs 23.7 +/- 11.9% for increase in systolic AP and 59.8 +/- 22.6% vs 26.2 +/- 11.0% for increase in HR, P < 0.05 respectively). There were no differences between the baroreflex sensitivities in the pressor (phenylephrine) test groups (3.77 +/- 1.08 vs 4.41 +/- 1.66 msec.mmHg-1). In contrast, the slopes of depressor (nitroglycerin) test groups were decreased in patients receiving clonidine (1.98 +/- 0.73 vs 3.68 +/- 1.72 msec.mmHg-1, P < 0.05). CONCLUSION: The results suggest that premedication with clonidine might enhance critical hypotension during anaesthesia and surgery, but restoration both of AP and HR decrease can be achieved effectively by phenylephrine and isoproterenol i.v., respectively.

Adrenergic alpha-Agonists↗
PubMed2006

Impaired baroreflex function in temporal lobe epilepsy.

Changes of cardiovascular function are frequent in temporal lobe epilepsy (TLE). The baroreflex - the most important reflex for cardiovascular stability - has not been studied systematically in TLE. We evaluated cardiovascular variability and baroreflex function in TLE. In 22 TLE patients and 20 controls, we continuously monitored heart rate (HR) and blood pressure (BP). Time-domain parameters were derived from recordings at rest and from standard cardiovascular reflex tests. Spectral analysis determined sympathetic and parasympathetic modulation of HR and BP in the low (LF-power) and high frequency range (HF-power). We calculated the relative LF- and HF-powers of HR in relation to the sum of LF- and HF-powers. LF/HF-ratio of HR was assessed as a parameter of sympatheticovagal balance. LF-transfer function gain between BP and HR determined baroreflex function.Time-domain parameters did not differ between TLE patients and controls. Spectral analysis showed decreased absolute LF- and HF-powers but increased relative LF-power and LF/HF-ratio of HR in TLE. LF-transfer function gain between BP and HR was reduced in TLE (p<0.05). The reduction of absolute LF- and HF-powers indicates decreased total autonomic variability in TLE. However, increased relative LF-power and LF/HF-ratio of HR in TLE show a relative increase of sympathetic tone. Most importantly, we demonstrate an impaired baroreflex function in TLE. These cardiovascular autonomic abnormalities may contribute to cardiac arrhythmia in TLE.

Adult↗
PubMed2004

Strength training does not affect vagal-cardiac control or cardiovagal baroreflex sensitivity in young healthy subjects.

The purpose of this study was to test the hypothesis that high-intensity strength training increases vagal-cardiac control and cardiovagal baroreflex sensitivity. Twenty-two subjects [age 22 (0.8) years] were assigned to either strength training (ST, n=12) or control (CON, n=10) groups. Subjects in the ST group trained each major muscle group 3 days per week for 8 weeks with three sets of 10 repetitions and 2-min rest periods. Resistance was increased progressively when possible. Subjects in the CON group were active recreationally but did not lift weights. Before and after training, resting arterial pressure was measured with an automated sphygmomanometer, and ECG, respiratory rate, and finger photoplethysmographic arterial pressures were recorded with subjects supine and breathing at a set rate (0.25 Hz) for 5 min. Data were analyzed in both time and frequency domains. Arterial baroreflex sensitivity was estimated with the sequence method and cross-spectral transfer function analysis of systolic pressures and R-R intervals. Training increased whole-body muscular strength and decreased arterial blood pressure at rest (the exercise and pressure data have been published elsewhere). R-R intervals and standard deviations, and R-R interval spectral power at the respiratory frequency were unaffected by training. Similarly, training did not affect respiratory or low-frequency systolic pressure spectral power or cardiovagal baroreflex sensitivity. Although evidence supports beneficial cardiovascular adaptations to resistance training, our results demonstrate that resistance training does not affect vagal-cardiac control or cardiovagal baroreflex sensitivity in young healthy subjects.

Adaptation, Physiological↗
PubMed2005

Abnormal heart rate and blood pressure responses to baroreflex stimulation in multiple sclerosis patients.

Cardiovascular autonomic neuropathy has been previously reported in patients with multiple sclerosis (MS) using standard reflex tests. However, no study has separately evaluated both parasympathetic and sympathetic cardiovascular autonomic regulation. We therefore assessed the baroreflex-mediated vagal and sympathetic control of the heart rate and sympathetic control of the blood vessels in MS patients using sinusoidal neck stimulation. We studied 13 multiple sclerosis patients aged 28-58 years and 18 healthy controls aged 26-58 years. The carotid baroreflex was stimulated by sinusoidal neck suction (0 to -30 mmHg) at 0.1 Hz to assess the autonomic control of the heart and blood vessels, and at 0.2 Hz to assess the vagal control of the heart. Continuous recordings were made of blood pressure, electrocardiographic RR-interval and respiration, with breathing paced at 0.25 Hz. Spectral analysis was used to evaluate the magnitude of the low frequency (LF, 0.03-0.14 Hz) and high frequency (HF, 0.15-0.50 Hz) oscillations in RR-interval and blood pressure in response to the sinusoidal baroreceptor stimulation. Responses to the applied stimulus were assessed as the change in the spectral power of the RR-interval and blood pressure fluctuations at the stimulating frequency from the baseline values. The increase in the power of 0.1 Hz RR-interval oscillations during the 0.1 Hz neck suction was significantly smaller (p<0.01) in the MS patients (4.47+/-0.27 to 5.62+/-0.25 ln ms(2)) than in the controls (4.12+/-0.37 to 6.82+/-0.33 ln ms(2)). The increase in the power of 0.1 Hz systolic BP oscillations during 0.1 Hz neck suction was also significantly smaller (p<0.01) in the MS patients (0.99+/-0.19 to 1.96+/-0.39 mmHg(2)) than in the healthy controls (1.27+/-0.34 to 9.01+/-4.10 mmHg(2)). Neck suction at 0.2 Hz induced RR-interval oscillations at 0.2 Hz that were significantly smaller (p<0.05) in the patients (3.22+/-0.45 ln ms(2)) than in the controls (5.27+/-0.29 ln ms(2)). These results indicate that in MS patients, baroreflex dysfunction is not only restricted to the cardiovagal limb of the baroreflex, but that the sympathetic modulation of the blood vessels is also affected.

Adult↗
PubMed1994

Baroreflex function during 45-degree passive head-up tilt before and after long-term thiazide therapy in the elderly with systolic systemic hypertension.

The ratio of the 30th to the 15th cardiac cycle duration on an electrocardiogram (30:15 ratio) immediately after active standing from the supine position has been used as one of the markers of baroreflex function. A ratio of < or = 1.0 has been suggested to indicate baroreflex dysfunction. Blood pressure (BP) changes were measured and the 30:15 ratio was calculated after standing and during 45-degree passive head-up tilt from the supine position in 10 nondiabetic men (mean age +/- SE 70.1 +/- 1.05 years, and BP < 150/90 mm Hg). After tilt the decrease in systolic BP (from 132 +/- 4.8 to 117 +/- 6.3 mm Hg; p < 0.001) appeared to be larger than that after standing (from 132 +/- 4.6 to 123 +/- 5.8 mm Hg; p < 0.01), whereas the 30:15 ratios were 0.965 +/- 0.006 and 0.970 +/- 0.014, respectively, which suggested baroreflex dysfunction. Although the mean of the 2 ratios did not differ, the variance appeared to be less during tilting than after standing. Thus, the 45-degree passive head-up tilt appeared to be a better and more uniform inducer of orthostatic stress than active standing. Therefore, 45-degree head-up tilt was used in a group of 10 nondiabetic male patients (aged 70 +/- 1.46 years) with isolated systolic hypertension (systolic BP > 160 mm Hg, diastolic BP of < 90 mm Hg) to assess their baroreflex function. Upon tilting, their systolic BP decreased from 190 +/- 5.5 to 179 +/- 5.8 mm Hg (p < 0.05) and their 30:15 ratio was 0.985 +/- 0.011.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗