PubMed Health⌕ Search

Biomedical subjects

J L Elghozi

Publications and source records attributed to J L Elghozi.

At least 19 recordsLinked to original sources
PubMed1992

Effects of plasmapheresis on short-term variability of blood pressure in healthy donors.

The acute effect of mild central hypovolaemia induced by plasmapheresis on the short-term variability of blood pressure and heart rate was evaluated in ten healthy donors. Indirect finger blood pressure was measured by a non-invasive device (Finapres). Analogue-to-digital conversion of the blood pressure was used to determine systolic, diastolic and mean blood pressure and heart rate every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. Blood pressure and heart rate were maintained while an increased overall variability of blood pressure was observed after plasmapheresis. The increased total area under the curve of the systolic and diastolic blood pressure spectra was documented with the selective analysis of the three main components of the spectra: the increase in the oscillations of blood pressure following plasmapheresis predominated in the 66-129 mHz region, corresponding to Mayer waves. The spectral profile of HR was unaffected by plasmapheresis. The significant increase in the 10-s period oscillations of blood pressure after the mild central hypovolaemia could result from the unloading of cardiopulmonary (and arterial) baroreceptors which in turn could buffer the arterial pressure through sympathetic activation, detected on the systolic and diastolic pressure spectra in the low-frequency range.

Adult↗
PubMed1992

Differential effects of enalapril and hydralazine on short-term variability of blood pressure and heart rate in rats.

Using a spectral procedure, we studied the acute and chronic effects of enalapril and hydralazine on the variability of blood pressure (BP) and heart rate (HR) in conscious Wistar rats. In the acute protocol, rats received two injections 25 min apart (saline followed by enalaprilic acid or hydralazine hydrochloride). In the chronic protocol, animals received oral enalapril maleate, hydralazine hydrochloride, or distilled water. A 5-min recording session was initiated on day 12. Acute enalapril and hydralazine amplified the low-frequency (LF) component of the systolic BP (SBP) spectrum. Chronic enalapril reduced the variability of BP, as indicated by the lower variance in SBP distribution. Chronic enalapril preferentially reduced the amplitude of the 400-mHz oscillations of SBP. Acute administration of enalapril or hydralazine resulted in BP variability profiles, suggesting a reflexly mediated vascular sympathetic activation. In contrast, chronic angiotensin-converting enzyme (ACE) blockade with enalapril caused a significant decrease in the LF oscillations of BP. This could reflect a reduced sympathetic outflow to vascular smooth muscles.

Angiotensin II↗
PubMed1992

Spectral analysis of short-term blood pressure and heart rate variability in uremic patients.

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were quantified to assess autonomic nervous system (ANS) dysfunction in six dialysis patients, compared to six control subjects of similar age. Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic BP (SBP), diastolic BP (DBP) and HR every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. Uremic patients exhibited reduced BP and HR short-term variabilities, with a dramatic reduction in the amplitude of the 0.1 Hz component (Mayer waves) of SBP and DBP spectra. Dialysis did not produce any consistent immediate improvement in the amplitude of the Mayer waves. Our study thus indicates impaired cardiovascular ANS function in uremic patients.

Adult↗
PubMed1991

Effects of the converting enzyme inhibitor trandolapril on short-term variability of blood pressure in essential hypertension.

Short-term fluctuations in blood pressure and heart rate were analysed in a group of eight males with essential hypertension. Indirect finger blood pressure was measured by a non-invasive device (Finapres). Analogue-to-digital conversion of the blood pressure was used to determine systolic and diastolic blood pressure and heart rate every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transformation algorithm. The effect of 7-day administration of the angiotensin converting enzyme inhibitor, transolapril (2 mg/day), was assessed in a double-blind, randomized, placebo-controlled cross-over study. After trandolapril there was a significant reduction in systolic blood pressure levels (-15 mmHg). The reduction in diastolic blood pressure did not reach significance. The standard deviation of systolic and diastolic blood pressure levels were significantly reduced (-20% and -22% for systolic and diastolic respectively). Neither average heart rate nor standard deviations of heart rate time series was affected by the angiotensin converting enzyme inhibitor. Spectral analysis of fluctuation in blood pressure showed a reduction in the variability underlying the standard deviation changes of systolic and diastolic blood pressure. Trandolapril selectively reduced the amplitude of systolic and diastolic oscillations in the 66-129 mHz region, corresponding to Mayer waves. The significant decrease in the 10 s period oscillations of blood pressure after chronic angiotensin converting enzyme blockade with trandolapril could reflect reduced sympathetic outflow to vascular smooth muscle.

Adult↗
PubMed1991

Cardiovascular and adrenaline-releasing effects of the 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin in streptozotocin diabetic rats.

The 5-hydroxytryptamine1A (5-HT1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) has been reported to trigger sympathoinhibition, as evidenced by its cardiovascular effects, and adrenal catecholamine secretion. The purpose of this study was to analyze the cardiovascular and adrenaline-releasing effects of 8-OH-DPAT in 1 week streptozotocin diabetic rats. 8-OH-DPAT-induced changes in mean arterial pressure (MAP) and heart rate (HR) were determined directly in anesthetized rats, whilst changes in plasma adrenaline (and plasma corticosterone and glucose) levels were analyzed in conscious rats. Resting blood pressure and heart rate were diminished in diabetics, when compared with controls. These changes were associated with a decrease in body weight and a marked increase in resting plasma glucose levels. Diabetes did not affect MAP response to 8-OH-DPAT, except for a decrease in the amplitude of MAP maximal fall, which was associated with a diminished bradycardic response to 8-OH-DPAT. Blood pressure response to prazosin (0.5 mg/kg) in 8-OH-DPAT-pretreated rats was also diminished in diabetics. Lastly, diabetes prevented the adrenaline-releasing and hyperglycemic effects of 8-OH-DPAT (250 ug/kg).

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Clonidine reduces blood pressure and heart rate oscillations in hypertensive patients.

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analyzed in a group of eight men with essential hypertension. Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP) and HR every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. The effects of an oral dose of clonidine (150 micrograms) were studied in a double-blind, crossover, placebo-controlled study. Clonidine markedly reduced the variability of BP and HR after 90 min as indicated by a reduction in the standard deviations of BP by 36.7% for SAP, 21.0% for DAP, 22.1% for MAP, and 26.0% for HR. At this time clonidine reduced the average BP by 19.7 mm Hg for SAP, 10.6 mm Hg for DAP, 16.0 mm Hg for MAP, and 1.0 beat/min for HR. Spectral profiles of BP and HR illustrated the alterations in the spontaneous oscillations underlying the standard deviation changes. Clonidine dramatically reduced the amplitude of BP and HR oscillations in the mid-frequency region 66-129 mHz, which depends on the activity of the autonomic nervous system. We suggest that an increased sensitivity of the baroreflex is responsible for the apparent better control of BP and HR with clonidine.

Adult↗
PubMed1991

Effects of clonidine on blood pressure and heart rate responses to an emotional stress in the rat: a spectral study.

1. The fluctuations that underlie the spontaneous variability of blood pressure (BP) and heart rate (HR) were investigated in conscious normotensive rats using power spectral analysis. 2. Air jet stimulation determined a significant BP rise associated with a tachycardia. This environmental mild stressor amplified the 195-605 mHz oscillations of HR which are under autonomic control. No habituation to this stressor was observed since a second stimulation determined similar responses. 3. Clonidine (10 micrograms/kg, i.v.) prevented the BP rise normally associated with air jet stimulation. In addition, clonidine dramatically reduced the amplitude of BP and HR oscillations in the frequency region of 195-605 mHz. 4. It is concluded that a mild emotional stressor elicits in normotensive rats a rise in BP and HR associated with modified spectral profiles reflecting sympathetic hyperactivity. Clonidine minored the effects of stress on BP and HR variability and also prevented BP elevation.

Animals↗
PubMed1991

Effects of respiration on blood pressure and heart rate variability in humans.

1. Non-invasive continuous finger blood pressure (BP) measurement and a spectral technique based on the Fourier transform (FT) were recently combined to quantify short-term fluctuations in haemodynamic variables. 2. Systolic BP (SBP) recording combined low frequency (LF, Mayer waves) plus high frequency (HF, respiratory) oscillations. The presence of HF oscillations of SBP probably reflects fluctuations in cardiac output. Heart rate (HR) also exhibited a combination of low and HF (respiratory) oscillations. The vagus nerve mediates the efferent control of the respiratory sinus arrhythmia (RSA). 3. During controlled breathing in a supine position, a change in SBP is associated with an opposite consequent change in HR. Respiratory sinus arrhythmia could therefore depend on the baroreceptor-HR response to underlying SBP oscillations. 4. The fast regulation of R-R interval by SBP through the baroreceptor-HR reflex may explain why the respiratory variations in the diastolic BP are small.

Blood Pressure↗
PubMed1991

Contribution of alpha 2-adrenoceptors to the central cardiovascular effects of clonidine and S 8350 in anaesthetized rats.

1. The alpha 2-adrenoceptor agonist clonidine elicits centrally mediated effects through an interaction with both alpha 2-adrenoceptors and imidazoline binding sites. 2. We selected a new oxazoline derivative, S 8350, which competes with [3H]-yohimbine for binding to cerebral alpha 2-adrenoceptors (IC50, 67 +/= 17 nmol/L) and displays a higher affinity (35-fold) for alpha 2- than for alpha 1-adrenoceptors. 3. As observed for clonidine, intravenous (i.v.) administration of S 8350 resulted in a brief pressor effect followed by a prolonged hypotension. When S 8350 was administered i.v. to spinally pithed rats, only a rise in blood pressure was observed. 4. In order to discriminate the cardiovascular effects related to the central imidazoline receptor or alpha 2-adrenoceptor activation, the effects of intracisternal (i.c.) administration of clonidine and S 8350 were investigated in the rat. 5. In the anaesthetized rat, both clonidine and S 8350 displayed a profound central (i.c. route) hypotensive effect associated with a bradycardia. 6. The cardiovascular effects of S 8350 were abolished by the central administration of the selective alpha 2-adrenoceptor antagonist rauwolscine. Conversely, rauwolscine completely prevented bradycardia but it induced only a partial reversion of the hypotension elicited by clonidine. 7. These results suggest that central alpha 2-adrenoceptors are responsible for hypotension and bradycardia while imidazoline binding sites do not apparently contribute to heart rate control.

Adrenergic alpha-Agonists↗
PubMed1991

[Short-term variability in arterial pressure and heart rate in man].

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analysed in a group of seventeen males with essential hypertension (n = 8) or with normotension (n = 9). Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic, diastolic, and mean arterial pressure and HR every s. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. BP recordings combined low frequency plus high frequency oscillations. The presence of high frequency oscillations of SBP probably reflects fluctuations in cardiac output. HR exhibited a combination of low and high frequency oscillations, such as systolic pressure. The corresponding spectra illustrate these observations. The high frequency (respiratory) oscillation corresponded to one peak easily detected on the spectrum of SBP and/or HR. Slow waves were detected in a 4-129 mHz range and divided into a 4-66 mHz low frequency region and a 66-129 mHz mid frequency region (Mayer waves). The sum of the values of consecutive bands was calculated to represent an integrated spectrum of each series of treatment. Controlled respiration produced at rest a marked increase in the high frequency component. HR variability increased with the level of HR. This study illustrates the applicability of a spectral procedures combined to an indirect BP measurement to study short-term oscillations of BP and HR.

Adult↗
PubMed1990

Spectral analysis of blood pressure and heart rate in conscious rats: effects of autonomic blockers.

We investigated the fluctuations which underly the spontaneous variability of blood pressure and heart rate in conscious rats. Intrafemoral blood pressure was computed to generate evenly spaced signals (systolic, diastolic, mean blood pressure, heart rate) at 200 ms intervals. This equidistant sampling allowed a direct spectral analysis using a Fast Fourier Transform algorithm. Systolic blood pressure and heart rate exhibited low-frequency oscillations (Mayer waves, 20-605 mHz) and a high- frequency oscillation related to respiration (1855 mHz). The respiratory fluctuations in heart rate were almost abolished by vagal blockade (atropine). Heart rate fluctuations in the low-frequency regime were diminished by vagal blockade or cardiac sympathetic blockade (atenolol). The respiratory frequency fluctuations in systolic blood pressure were markedly increased by alpha-sympathetic blockade (prazosin). In contrast, the low-frequency oscillations in systolic blood pressure were reduced by alpha-sympathetic blockade. These data indicate that in conscious rats: (1) the heart rate oscillation with respiration is vagally mediated; (2) the heart rate fluctuation in the low-frequency range is jointly mediated by beta-sympathetic and parasympathetic activities; (3) the respiratory oscillation in systolic blood pressure depends on fluctuations in cardiac output and is normally counteracted by the sympathetic tone; (4) the low-frequency oscillations in systolic blood pressure reflect the sympathetic activity to the resistance vessels.

Animals↗
PubMed1990

Clonidine reduces blood pressure and heart rate oscillations in the conscious rat.

We investigated the effects of clonidine on the fluctuations that underlie the spontaneous variability of blood pressure (BP) and heart rate (HR) in conscious rats. Analog-to-digital conversion of the intrafemoral BP was used to determine systolic, diastolic, and mean BP and HR every 200 ms. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. An i.v. dose of 10 micrograms/kg of clonidine markedly reduced the variability of BP and HR after 20 min as indicated by a reduction in the variances by approximately one-half of the control value for BP and to one-third of the control value for HR. At this time, clonidine had not significantly altered BP or HR. Spectral profiles of systolic BP and HR illustrated the alterations in the spontaneous oscillations underlying these variance changes. Clonidine dramatically reduced the amplitude of BP and HR oscillations in the frequency region of 195-605 mHZ, which depends on the activity of the autonomic nervous system. We suggest that an increased sensitivity of the baroreflex is responsible for the apparent better control of BP and HR with clonidine.

Animals↗
PubMed1990

A method for the in vivo investigation of the serotonergic 5-HT2 receptors in the human cerebral cortex using positron emission tomography and 18F-labeled setoperone.

Following previous validation in baboons, we have studied the characteristics of [18F]setoperone as a radioligand for investigating serotonergic 5-hydroxytryptamine2 (5-HT2) receptors in the normal, unmedicated human brain with positron emission tomography (PET); subjects orally pretreated with therapeutic amounts of ketanserin, sulpiride, or prazosin were also studied to evaluate the specificity and sensitivity of [18F]setoperone brain specific binding. In controls (n = 10), the tracer showed a clear-cut retention in both frontal cortex and striatum (known to contain a high density of 5-HT2 receptors) relative to cerebellum (known to be devoid of 5-HT2 receptors). In the seven young controls (20-39 years old), the frontal cortex/cerebellum and striatum/cerebellum ratios increased during the first hour to reach similar values of 2.53 +/- 0.12 and 2.38 +/- 0.11 (mean +/- SEM), respectively, and were essentially stable during the second hour. Pretreatment with ketanserin (a 5-HT2 blocker) significantly reduced the frontal cortex/cerebellum ratio to 0.7-1.0 at 65 min, whereas the striatum/cerebellum ratio was significantly, but only partially, reduced. During sulpiride treatment (a D2 blocker), the frontal cortex/cerebellum ratio was not altered, whereas the striatum/cerebellum ratio was significantly, but only partially, reduced. With prazosin pretreatment (an alpha 1-adrenergic blocker), neither the frontal cortex/cerebellum nor the striatum/cerebellum ratio was modified. These data in humans with PET demonstrate that [18F]setoperone labels with high sensitivity and selectivity 5-HT2 receptors in the frontal cortex; in striata, however, binding is to both 5-HT2 and D2 receptors. The deproteinated-to-whole plasma radio-activity concentration ratio increased with time following injection. The mean percentage of intact [18F]setoperone, in deproteinated plasma, was 82, 74, 53, 45, 30, and 22% at 5, 10, 20, 30, 60, and 110 min following injection, respectively. These data indicate that [18F]setoperone (a) is significantly bound to plasma proteins and (b) is significantly metabolized into several labeled metabolites that are much more hydrophilic than setoperone and, hence, presumably do not cross the blood-brain barrier. These results suggest the suitability of [18F]setoperone data for modeling of 5-HT2 receptor binding in brain.

Adult↗
PubMed1990

Determination of cerebrospinal fluid production rate using a push-pull perfusion procedure in the conscious rat.

The inulin dilution technique was used to determine the cerebrospinal fluid (CSF) production rate by means of a push-pull cannula implanted into a lateral ventricle. Artificial CSF containing trace amount of 3H-inulin was perfused for 2 h in conscious rats. 3H-inulin in the effluent reached a plateau level depending on the CSF production rate. The control lateroventricular CSF production was 0.98 microliters/min. Production was reduced to 0.34 microliters/min during a perfusion with acetazolamide (1 mM), a carbonic anhydrase inhibitor.

Acetazolamide↗
PubMed1990

Spinal noradrenergic pathways and pressor responses to central angiotensin II.

We have investigated the contribution of spinal noradrenergic (NA) pathways to the central pressor effects of angiotensin II (ANG II) in conscious rabbits with intact baroreceptors and after sinoaortic denervation (SAD). Very low intracisternal (ic) doses of ANG II [half maximum dose (ED50) = 6 x 10(-15) mol] produced increases in mean arterial pressure (MAP) and decreases in heart rate. Pressor responses to intracisternal ANG II were markedly reduced by 100 pmol of the ANG II antagonist [( Sar1, Ile8] ANG II, ic) and by intravenous prazosin, suggesting that central activation of ANG II receptors increased sympathetic vasoconstrictor tone. After SAD, the rabbits exhibited a 900-fold increase in sensitivity to ANG II (i.e., responded to very much lower doses, ED50 = 5 x 10(-18) mol). Intraspinal 6-hydroxydopamine (6-OHDA) injections given 1 mo earlier did not alter dose-response curves in baroreceptor-intact rabbits. However, the SAD-induced increase in sensitivity to ANG II was not observed in rabbits with depletion of spinal NA pathways. The results suggest intracisternal administration of ANG II activates two functionally distinct pathways: 1) a very sensitive site that utilizes NA projections to the spinal cord, and 2) a less sensitive site that uses non-NA descending pathways. Under normal baroreceptor input the former pressor pathway is completely inhibited. Thus the role of the central renin-angiotensin system may be of greater physiological importance in conditions where the baroreflex is suppressed.

Angiotensin II↗
PubMed1990

[Nervous mechanisms of spontaneous oscillations of systolic blood pressure and heart rate].

The phenomenon of rhythmic fluctuations in cardiovascular variables such as heart rate (HR) or arterial blood pressure (BP) has attracted the attention of workers in both pure and applied research. In recent years, the possibility of quantifying these oscillations by using power spectral analysis has aroused a growing interest. We investigated the fluctuations which underly the spontaneous variability of BP and HR in conscious rats. Intrafemoral pulsatile BP was computed to generate evenly spaced signals (systolic, diastolic, mean BP, HR) at 200 ms intervals. This equidistant sampling allowed a direct spectral analysis using a Fast Fourier Transform algorithm. Systolic Blood Pressure (SBP) and HR exhibited low frequency oscillations (Mayer waves, 20-605 mHz) and a high frequency oscillation related to respiration (1,855 mHz). The respiratory fluctuations in HR were almost abolished by vagal blockade (atropine). HR fluctuations in the low frequency regime were diminished by vagal blockade or cardiac sympathetic blockade (atenolol). The respiratory frequency fluctuations in SBP were markedly increased by alpha sympathetic blockade (prazosin). On the contrary the low frequency oscillations in SBP were reduced by alpha sympathetic blockade. These data indicate that in conscious rats: 1) the HR oscillation with respiration is vagally mediated, 2) the HR fluctuation in the low frequency regime is jointly mediated by beta sympathetic and parasympathetic activities, 3) the respiratory oscillation in SBP depends on fluctuations in cardiac output and is normally counteracted by the sympathetic tone, 4) the low frequency oscillations in SBP reflect the sympathetic activity to the resistance vessels.

Animals↗
PubMed1989

Importance of spinal noradrenergic pathways in cardiovascular reflexes and central actions of clonidine and alpha-methyldopa in the rabbit.

We have examined in conscious rabbits the chronic effects of 6-hydroxydopamine (6-OHDA)-induced local lesions of the spinal noradrenaline (NA) pathways on (i) resting mean arterial pressure (MAP) and heart rate (HR), (ii) the nasopharyngeal pressor response, (iii) the sympathetic component of the baroreceptor-heart rate reflex (iv) the acute responses to intracisternal (i.c.) clonidine and alpha-methyldopa (alpha-MD), and (v) the acute NA release response produced by i.e. 6-OHDA. One month after injection of 6-OHDA (40 nmol in 4 microliters) into the first cervical spinal cord segment (C1), the NA content was reduced to 29% in C2, 45% in T4 and 61% in L3 with little non-specific damage. Basal MAP was 14% higher (P less than 0.05) than in sham-operated rabbits suggesting increased vasoconstrictor tone. Basal cardiac sympathetic tone was enhanced, but a corresponding increase in cardiac vagal tone resulted in little net effect on resting HR in the spinal NA-depleted group. Spinal NA lesions attenuated the nasopharyngeal pressor reflex by 27% in baroreceptor-intact rabbits and by 38% in sino-aortically denervated (SAD) animals. The lesion did not affect HR range, gain and BP50 of the sympathetic baroreflex. In SAD rabbits, the acute MAP responses to i.c. 6-OHDA (early hypotension, late hypertension) were not affected by spinal NA depletion, but the early fall in HR (cardiac sympathetic inhibition) was abolished. The hypotension produced by i.c. clonidine or alpha-MD was not affected by the lesion, probably because many of the NA terminals in the lower thoracic and upper lumbar cord were still intact. Our results suggest that intraspinal NA fibers have a tonic inhibitory action on spinal preganglionic vasoconstrictor and cardiac motoneurons. The spinal NA neurons affecting vasomotor tone (but not cardiac sympathetic tone) are in turn inhibited by higher vasomotor centers receiving projections from the arterial and trigeminal afferents and thereby participate in vasoconstrictor reflexes.

Animals↗