Biomedical subjects

A U Ferrari

Publications and source records attributed to A U Ferrari.

At least 19 recordsLinked to original sources

PubMed2001

Nitric oxide-dependent vasodilation and the regulation of arterial blood pressure.

Conflicting evidence has been reported on the hypothesis that vascular nitric oxide (NO) release is modulated by autonomic influences. Another controversial question is whether an insufficient degree of NO-dependent vasodilation may play a contributory role in the genesis of arterial hypertension. To address these questions we evaluated NO-dependent vasodilation in conscious rats subjected to various experimental manipulations that interfere with autonomic function: chronic chemical sympathectomy (CCSx), acute ganglionic blockade (AGx) and chronic sinoaortic denervation (CSAD). Experiments were also carried out on 6- and 12-week-old spontaneously hypertensive rats (SHR) (i.e. during the pre-hypertensive and the early established hypertensive stage) and in age-matched Wistar-Kyoto (WKY) rats. Nitric oxide-dependent vasodilation was quantified from the extent of blood pressure (BP) elevation in response to acute inhibition of NO synthesis by L-nitromonomethyl-L-arginine (L-NMMA). Chronic chemical sympathectomy was produced by repeated 6-hydroxydopamine injections; AGx was induced by hexamethonium infusion; and CSAD was obtained by aortic nerve section and carotid sinus wall stripping. Nitric oxide synthesis inhibition by L-NMMA was followed by a marked BP elevation in all groups. Rats with CCSx, Agx or CSAD never showed reduced BP responses to L-NMMA compared to intact, control rats. Neither 6- nor 12-week-old SHR had attenuated pressor responses to L-NMMA compared to age-matched WKY rats. In conclusion, the data indicate that (i) in unanaesthetized quietly-behaving rats there is no significant modulation of NO release by autonomic influences and (ii) young SHR have unimpaired NO-dependent vasodilation so it is unlikely that a deficit of vascular NO release plays any etiologic role in the BP elevation of this experimental model.

Animals↗

PubMed2000

Enhanced vascular reactivity in the sympathectomized rat: studies in vivo and in small isolated resistance arteries.

OBJECTIVE: In the conscious rat, sympathectomy (6-hydroxydopamine pretreatment, 100 mg/kg intraperitoneally, twice in the previous 5-6 days) induces, among various homeostatic modifications, the frequent occurrence of sudden and wide oscillations of blood pressure. Since one of the mechanisms underlying this, as yet unexplained, phenomenon may be an enhanced vascular reactivity, we tested the hypothesis that sympathectomized rats exhibit such a hyper-reactivity. We examined the response to a variety of vasoactive agents both in vivo (chronically instrumented conscious animals) and in vitro (small isolated resistance arteries). DESIGN AND METHODS: Wistar-Kyoto sympathectomized rats (6-hydroxydopamine pretreatment, n = 19) and control rats (vehicle pretreatment, n = 23) were studied. In conscious animals, concentration-blood pressure response curves to intra-venous bolus injections of vasopressin, phenylephrine and angiotensin II were obtained. In isolated vessels, concentration-wall tension response curves were obtained for norepinephrine, phenylephrine, vasopressin, serotonin and potassium. Vasodilator responses to acetylcholine (with or without L-NAME), bradykinin and sodium nitroprusside were also evaluated after precontraction with norepinephrine (mesenteric arteries) or vasopressin (cerebral arteries). RESULTS: In sympathectomized rats in vivo the pressor responses to vasopressin, phenylephrine and angiotensin II were significantly larger than in control rats, the difference amounting to 46.5, 40.2 and 57.1%, respectively (all P < 0.05). In vitro, the vascular reactivity of isolated cerebral arteries was similar in sympathectomized and control rats. In contrast, the mesenteric arteries showed significantly increased contractions in sympathectomized compared to control rats in response to norepinephrine, phenylephrine and vasopressin but not to serotonin and potassium, whereas the vasodilator responses to acetylcholine and sodium nitroprusside (but not to bradykinin and acetylcholine+L-NAME) were reduced. CONCLUSIONS: In conclusion, we showed that sympathectomy produces complex alterations of vascular reactivity both in vivo and in isolated vessels, which shift the balance of the sensitivity of the vessel between vasoconstrictor and vasodilating agents towards an increased constriction. These results are unlikely to simply reflect denervation supersensitivity; their underlying receptor, post-receptor and/or contractile mechanisms are yet to be identified.

Animals↗

PubMed1999

Endothelin and mechanical properties of the carotid artery in Wistar-Kyoto and spontaneously hypertensive rats.

The aim of this study is to evaluate the role of endothelin in the control of the static mechanical properties of in vitro carotid arteries from 14-week-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). An in vitro preparation in which the artery was allowed to longitudinally elongate similarly to the in situ carotid artery was employed. The diameter of in vitro carotid arteries subjected to static pressures (from 25 to 200 mmHg in 25 mmHg steps) was determined by videomicroscopy and computer-assisted image analysis, the cross-sectional compliance- and distensibility-pressure curves being then derived. The role of endothelin was assessed by incubating carotid arteries with the selective ETA and ETB endothelin receptor antagonists BQ123 and BQ788, respectively. These effects were compared with those observed under control conditions, as well as with those following complete abolition of vascular smooth muscle tone by potassium cyanide (KCN). Carotid diameter was significantly larger, and compliance and distensibility significantly smaller, in SHR compared to WKY rats. Local incubation with BQ123 was associated with significant dilations as well as significant increases in cross-sectional compliance and distensibility in both strains. This was even more pronounced with KCN, while BQ788 had no effect. The results of the present study suggest that: (i) endothelin exerts a tonic stiffening effect on the in vitro common carotid artery; (ii) this effect is mediated via the ETA endothelin receptor, and (iii) the stiffening effect of endothelin is exerted to a similar extent in the carotid arteries of normotensive WKY and SHR rats.

Animals↗

PubMed1999

Sympathectomy inhibits the vasoactive effects of nicotine in conscious rats.

OBJECTIVE: The mechanisms underlying the pressor response to nicotine are incompletely understood. Although sympatho-adrenergic activation plays a major role, the relative contribution of adrenal vs. neurally released catecholamines and the possible role of non-adrenergic factors (e.g. vasopressin release) is not established. METHODS: We examined the cardiovascular responses to graded i.v. injections of nicotine (1 to 100 micrograms kg-1) in conscious Wistar-Kyoto rats under control conditions and (i) after chemical sympathectomy by 6-hydroxydopamine, which destroys sympathetic endings but spares the adrenal medulla; (ii) after an alpha-adrenergic blockade by phenoxybenzamine; (iii) after a V1 vasopressin receptor blockade by a specific antagonist. RESULTS: In control rats, nicotine caused a dose-dependent tachycardiac and pressor response. Both responses were abolished by sympathectomy, whereas the alpha-blockade left the tachycardiac response unaffected but inhibited the pressor response: the V1 vasopressin receptor blockade had no effect on either the tachycardiac or pressor response. CONCLUSIONS: We conclude that in the conscious rat; (1) the pressor response to nicotine mainly depends on peripheral alpha-adrenergically-mediated vasoconstriction; (2) the vasomotor effect is caused by neural rather than adrenomedullary catecholamine release; (3) the nicotine-induced increase in heart rate (and presumably cardiac output) is per se unable to raise blood pressure, and (4) the nicotine-induced release of vasopressin plays no significant role in the pressor response.

Adrenergic alpha-Antagonists↗

PubMed1999

Altered blood pressure variability in patients with congestive heart failure.

OBJECTIVE: Congestive heart failure (CHF) is characterized by sympathetic overactivity but reduced variability of heart interval and sympathetic nerve activity; little information exists, however, about the alterations in blood pressure variability in this syndrome, especially during excitatory manoeuvres such as tilting or exercise. DESIGN AND METHODS: Nine patients with CHF (age 62+/-1 years, NYHA class II-III, ejection fraction 33+/-1%, peak VO2 14.1+/-3.2 ml/min per kg body weight [mean +/- SEM]) and eight healthy control subjects (age 58+/-1 years) with normal left ventricular function were studied. Blood pressure (Finapres), R-R interval (ECG) and respiration (nasal thermistor) were recorded during 15-min periods of supine rest, 70 degree head-up tilting, submaximal bicycling exercise and post-exercise recovery. Total variance and the power of the spectral components of blood pressure (HF, respiratory-related; LF, 0.03-0.14 Hz; and VLF, 0.02-0.003 Hz) were measured. RESULTS: Compared with control subjects, CHF patients have, first, a normal overall blood pressure variability during supine rest but a failure to increase this variability in response to head-up tilt and exercise; second, a suppressed LF spectral component of blood pressure at rest and in response to head-up tilt and exercise; and third, reappearance of LF blood pressure power during postexercise recovery. CONCLUSIONS: In CHF patients, overall blood pressure variability and its LF spectral component are altered at rest and during sympathoexcitatory manoeuvres. Somewhat paradoxically, however, the depressed LF blood pressure power is partially restored during a 15-min recovery period, indicating that at least part of the CHF-related alterations of blood pressure variability have the potential to revert back towards normal under appropriate physiological circumstances.

Bicycling↗

PubMed1999

Protection by shear stress from collar-induced intimal thickening: role of nitric oxide.

Nitric oxide (NO) has potent relaxant and antiproliferative effects on vascular smooth muscle cells, which may represent an important antiatherosclerotic mechanism. Since one of the major stimuli for NO release is flow-related shear stress, we have investigated (1) the effect of increased shear stress on neointimal formation induced in the rabbit carotid artery by enclosing the vessel in a nonconstrictive silicone soft collar and (2) the role of NO in the antiproliferative effect of increased shear stress. Forty-three New Zealand White rabbits were used. High shear stress in the left common carotid artery (CCA) was induced by ligature of the contralateral right internal carotid artery; intimal thickening was produced by the positioning a nonconstrictive silicone soft collar around the left CCA. To evaluate the role of NO, N(G)-nitro-L-arginine methyl ester (L-NAME) was orally administered at a subpressor dose. In all rabbits, arterial blood pressure, heart rate, arterial diameters, and blood flow velocities of both CCAs were determined at days 0, 3, 7, and 14. At the end of the study, all rabbits were euthanized, and histological analyses were performed on both CCAs of each animal. The presence of the collar was associated with a marked degree of intimal hyperplasia (intimal/medial area ratio 29+/-3.0% in collared arteries compared with 3+/-0.7% in sham control [noncollared] arteries, P<0.001). The increase in blood flow almost completely inhibited neointimal formation and induced an increase in arterial diameter of approximately 30%. The effects of increased blood flow were reversed by the administration of L-NAME. In conclusion, we demonstrate that in collar-induced intimal thickening, a chronic increase in shear stress (1) almost completely inhibits intimal thickening, and (2) this protective effect is mediated by NO production.

Animals↗

PubMed1999

Heart rate-dependent stiffening of large arteries in intact and sympathectomized rats.

In the anesthetized rat, acute increases in heart rate are accompanied by a reduction in arterial distensibility, which is a significant phenomenon in elastic-type vessels such as the common carotid but much less evident in muscle-type vessels such as the femoral artery. Because the sympathetic nervous system importantly reduces arterial distensibility, the present study aimed to determine whether sympathetic influences (1) are involved in the heart rate-dependent changes in arterial distensibility and (2) exert differential effects on elastic-type versus muscle-type arteries. To address this issue, 9 sympathectomized (6-hydroxydopamine) and 10 vehicle-treated, 12-week-old, pentobarbitone-anesthetized Wistar-Kyoto rats were subjected to atrial pacing via a transjugular catheter at 5 different randomly sequenced rates (280, 310, 340, 370, and 400 bpm). After each step, spontaneous sinus rhythm was allowed to return to normal. Common carotid and femoral artery diameters were measured by an echo Doppler device (NIUS 01), and blood pressure was measured via catheter inserted into the contralateral vessel. Arterial distensibility was calculated over the systolic-diastolic pressure range according to the Langewouters formula. In the common carotid artery, progressive increases in heart rate determined progressive and marked reductions of distensibility (range, 15% to 43%) in sympathectomized and intact rats. In the femoral artery, the stiffening effect of tachycardia was present in sympathectomized rats (range, 21% to 42%), at variance with the inconsistent changes observed in intact rats. In conclusion, our experiments support the notions (1) that in predominantly elastic-type arteries, the stiffening effect of tachycardia is exerted independently of sympathetic modulation of the vessel wall properties and (2) that in predominantly muscle-type arteries, removal of sympathetic influences unmasks the stiffening effect of tachycardia.

Animals↗

PubMed1998

Lack of autonomic contributions to tonic nitric oxide-mediated vasodilatation in unanesthetized free-moving rats.

OBJECTIVE: To clarify the controversial issue of whether autonomic influences modulate vascular nitric oxide-mediated vasodilatation or even directly contribute to production of nitric oxide (NO) via nitroxidergic fibers. METHODS: Chronic venous and arterial catheters were implanted in Wistar-Kyoto rats (n = 65) for continuous blood pressure measurement, drug administration and blood sampling. Tonic NO-dependent vasodilatation in the conscious free-moving animal was evaluated as the pressor response to inhibition of NO synthesis by intravenous L-monomethylarginine (a 100 mg/kg intravenous bolus plus 0.5 mg/kg per min infusion for 30 min). Experiments were performed under control conditions, chemical sympathectomy by 6-hydroxy-dopamine, ganglionic blockade by hexamethonium, and surgical denervation of sino-aortic baroreceptors. RESULTS: Baseline mean arterial pressure was 100+/-4 mmHg (mean +/- SEM) in control rats and 73+/-3, 62+/-5, and 105+/-10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. The peak increase in mean arterial pressure after administration of L-monomethylarginine was 38+/-3 mmHg in control rats and 51+/-3, 50+/-6, and 63+/-10 mmHg in sympathectomized, ganglion-blocked, and denervated rats, respectively. Epinephrine and norepinephrine levels in rats of separate groups of unanesthetized control, sympathectomized and ganglion-blocked animals were measured by high-performance liquid chromatography from an arterial blood sample, the results indicating drastic reductions in levels of both catecholamines in the ganglion-blocked (but not in the sympathectomized) rats compared with those in the control rats. CONCLUSIONS: Tonic NO-dependent vasodilatation can normally be maintained in the unanesthetized unrestrained rat irrespective of autonomic or humoral adrenergic influences.

Animals↗

PubMed1998

Nitric oxide dependent vasodilation in young spontaneously hypertensive rats.

Conflicting evidence exists on the possible impairment of tonic nitric oxide (NO) mediated vasodilation as a causative factor in the genesis of human as well as experimental hypertension. We evaluated the tonic NO-dependent vasodilation from the pressor response to NO synthesis inhibition by NG-monomethyl-L-arginine (L-NMMA) in 9 conscious, chronically instrumented spontaneously hypertensive rats (SHR) at 12 weeks of age, ie, during the early established hypertensive stage. Nine age-matched Wistar-Kyoto rats (WKY) were used as controls. The pressor responses to L-NMMA (100 mg . kg-1 IV bolus plus 1.5 mg . kg-1 . min-1 infusion for 60 minutes) as well as to non NO-dependent pressor stimuli, namely, vasopressin (2, 4, and 8 ng . kg-1) and phenylephrine (0.5, 1, and 2 microg . kg-1) given as IV boluses, were assessed both under control conditions and during suppression of autonomic reflexes by hexamethonium (30 mg . kg-1 IV bolus+1.5 mg . kg-1 . min-1 infusion). Rather than being reduced, the pressor responses to L-NMMA were 39% and 71% larger in the control and areflexic conditions, respectively, than those observed in WKY (both P<0.01). A similar pattern was observed for the pressor responses to vasopressin (+37% and +68% in the control and areflexic conditions, respectively; both P<0.01) and phenylephrine, (+20% and +52%; both P<0.05). Additional groups of 6-week-old prehypertensive SHR (n=11) and age-matched WKY (n=11) were subjected to an identical protocol: in these animals, the pressor responses to L-NMMA were similar in each strain, as were the pressor responses to vasopressin and phenylephrine in both control and areflexic conditions. In conclusion, our observations indicate that during the developmental phase of hypertension in the SHR model, namely, during the prehypertensive as well as the early established hypertensive stage, NO-dependent vasodilation is preserved (if not enhanced) so that a putative impairment of this function provides no significant pathogenic contribution to the onset of hypertension in this experimental model.

Aging↗

PubMed1998

Methods to quantify sympathetic cardiovascular influences.

This paper will critically review the main features of the various techniques (plasma noradrenaline assay, noradrenaline spillover technique, microneurographic recording of postganglionic muscle sympathetic nerve and power spectral analysis of blood pressure and heart rate signals in specific bands) currently employed to assess sympathetic cardiovascular control in humans. After highlighting the advantages and limitations of each approach, the paper will describe some of the results obtained by employing the above mentioned techniques to detect abnormalities in sympathetic cardiovascular tone in physiological and pathological conditions.

Arousal↗

PubMed1997

Differential alterations of common carotid and femoral artery distensibility in 12-week-old spontaneously hypertensive rats.

OBJECTIVE: In essential hypertension, the mechanical properties of the radial artery have been shown to be largely unaltered, whereas more controversial and less reliable data have been obtained for the common carotid artery. We therefore examined the distensibility/pressure relationships of the predominantly elastic common carotid artery and of the predominantly muscle-type femoral artery in 12-week-old normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: Eleven 12-week-old SHR and 10 age-matched WKY rats were anesthetized with sodium pentobarbitone. Blood pressure and pulse rate were measured by catheters inserted in the common carotid and in the femoral arteries, while contralateral arterial diameter was continuously recorded via an echo-tracking device. Arterial compliance was derived according to the Langewouters formula, and its values were normalized for the diameter, to obtain distensibility/pressure curves and to calculate the distensibility index. The Peterson elastic modulus was also calculated in order to obtain a pressure-independent estimate of arterial mechanical properties. RESULTS: Femoral artery distensibility/pressure curves and distensibility index were similar in the two groups of rats, the latter being 1.13+/-0.13 mm/mmHg10(-3) in SHR and 1.28+/-0.15 mm/mmHg10(-3) in WKY rats (means+/-SEM; NS). In contrast, in SHR, common carotid artery mechanical properties were clearly impaired, as shown by a marked reduction in distensibility index (2.55+/-0.16 mm/mmHg10(-3) in SHR versus 3.4+/-0.3 mm/mmHg10(-3) in WKY rats; P< 0.05), and by a significant increase in the Peterson elastic modulus. CONCLUSIONS: In the SHR model, high blood pressure alters the mechanics of large arteries even in the relatively early stage of the disease; however, the alterations are not homogeneous inasmuch elastic-type vessels are affected to a much greater extent than muscle-type vessels.

Animals↗

PubMed1997

Effect of sympathectomy on mechanical properties of common carotid and femoral arteries.

Sympathetic stimulation is accompanied by a reduction of arterial distensibility, but whether and to what extent elastic and muscle-type arterial mechanics is under tonic sympathetic restraint is not known. We addressed this issue by measuring, in the anesthetized rat, the diameters of the common carotid and femoral arteries with an echo-Doppler device (NIUS 01). Blood pressure was measured by a catheter inserted contralaterally and symmetrically to the vessel where the diameter was measured. Arterial distensibility over the systolic-diastolic pressure range was calculated according to the Langewouters formula. Data were collected in 10 intact (vehicle pretreatment) and 9 sympathectomized (6-hydroxydopamine pretreatment) 3-month-old Wistar-Kyoto rats. Compared with the intact animals, sympathectomized rats showed a marked increase in arterial distensibility over the entire systolic-diastolic pressure range. When quantified by the area under the distensibility-pressure curve, the increase was 59% and 62% for the common carotid and femoral arteries, respectively (P<.01 for both). In the femoral but not in the common carotid artery, sympathectomy was accompanied also by an increase in arterial diameter (+18%, P<.05 versus intact). Therefore, in the anesthetized normotensive rat, sympathetic activity exerts a tonic restraint on large-artery distensibility. This restraint is pronounced in elastic vessels and even more pronounced in muscle-type vessels.

Animals↗

PubMed1996

Heart rate-dependence of arterial distensibility in vivo.

OBJECTIVES: Viscous and inertial components contribute to arterial distensibility and compliance in vitro. The purpose of our study was to determine whether this phenomenon is of relevance in vivo, namely, whether arterial compliance is altered by an increase in heart rate. DESIGN: Arterial diameter was assessed by an echo-Doppler device in a common carotid and femoral artery, namely, in a large elastic and a muscle artery. The studies were performed in 12-week-old pentobarbitone-anaesthetized Wistar-Kyoto rats subjected to atrial pacing via a transjugular unipolar catheter at five different randomly sequenced rates (280, 310, 340, 370 and 400 beats/min). After each stage, spontaneous sinus rhythm was allowed to return. Blood pressure was measured via a catheter inserted into the carotid or femoral artery contralateral to the vessels in which the diameter was measured. Arterial compliance and distensibility values were derived according to the Langewouters formula. RESULTS: A progressive increase in heart rate caused by pacing was accompanied by progressive and marked reductions in carotid artery compliance and distensibility. When quantified by the area under the distensibility-pressure or compliance-pressure curve the reduction was in the range 15-43%. Although a tendency to a similar phenomenon was observed in the femoral artery, in the latter vessel the reduction in distensibility and compliance was less marked and statistically insignificant. CONCLUSIONS: In the anaesthetized rat acute increases in heart rate are accompanied by reductions in arterial compliance and distensibility. The effect is greater in elastic than in muscle arteries.

Animals↗

PubMed1996

Sympathovagal interplay in the control of overall blood pressure variability in unanesthetized rats.

The role of sympathetic and parasympathetic influences in the control of overall blood pressure variability was studied in chronically instrumented, freely behaving Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) subjected to sympathectomy by 6-hydroxydopamine (100 micrograms/kg ip) twice in 1 wk (effectiveness verified by abolition of pressor and tachycardic response to tyramine, 150 mg/kg i.v.) and/or to cholinergic blockade by atropine (0.7 mg/kg i.v.). Overall heart rate and blood pressure variabilities were measured as variation coefficients computed beat to beat on 90-min blood pressure recordings. As compared with the vehicle-treated controls, sympathectomized rats had much larger blood pressure variability (WKY, +61%, SHR, +86%, both P < 0.01). Cholinergic blockade superimposed to sympathectomy caused heart rate variability to markedly fall and the already augmented blood pressure variability to further rise 47% in WKY and 28% in SHR (both P < 0.01). Prolonged observation of the animals revealed the systematic occurrence of rapid blood pressure falls occurring at the onset of locomotor activity, accounting for a substantial fraction of the sympathectomy-related increase in blood pressure variability. It is concluded that 1) under undisturbed daily life conditions, sympathetic influences oppose blood pressure variations, presumably by adjusting their vasoconstrictor influences to compensate for the metabolic vasodilation occurring in functionally active tissues; 2) when sympathetic vascular control is lost, vagally mediated heart rate variations oppose the rise in blood pressure variability, possibly via rapid changes in cardiac output that partly offset the fluctuations in total peripheral resistance; and 3) chronic hypertension fails to alter these cardiovascular regulatory mechanisms.

Animals↗

PubMed1995

Autonomic and ventilatory components of heart rate and blood pressure variability in freely behaving rats.

The relative role of parasympathetic, sympathetic, and ventilatory influences in the genesis of blood pressure and R-R interval variability is controversial. In 13 freely behaving WKY rats instrumented with venous and arterial catheters and chest electrodes, mean arterial pressure (MAP, mmHg), R-R interval (ms), and respiratory fluctuations were monitored for 90 min in the control condition and after intravenous atropine (0.75 mg/kg) and/or propranolol (1 mg/kg). Spectral power (pw) in the 0.25- to 0.75-Hz (midfrequency, MF) and the 0.75- to 3.0-Hz (high-frequency, HF, respiratory-synchronous) bands was computed in sequences of 400 heartbeats by use of a combined autoregressive analysis. Atropine reduced but did not abolish HF R-R interval pw (from 1.73 +/- 0.50 to 0.39 +/- 0.27 ms2, P < 0.01) and halved HF MAP pw (from 0.41 +/- 0.30 to 0.21 +/- 0.12 mmHg2, P < 0.05), whereas propranolol did not affect HF pw of the R-R interval or MAP. Propranolol also failed to significantly modify MF R-R interval pw (from 0.48 +/- 0.44 to 0.40 +/- 0.34 ms2, P = NS) or MF MAP pw (from 0.54 +/- 0.39 to 0.42 +/- 0.20 mmHg2, P = NS), whereas atropine virtually abolished MF R-R interval pw (from 0.48 +/- 0.44 to 0.01 +/- 0.01 ms2, P < 0.01) and also significantly reduced MF MAP pw (from 0.54 +/- 0.39 to 0.33 +/- 0.24 mmHg2, P < 0.01). The effects of combined blockade were similar to those of atropine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Sympathectomy and cardiovascular spectral components in conscious normotensive rats.

We examined the extent to which sympathetic influences are reflected by spectral powers of blood pressure and pulse interval in specific frequency bands in spontaneously behaving Wistar-Kyoto rats subjected to continuous intraarterial blood pressure recording. The rats were pretreated with 6-hydroxydopamine (150 mg/kg twice in 1 week, n = 19) to produce chemical sympathectomy or received vehicle (n = 15). In the sympathectomized group, additional monitoring sessions were performed with rats under alpha-adrenergic receptor blockade with phenoxybenzamine (n = 8), beta-receptor blockade with propranolol (n = 7), or cholinergic receptor blockade with atropine (n = 8). Blood pressure signals were analyzed by a computer to calculate spectral powers (fast Fourier transform) in the low-frequency (0.025 to 0.1 Hz), mid-frequency (0.1 to 0.6 Hz), and high-frequency (0.8 to 3.0 Hz) bands. In sympathectomized rats, low-frequency power of blood pressure was 70% greater than in intact rats, whereas mid-frequency power was 60% smaller (P < .05 for both) and high-frequency power was unchanged. High-frequency power of pulse interval was also unchanged in sympathectomized rats, whereas low- and mid-frequency powers were reduced by approximately 50% (P < .05). No further alterations in spectral powers were observed by adding alpha- or beta-adrenergic blockade to sympathectomy, whereas adding cholinergic blockade caused a striking reduction in all pulse interval powers. Thus, mid-frequency blood pressure power depends on sympathetic but also to a substantial extent on nonsympathetic influences. Sympathetic influences do not contribute to low-frequency blood pressure power, having instead a restraining effect. The low- and mid-frequency pulse interval powers depend on both sympathetic and vagal influences. Thus, no blood pressure or pulse interval power in the mid- and low-frequency ranges can be regarded as a specific marker of sympathetic activity.

Adrenergic alpha-Antagonists↗

PubMed1995

Sympathetic, parasympathetic and non-autonomic contributions to cardiovascular spectral powers in unanesthetized spontaneously hypertensive rats.

OBJECTIVE: To determine whether spectral powers of blood pressure and pulse interval can specifically reflect sympathetic and parasympathetic effects in unanesthetized, free-moving spontaneously hypertensive rats (SHR). DESIGN: Spectral powers were observed before and after various autonomic interventions in chronically instrumented rats. MATERIALS AND METHODS: Chemical sympathectomy was produced in 12-week-old SHR by repeated injections of 6-hydroxydopamine, while control rats were given vehicle alone. Chronic arterial and venous catheters were inserted in the femoral artery and vein. Blood pressure was recorded beat-to-beat for 90 min in free-moving rats; further recording sessions were obtained under additional alpha-receptor blockade with phenoxybenzamine at 1 mg/kg and/or additional cholinergic blockade with atropine at 0.8 mg/kg. Off-line computer analysis (fast Fourier transform) provided estimates of low- (0.025-0.1 Hz), mid- (0.1-0.6 Hz) and high-frequency (0.8-3.0 Hz) powers for blood pressure and pulse interval over consecutive periods of 100 s. RESULTS: The most noticeable findings were that sympathectomy produced a striking increase in the low-frequency power of blood pressure and a tendency (borderline statistical significance) to reduce the mid-frequency power of blood pressure. Additional alpha-receptor blockade had no effect on any spectral power whereas additional cholinergic blockade caused a further increase in the low-frequency blood pressure power and a drastic reduction in all pulse interval powers. CONCLUSIONS: In the unanesthetized SHR, sympathetic activity opposes low-frequency and marginally promotes mid-frequency blood pressure fluctuations; the pulse interval spectral expression of vagal effects is spread throughout the range of frequencies explored and is not confined to the high-frequency band. These data indicate that in SHR no spectral power can specifically reflect the effects of either autonomic limb.

Adrenergic Fibers↗

PubMed1995

Reproducibility of ultrasound assessment of common carotid and femoral artery compliance and distensibility in the anesthetized rat.

OBJECTIVE: To validate ultrasound assessment of common carotid and femoral artery compliance and distensibility in the anesthetized rat. MATERIALS AND METHODS: A reproducibility study was performed by taking measurements twice on two different days in anesthetized Wistar-Kyoto (WKY) rats. The common carotid or femoral arterial diameter on one side and the contralateral arterial blood pressure were measured using a 10-MHz probe echo-Doppler device and an arterial catheter, respectively. The pressure and diameter data were stored in a computer programmed to calculate the arterial compliance and distensibility coefficients (Reneman formulas) and compliance and distensibility indices (arctangent model of Langewouters). A second experimental session was repeated 1 day later, and mean values, day-to-day mean differences and repeatability coefficients were calculated for each parameter. RESULTS: For both the common carotid and the femoral artery, the mean values for heart rate, mean arterial pressure, arterial diameter, arterial compliance and arterial distensibility were similar on the first and second days; mean day-to-day differences were small and repeatability coefficients were in the range 5-10% of the mean value for diameter and mean arterial pressure and 10-20% of the mean value for compliance and distensibility. CONCLUSIONS: In the anesthetized rat, ultrasound evaluation of the mechanical properties of the common carotid and femoral arteries is a reliable and reproducible technique.

Anesthesia, General↗