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J L Elghozi

Publications and source records attributed to J L Elghozi.

At least 19 recordsLinked to original sources
PubMed1999

Beneficial effect of renin-angiotensin system for maintaining blood pressure control following subarachnoid haemorrhage.

Subarachnoid haemorrhage is a serious condition often accompanied by delayed cerebral ischaemia. Earlier reports have provided evidence suggesting a role for angiotensin II in the development of cerebral vasospasm following subarachnoid bleeding. We sought to examine the influence of angiotensin II blockade with losartan on blood pressure and survival in animals following experimental subarachnoid haemorrhage, induced in conscious rats by injecting homologous blood via a catheter placed along the surface of the brain. We combined measurements of plasma renin activity with blood pressure recording in order to examine renin-angiotensin system activation following experimental subarachnoid haemorrhage. Following subarachnoid injury an approximately three-fold increase in plasma renin activity occurred (3.4 +/- 1.0 vs. 10.1 +/- 1.8 ng angiotensin I produced/ml/h, p < 0.01). In animals treated with losartan (20 mg/kg) prior to the induction of subarachnoid haemorrhage blood pressure fell dramatically following the cerebral injury (124 +/- 5 vs. 94 +/- 7 mmHg, p < 0.001), whereas blood pressure remained unchanged in control animals. Survival was markedly reduced in those animals treated with losartan. Given the pronounced decrease in blood pressure and impaired survival following subarachnoid haemorrhage in animals treated with losartan, it would appear that the acute activation of the renin-angiotensin system following this insult is in fact a desirable, compensatory response.

Animals↗
PubMed1999

Short-term variability of blood pressure and heart rate in Guillain-Barré syndrome without respiratory failure.

The effect of Guillain-Barré syndrome (GBS) on the short-term variability of blood pressure and heart rate was evaluated in six patients presenting with a moderate form of the syndrome, i.e. unable to stand up unaided and without respiratory failure, at the height of the disease and during recovery. The patients were compared with six age-matched healthy volunteers. During the acute phase of the syndrome, GBS patients exhibited a significant heart rate elevation (+26 beats/min compared with healthy subjects), but the acceleratory response to atropine, or to 60 degrees head-up tilt, was maintained. Resting plasma noradrenaline levels were high in acute GBS, but the secretory response to tilt was preserved. Desensitization to noradrenaline was observed in acute GBS with a reduced pressor action of this alpha-adrenoceptor agonist. Blood pressure levels were normal and head-up tilt did not induce orthostatic hypotension in this moderate form of GBS. Power spectral analysis demonstrated marked alterations in cardiovascular variability. The overall heart period variability was markedly reduced with the reduction predominantly in the high-frequency (respiratory) range (-73%). The low-frequency component of heart period variability was also reduced (-54%). This cardiovascular profile of moderate GBS at the height of the disease could result from a demyelination of the reflex loop controlling respiratory oscillations in heart rate and from a desensitization of the arterial tree to an elevated plasma noradrenaline. Sympathetic nervous activation may contribute to the high resting heart rate in acute GBS.

Acute Disease↗
PubMed1999

[Cardiovascular responses to a acoustic startle stimulus in man].

OBJECTIVE: To describe the effects of an auditory startle stimulus on blood pressure (BP) and heart rate (HR) in man. Three sound levels were tested. DESIGN AND METHODS: Twelve normotensive volunteers were studied in supine position. Polygraphic recordings were obtained for finger BP, R-R interval using an electrocardiograph, respiratory movements using a thoracoabdominal belt and for electrooculomyogram using adhesive electrodes. A background noise of 55 dB was administered through headphones and the acoustic startle was generated using 3 synthetized white noises of 95, 110 or 120 dB administered at 5-min intervals during the tele-expiratory phase in a randomized order. Noise duration was fixed to 150 msec. The sham stimulation (0 dB, event marker) was compared to the 3 levels of noise (one way ANOVA with repeated measures followed by multiple comparisons). Confidence intervals (95%) were calculated for BP and HR using the 30 sec period preceding each stimulation to obtain individual significance of the responses for the 30 sec following each stimulation. RESULTS: A biphasic cardiovascular profile was observed following noise stimulation. The early response (0-10 sec) observed after the immediate motor contraction (blink) combined BP and HR increases. The average systolic BP rise was 15.9 +/- 2.6 mmHg (peak at 4.8 sec) and the average HR increase was 11.9 +/- 1.6 bpm (peak at 2.8 sec) for the 110 dB noise. These effects were highly significant compared to the sham response (P < 0.001). This 110 dB intensity determined 44% of significant systolic BP values and 25% significant HR values during this early period. Similar profiles were obtained with 95 and 120 dB with a lesser amplitude. The delayed response (10-30 sec) combined moderate BP and HR decreases. CONCLUSION: This is the first description of the BP response to an acute loud noise in man. The early (within 10 sec) BP and HR rises may depend upon the autonomic component of the startle reflex. The reproducibility of this cardiovascular profile obtained with a 110 dB white noise makes this test applicable to the clinical trials of antihypertensive drugs.

Acoustic Stimulation↗
PubMed1999

Pulse rate variability is not a surrogate for heart rate variability.

To investigate the differences between heart rate (HR) variability and pulse rate (PR) variability, short-term variability of finger pulse wave and ECG signals were studied in 10 children with a fixed ventricular pacemaker rhythm (80 beats/min). Ten healthy children in sinus rhythm served as a reference population. Distal PR and HR were measured continuously using a Finapres device and an ECG respectively. Power spectra for HR and PR were calculated in both the supine and orthostatic positions. In paced subjects, PR spectra exhibited the characteristic respiratory peak, although the HR spectra were flat. Similarly, in healthy children the respiratory fluctuations were more pronounced when calculated from the finger pulse wave signal compared with the ECG signal. The overestimation of HR respiratory fluctuation resulting from distal PR measurement was more pronounced in the standing position; however, this postural effect was demonstrated only in healthy subjects. We observed mechanical respiratory modulation of distal PR independent of classical HR modulations. Our results suggest a mechanical respiratory influence via cardiac output and aortic transmural pressure changes on pulse wave velocity. We conclude that respiratory PR variability does not precisely reflect respiratory HR variability in standing healthy subjects and in patients with low HR variability. Consequently, HR modulation should be studied using the ECG signal rather than the distal pulse wave signal. However, when ECG recording is not available, the distal pulse wave is an acceptable alternative.

Adolescent↗
PubMed1998

Contribution of the autonomic nervous system to blood pressure and heart rate variability changes in early experimental hyperthyroidism.

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous system activity and thyroid hormones in the control of heart rate and blood pressure. We now report on thyrotoxicosis produced by daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt. in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvent. In order to estimate the degree of autonomic activation in hyperthyroidism, specific blockers were administered intravenously: atropine (0.5 mg/kg), prazosin (1 mg/kg), atenolol (1 mg/kg) or the combination of atenolol and atropine. A jet of air was administered in other animals to induce sympathoactivation. Eight animals were studied in each group. The dose and duration of L-thyroxine treatment was sufficient to induce a significant degree of hyperthyroidism with accompanying tachycardia, systolic blood pressure elevation, increased pulse pressure, cardiac hypertrophy, weight loss, tachypnea and hyperthermia. In addition, the intrinsic heart period observed after double blockade (atenolol + atropine) was markedly decreased after treatment with L-thyroxine (121.5+/-3.6 ms vs. 141.2+/-3.7 ms, P < 0.01). Of the autonomic indices, vagal tone (difference between heart period obtained after atenolol and intrinsic heart period) was negatively linearly related to intrinsic heart period (r = 0.71, P < 0.05). Atenolol modified neither the heart period nor blood pressure variability in rats with hyperthyroidism and in these rats the jet of air did not significantly affect the heart period level. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of blood pressure variability (analyses on 102.4 s segments, modulus 1.10+/-0.07 vs. 1.41+/-0.06 mm Hg, P < 0.01) and prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic heart rate could be the main determinant of tachycardia. The blood pressure elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Adrenergic alpha-Antagonists↗
PubMed1998

Short-term variability of blood pressure and heart rate in hyperthyroidism.

The effect of hyperthyroidism on the short-term memory variability of blood pressure and heart rate was evaluated in 12 untreated hyperthyroid patients during thyrotoxicosis and after a 6 1/2 month treatment designed to achieve a stable euthyroid state. Beat-by-beat finger blood pressure was measured with a Finapres device. The pulse interval, from which pulse rate was derived, was obtained from the blood pressure signal. Due to the significant change in heart rhythm associated with thyrotoxicosis, both pulse interval (taken as a surrogate of heart period) and pulse rate (taken as a surrogate of heart rate) were computed. Power spectral analysis showed a reduction in the overall heart period variability in the supine position in the hyperthyroid compared to the euthyroid state. This effect was observed in the low-frequency (0.005-0.068 Hz), mid-frequency (0.068-0.127 Hz) and high-frequency (respiratory) domains as well, with a significant reduction of the modulus of these bands of 31%, 35% and 47%, respectively. The heart rate spectral modulus also exhibited a reduction of the high-frequency component (31%) in the supine position in the hyperthyroid subjects. These changes in heart rhythmicity corroborate a vagal deficit in hyperthyroidism. In addition, blood pressure spectral power exhibited a significant deficit in the orthostatism-induced mid-frequency systolic blood pressure rise in the hyperthyroid state (64%) compared with the euthyroid state. This observation may reflect a reduced vascular sympathetic activation with standing. The resulting vasodilatation could well contribute to normalize blood pressure in thyrotoxicosis in which cardiac output is increased.

Adult↗
PubMed1998

Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism.

OBJECTIVE: To study the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). DESIGN AND METHODS: Thyrotoxicosis was produced by injections of L-thyroxine (0.5 mg/kg/day for five days). Blockers were atropine (0.5 mg/kg), atenolol (1 mg/kg) or prazosin (1 mg/kg). Eight animals were studied in each group. Spectral analyses was performed using continuous BP time series obtained in conscious rats. RESULTS: Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423+/-6 vs 353+/-4 bpm, P < 0.001, unpaired Student's t test), systolic BP elevation (142+/-3 vs 127+/-2 mmHg, P < 0.001) and cardiac hypertrophy (1.165+/-0.017 vs 1.006+/-0.012 g, P < 0.001). The intrinsic HR was markedly increased after treatment with thyroxine (497+/-16 vs 373+/-10 bpm, P < 0.05). Vagal tone was positively linearly related to intrinsic HR (r = 0.84, P< 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyroidism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (modulus 1.10+/-0.07 vs 1.41+/-0.06 mmHg, P < 0.01). Prazosin was without effect on this 0.4 Hz component in hyperthyroid animals. CONCLUSIONS: These data show a functional diminution of the vascular and cardiac sympathetic tone in early experimental hyperthyroidism. The marked rise in the intrinsic HR could be the main determinant of tachycardia. The BP elevation may reflexly induce vagal activation and sympathetic (vascular and cardiac) inhibition.

Animals↗
PubMed1998

Acute effects of bisoprolol on respiratory sinus arrhythmia.

Respiratory sinus arrhythmia (RSA) is often quantified by computing the spectra of heart period (HP) or of its reciprocal heart rate (HR) at the respiratory frequency. This study was undertaken to describe the effect of an acute beta-blockade achieved with bisoprolol on RSA, obtained during a calibrated breathing (breathing frequency 0.25 Hz, tidal volume VT 500 or 700 mL) in 15 normal volunteers, using a double-blind, placebo-controlled, cross-over method. The two heart signals were computed and the RSA values were compared to the individual estimates of vagal tone obtained using an additional atropine injection. The difference between the HP (or HR) value obtained after beta-blockade and the HP (or HR) value observed following the double blockade (bisoprolol plus atropine) was taken as an index of cardiac vagal tone. Bisoprolol administration resulted in a significant reduction in HR reaching 60.3 +/- 1.4 bpm at VT of 500 mL (compared to 70.5 +/- 1.8 bpm with placebo, P < 0.001). Changes in HP were also significant with an increase in HP reaching 1004.5 +/- 22.2 msec at this controlled VT (compared to 860.3 +/- 21.5 msec with placebo, P < 0.001). Similar changes were observed at a VT of 700 mL. The relationship between RSA in bpm and vagal tone was not significant for HR while a significant positive relationship was observed between RSA in msec and vagal tone for the two respiratory patterns (r = 0.65 for a tidal volume of 500 mL, P < 0.01, and r = 0.62 for 700 mL, P < 0.05). This demonstrates that the detection of the variability effect highly depends upon the unit. The parallelism between vagal tone and RSA supports the view that the HF component of HRV in msec quantifies the vagal tone. The increased RSA during beta-blockade could well reflect this vagotonic effect of this class of drugs.

Acute-Phase Reaction↗
PubMed1998

Mechanisms of the cardiovascular deconditioning induced by tail suspension in the rat.

The aim of the present work was to obtain insights into the pathophysiology of cardiovascular deconditioning (CVD) induced by tail suspension (TS) in the rat: during TS, when central venous pressure (CVP) has been normalized (E. Martel, P. Champéroux, P. Lacolley, S. Richard, M. Safar, and J. L. Cuche. J. Appl. Physiol. 80: 1390-1396, 1996), and during simulated orthostatism (SO), when transient episodes of hypotension and bradycardia are disclosed, bradycardia with SO represents a response that seems peculiar to the rat compared with humans. According to basic physiology, a reduced activity of the sympathetic system induced by increased CVP was suspected but was not supported by data obtained through spectral analysis of blood pressure (BP) and heart rate (HR) variability or measurements of plasma catecholamine concentration during TS. Nonetheless, indirect evidence was obtained. During SO, plasma catecholamine concentration was lower in TS rats than in controls, suggesting a reduced synthesis of catecholamines, itself secondary to reduced activity of the sympathetic system. Furthermore, after 48 h of TS, the number of binding sites and affinity of alpha-receptors in rat aorta were increased, compatible with a reduced level of neurotransmitter in the synaptic cleft. A second series of experiments was carried out to study hypotension and bradycardia in TS rats during SO. Hypersensitivity of serotonergic mechanisms was suspected. Two 5-HT3 receptor antagonists (ondansetron and MDL-72222) blocked hypotension and restored tachycardia, basic features of orthostatic adaptation of the circulatory system. Response to the 5-HT3 receptor agonist was measured through dose-response curves of BP and HR after injection of 2-methylserotonin. After low doses, hypotension (10 micrograms/kg) and bradycardia (3 and 10 micrograms/kg) were significantly greater in 48-h TS rats than in controls. Thus CVD in the rat induced by TS appears to implicate at least two mechanisms: reduced activity of the sympathetic system and hypersensitivity of serotonergic mechanisms.

Animals↗
PubMed1998

Heart rate control of blood pressure variability in children: a study in subjects with fixed ventricular pacemaker rhythm.

1. To investigate the influence of heart rate variability on blood pressure variability, short-term variability in heart rate and blood pressure was studied in 10 children with fixed ventricular pacemaker rhythm (80 beats/min). Ten healthy children, in sinus rhythm, served as a reference population. 2. Arterial blood pressure and heart rate were measured continuously using a finger arterial device and an ECG respectively. Power spectra for heart rate and blood pressure (systolic and diastolic) were calculated in both supine and orthostatic positions. In addition, acute changes in blood pressure and heart rate during active standing were studied. 3. Healthy children exhibited considerable heart rate variability, which was slightly more pronounced in the supine position, while children with a fixed ventricular rate had no heart rate variability in either position. 4. Despite the differences in heart rate variability, mean systolic blood pressure and its variability profiles were poorly affected by the suppression of heart rate variability. The lack of autonomic control on the sinus node was associated with a reduction in magnitude of the changes in systolic blood pressure variability induced by orthostatic posture. 5. The suppression of heart rate fluctuations induced a noticeable decrease in diastolic blood pressure fluctuations, which was most conspicuous in the children with fixed cardiac rhythm when in the supine position. This may be explained by the lack of diastolic blood pressure fluctuations, physiologically due to heart rate fluctuations through the run-off effect: the longer the cardiac cycle, the greater the diastolic pressure decay. These results may challenge the classical theory of baroreflex-mediated diastolic blood pressure control described in adult patients. 6. During active standing, the early drop in systolic blood pressure was greater in subjects with fixed ventricular rhythm. A rise in heart rate of 36 beats/min was observed in the healthy subjects in response to active standing. 7. We conclude that in normal children, heart rate fluctuations increase the blood pressure variability rather than buffering it. However, during acute orthostatic stress, the abrupt baroreflex-mediated heart rate rise may partly compensate for the reduction in blood pressure.

Adolescent↗
PubMed1998

Clinical relevance blood pressure variability.

Blood pressure fluctuates continuously over time, either spontaneously or in response to a variety of external stimulations. The occurrence of these continuous and often marked blood pressure variations is not only of pathophysiologic interest, but it may also have a clinical relevance. Indeed, it has been shown that the occurrence of pronounced blood pressure changes at the time of the physician's visit may introduce errors in the diagnosis of hypertension and in the assessment of the efficacy of antihypertensive treatment. Moreover, several studies have reported that the end-organ damage of hypertension is significantly and independently related to the degree of blood pressure variability during the day and night. This was shown by reports that assessed blood pressure variability by a variety of different methods, i.e. by computing the 24 h or daytime blood pressure standard deviation, the degree of morning blood pressure rise or that of night-time blood pressure fall, the frequency of blood pressure peaks over the 24 h, and the blood pressure increases under stressful conditions or during physical exercise. Results from a recent follow-up study have provided evidence that the degree of blood pressure variability may also have prognostic relevance in hypertensive patients. Thus, optimal antihypertensive treatment might also need to reduce the degree of blood pressure fluctuations together with the 24 h average blood pressure levels. Until recently, however, available antihypertensive drugs have been ineffective in buffering blood pressure variability or have even been responsible for an increase in the degree of blood pressure fluctuations. Further studies are needed to assess whether recently developed antihypertensive agents, and in particular those able to induce a smooth reduction in blood pressure over the 24 h or to modulate the sympathetic influences exerted on the cardiovascular system, may represent better tools to reduce the magnitude of an enhanced blood pressure variability in hypertensive patients over the 24 h. Recent progress in technology has offered us more powerful tools to address this issue. They include devices for continuous noninvasive ambulatory blood pressure monitoring (Portapres, TNO), and techniques for a more comprehensive analysis of all components which contribute to overall blood pressure variability (broad-band spectral analysis).

Blood Pressure↗
PubMed1998

[Autonomic contribution to the blood pressure and heart rate variability changes in early experimental hyperthyroidism].

A great deal of uncertainty persists regarding the exact nature of the interaction between autonomic nervous activity and thyroid hormones in the control of heart rate (HR) and blood pressure (BP). Thyrotoxicosis was produced by a daily intraperitoneal (i.p.) injection of L-thyroxine (0.5 mg/kg body wt in 1 ml of 5 mM NaOH for 5 days). Control rats received i.p. daily injections of the thyroxine solvant. Autonomic blockers were administered intravenously: atropine (0.5 mg/kg), atenolol (1 mg/kg), atenolol + atropine or prazosin (1 mg/kg). Eight animals were studied in each group. Thyroxine treatment was sufficient to induce a significant degree of tachycardia (423 +/- 6 vs 353 +/- 4 bpm; p < 0.001, unpaired Student's tests), systolic BP elevation (142 +/- 3 vs 127 +/- 2 mmHg; p < 0.001), pulse pressure increase (51 +/- 2 vs 41 +/- 2 mmHg, p < 0.01), cardiac hypertrophy (1.165 +/- 0.017 vs 1.006 +/- 0.012 g, p < 0.001), weight loss (-21 +/- 2 g; p < 0.001) and hyperthermia (37.8 +/- 0.1 vs 37.0 +/- 0.1 degrees C, p < 0.001). The intrinsic HR observed after double blockade (atenolol + atropine) was markedly increased after treatment with thyroxine (497 +/- 16 vs 373 +/- 10 bpm, p < 0.05). Vagal tone (difference between HR obtained after atenolol and intrinsic HR) was positively linearly related to intrinsic HR (r = 0.84; p < 0.01). Atenolol neither modified HR nor BP variability in rats with hyperthyrodism. The thyrotoxicosis was associated with a reduction of the 0.4 Hz component of BP variability (analyses on 102.4 sec segments, modulus 1.10 +/- 0.07 vs 1.41 +/- 0.06 mmHg; p < 0.01). Prazosin was without effect on this 0.4 Hz component in these animals. These data show a functional diminution of the vascular and cardiac sympathetic tone in experimental hyperthyroidism. Increased intrinsic HR resulting from the direct effect of thyroid hormone on the sinoatrial node is the main determinant of a tachycardia leading to a subsequent rise in cardiac output. The resulting BP elevation could reflexly induce a vagal activation and a sympathetic (vascular and cardiac) inhibition.

Animals↗
PubMed1997

Autonomic components of the cardiovascular responses to an acoustic startle stimulus in rats.

1. A loud acoustic stimulus was administered to rats prior to and after treatment with autonomic blockers in order to unravel the autonomic mechanisms of the blood pressure (BP) and heart rate (HR) responses to startle. 2. Six rats, implanted with a BP telemetric system, were used in a randomized crossover saline-controlled (saline vs. autonomic blocker) study with a washout period of 7 days between each active session. A first acoustic stimulus (110 dB, 0.7 s) was administered. An autonomic blocker i.e. atropine methylnitrate (15 mg. kg-1), atenolol (15 mg. kg-1) or prazosin HCl (1 mg. kg-1), or physiological saline was administered i.p. 40 min prior to a second identical acoustic stimulus. 3. The average BP rise following the first stimulus was +25 mmHg and the average HR change was +17 bpm. The responses after autonomic blockades were affected as follows: atropine increased the HR rise (+45.1 +/- 1.7 bpm), atenolol reversed the HR changes to a bradycardic response (-21.4 +/- 9.1 bpm), after prazosin treatment the BP rise was reversed into a BP decrease (-11.3 +/- 3.2 mmHg) and the HR increase was amplified (+76.0 +/- 10.0 bpm). Finally, the delay for obtaining the maximal BP change was increased from 1.9 to 2.6 s following prazosin pretreatment. 4. These results indicate that the BP rise resulting from an acute loud noise depends on a vascular sympathetic activation (prevented with prazosin), which is partly blunted by vasodilation (revealed with prazosin). The evoked HR changes combine a sympathetic activation (fully expressed following atropine) and a vagal activation (unmasked with atenolol). Further experiments are necessary to document the vasodilatory component unmasked with prazosin.

Acoustic Stimulation↗
PubMed1997

Contribution of humoral systems to the recovery of blood pressure following severe haemorrhage.

1. Profound haemorrhage activates a number of pressor mechanisms, including the release of catecholamines, angiotensin II and arginine-vasopressin, which contribute to the subsequent cardiovascular recovery. Using specific single or combined blockade with prazosin, losartan and Manning compound (AVPX), the aim of this study was to evaluate the involvement of the three pressor systems in blood pressure recovery following severe haemorrhage (20 ml kg-1). 2. Haemorrhage of conscious, unrestrained rats resulted in a significant initial decrease in blood pressure of approximately 60 mmHg, and heart rate of approximately 70 bpm. Then, blood pressure tended to return to the control level within 10 min. The total cardiovascular recovery corresponded to increments of 52 +/- 5 mmHg (81% of the acute fall) for systolic blood pressure, and of 92 +/- 22 bpm (124%) for heart rate at 60 min post-bleeding. Significant falls in haematocrit (-10.5 +/- 1.2%, P < 0.01), in plasma concentrations of proteins (-10.3 +/- 0.9 g l-1, P < 0.01) and haemoglobin (-2.58 +/- 0.72 g 100 ml-1, P < 0.05) were observed at 60 min post-bleeding. 3. Pretreatment with one or two specific antagonists did not exaggerate the initial fall in blood pressure. The initial bradycardia was weakened only by combined blockade with losartan and AVPX. 4. The blood pressure recovery from a haemorrhage was delayed by approximately 25 min by the inhibition of vasopressin activity. The systolic blood pressure recovery in control animals (81% of the acute fall) was blunted by losartan (55% of the acute fall), prazosin (49%), combined losartan and AVPX (36%), prazosin and AVPX (36%), and also by prazosin plus losartan (13%). The diastolic blood pressure recovery was blunted only in the groups where the activity of angiotensin II was inhibited by losartan. 5. In conclusion, we have shown that neither catecholamines, angiotensin II nor vasopressin, although activated, individually compensate the acute hypotensive response to haemorrhage. The contribution of vasopressin to the blood pressure recovery post-bleeding is transient and is rapidly replaced by the pressor activity of the catecholamines and angiotensin II. The full systolic blood pressure recovery from severe haemorrhage requires the combined activity of these two pressor systems, while the diastolic blood pressure recovery seems to be only dependent upon angiotensin II activity.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1997

Social isolation affects the pattern of cardiovascular responses to repetitive acoustic startle stimuli.

1. The aim of this study was to investigate the cardiovascular responses to repetitive alerting stimuli in rats subjected to intermittent social isolation, in comparison with animals housed in pairs. 2. Ten male Wistar rats were implanted with a blood pressure (BP) telemetric system and enrolled in a randomized cross-over study design. Rats were either isolated or housed in pairs for an 8 day period. At the end of each period, the animals were exposed to five acoustic stimuli (110 dB at 15 kHz, 80 ms after the impact, duration 700 ms) at 60 s intervals. For each stimulus, maximal BP and heart rate (HR) responses were calculated. BP variability was analysed in the frequency domain before the first stimulation using power spectral analysis. 3. Isolated animals showed more faster breathing (1.71 vs 1.42 Hz in the paired condition). The 0.4 Hz zone of the systolic BP spectral power was not significantly affected by isolation (1.11 vs 0.85 mmHg2). BP and HR resting levels of isolated rats (121 mmHg for the systolic BP and 290 b.p.m.) were similar to those of animals housed in pairs (119 mmHg for the systolic BP and 279 b.p.m.). 4. The first acoustic stimulus caused a brief rise in BP of a comparable amplitude in both conditions (24 +/- 2 mmHg). A biphasic HR response was also observed, but the delayed bradycardia was more marked during isolation (37 vs 6 b.p.m. decrease). BP and HR levels were restored within 20 s. 5. Interestingly, BP responses were progressively attenuated to become negligible at the fifth presentation (1 mmHg) in the isolated state, while during the paired state a substantial pressor response (13 mmHg) after each successive stimulus was maintained. Paired rats exhibited a constant HR profile across the trials, consisting in a slight HR increase (< 5 b.p.m.), concomitant with the BP elevation, followed by a delayed bradycardia (around 15 b.p.m.). HR profiles in the isolated condition differed markedly: HR rises increased in magnitude with the trial number, reaching 30 b.p.m. after the 5th trial. 6. Spontaneous BP and HR increases, as observed throughout the experiment were quantitatively small (6 mmHg and < 10 b.p.m.) in the two conditions. 7. These data indicate that isolation markedly affects the BP habituation profile to repetitive alerting stimuli. The BP response attenuation might unmask a tachycardic response. Alternatively, the amplified tachycardia following the latter stimuli might express sensitization to the conditioned fear resulting from isolation.

Acoustic Stimulation↗
PubMed1997

Contribution of humoral systems to the short-term variability of blood pressure after severe hemorrhage.

The aim of this study was to generate hemorrhage-triggered fluctuations in blood pressure (BP) at low frequency (LF, < 0.2 Hz) in conscious rats and investigate with spectral analysis the relative roles of hemorrhage-activated catecholamines, the renin-angiotensin system (RAS), and arginine vasopressin (AVP) on the generation of these fluctuations. The individual contribution of these factors was assessed using a combination of the selective antagonists, prazosin, losartan, and Manning compound (AVPX). At rest, systolic BP (SBP) LF fluctuations were slightly increased by losartan. The mid-frequency (MF; 0.2-0.6 Hz) oscillations of SBP and diastolic BP (DBP) were decreased by prazosin alone or associated with AVPX or losartan. The high-frequency (HF; respiratory) oscillations of SBP were increased by prazosin, prazosin plus losartan, and prazosin plus AVPX. After severe hemorrhage (20 ml/kg), the spontaneous BP recovery was characterized by the occurrence of slow fluctuations of SBP and DBP, centered approximately 0.065 Hz, and by increases of MF (89%) oscillations of SBP. The HF component of SBP variability tended to be increased by blood loss. The occurrence of the SBP LF fluctuations was prevented when alpha 1-adrenergic activity was blocked by prazosin. These oscillations were always present, despite inhibition of angiotensin II, and were increased after inhibition of the AVP activity. Pretreatment with the specific inhibitors used in these studies favored the amplifying effect of hemorrhage on HF fluctuations while they prevented the postbleeding increase in MF oscillations. In conclusion, the present results show an association between the dependence of the postbleeding blood pressure level on catecholamines and the occurrence of slow fluctuations of BP. The buffering role of AVP suggests the establishment of a hierarchy between humoral systems in the genesis of the LF oscillations of BP, with the slow oscillations being generated by the main pressor system and being dampened by the other systems. The postbleeding rise in the MF component of SBP variability could be considered a reflection of the activations of both the sympathetic vasomotor drive and the RAS. The postbleeding increase in the HF component of BP variability was dampened by the activation of the humoral systems. These effects may reflect the low preload state due to hypovolemia.

Animals↗
PubMed1996

Contribution of the renin-angiotensin and kallikrein-kinin systems to short-term variability of blood pressure in two-kidney, one-clip hypertensive rats.

Spectral analysis was recently chosen to characterize the fast oscillations, depending on the autonomic nervous system, in heart rate and blood pressure variabilities. Humoral stimuli could impinge on the low-frequency domain of blood pressure variability since the time lag to humoral system activation is greater. This study was designed to analyse low-frequency components of short-term variability of blood pressure of conscious rats in conditions where humoral systems were activated. We studied rats with two-kidney, one-clip Goldblatt hypertension in which the blood pressure level was dependent upon the renin-angiotensin and kallikrein-kinin systems. Spectral powers of the systolic and diastolic blood pressure and heart rate were computed in the high (respiratory)-, mid (0.2-0.6 Hz)- and low (0.02-0.2 Hz)-frequency bands, as detected by the fast Fourier transform technique in consecutive 102-s stationary periods. Hypertensive rats exhibited a marked low-frequency component of systolic (+261%) and diastolic (+169%) blood pressure variabilities when compared to sham-operated animals. First, losartan, a selective non-peptide angiotensin AT1 receptor antagonist, reduced this low-frequency component (-44% and -25% for systolic and diastolic blood pressure). In a second series of hypertensive rats, HOE 140, D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]bradykinin, a bradykinin B2 receptor antagonist, decreased the low-frequency component of systolic (-28%) and diastolic (-40%) blood pressure. Losartan, added after HOE 140, induced a supplementary decrease of the low-frequency component (-60% and -42% for systolic and diastolic blood pressure). After the combined blockade, the low-frequency components of systolic and diastolic blood pressure variabilities of the hypertensive rats were equivalent to those of the control rats. Two-kidney, one-clip hypertension was also associated with an elevation of the mid-frequency component of the systolic blood pressure (+55%). The administration of HOE 140 did not change this component while losartan, alone or added after HOE 140, led to an increase (around +100%) in mid-frequency oscillations of systolic blood pressure. The high-frequency oscillations of systolic blood pressure were increased by losartan in the two series of hypertensive rats. Losartan increased the mid-frequency component of heart rate variability in sham-operated rats while the heart rate variability was not modified during any of the treatment periods in two-kidney, one-clip rats. In conclusion, an increase in the low-frequency component of blood pressure variability was observed in a model of hypertension where the blood pressure is dependent upon humoral activities. The reduction of the slow fluctuations following the combined blockade of the kallikrein-kinin and the renin-angiotensin systems suggested the contribution of these humoral systems to this low-frequency component of blood pressure variability.

Adrenergic beta-Antagonists↗