Biomedical subjects

S Perlini

Publications and source records attributed to S Perlini.

At least 19 recordsLinked to original sources

PubMed2001

Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of chamber geometry.

BACKGROUND: It is still unclear whether substantial regression of hypertensive left ventricular hypertrophy (LVH) and normalization of chamber geometry are associated with improved left ventricular (LV) myocardial function. METHODS AND RESULTS: Midwall mechanics were evaluated in 152 patients undergoing 1 year of effective antihypertensive treatment. Two-dimensionally directed M-mode echocardiography was performed as follows: (1) after a 4-week placebo "run-in" period, (2) after 1 year of treatment with 20 mg/d lisinopril (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3) after a final 1-month placebo period to allow blood pressure (24-hour average ambulatory monitoring) to return to pretreatment levels. Treatment-induced reductions in blood pressure (from 149+/-16/95+/-11 to 131+/-12/83+/-10 mm Hg, P:<0.05) and circumferential end-systolic wall stress (from 84+/-22 to 72+/-19 g/cm(2), P:<0.05) were associated with a marked reduction in LV mass index (from 159+/-30 to 133+/-26 g/m(2), P:<0.05). LVH regression was accompanied by an increase in midwall fractional shortening (from 19.7+/-2.7% to 20.9+/-2.7%, P:<0.05) and by a decrease in relative wall thickness (from 48.2+/-7.7% to 44.1+/-6.7%, P:<0.05). The improvement in midwall function associated with afterload reduction and substantial LVH regression persisted after antihypertensive therapy withdrawal and restoration of the hypertensive state. Despite a significant increase in end-systolic wall stress, further LV chamber remodeling did not occur. The preservation of relative wall thickness was associated with a persistent improvement in midwall systolic function. CONCLUSIONS: Regression of concentric LVH is associated with an improvement of midwall systolic function, which is more dependent on the normalization of LV geometry than on the reduction in LV systolic stress.

Adult↗

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↗

PubMed2001

Antiadrenergic effects of adenosine in pressure overload hypertrophy.

In the present study, we sought to evaluate whether the antiadrenergic action of adenosine in the heart is altered in pressure overload hypertrophy produced in rats by suprarenal aortic banding. Epicardial and coronary effluent adenosine and inosine concentrations and release were significantly elevated in compensated pressure overload hypertrophy but not in hearts with left ventricular failure. In pressure overload hearts, the contractile response to beta-adrenergic stimulation was less inhibited by incremental concentrations of either adenosine or the selective A(1) receptor agonist chloro-N:(6)-cyclopentyl adenosine than in controls. Furthermore, the extent of desensitization to the antiadrenergic actions of adenosine in pressure overload hypertrophy appeared to be proportional to the extent of chamber dilation and dysfunction. A 60-minute infusion of adenosine produced a sustained antiadrenergic effect that lasted up to 45 minutes after the infusion was terminated in both controls and hearts with compensated hypertrophy. This effect was not observed in the decompensated left ventricular failure group. Subsequent infusion with adenosine of the A(2A) receptor antagonist 8-(3-chlorostyryl)-caffeine to counteract the proadrenergic effect of A(2A) receptor stimulation did not alter the decreased sensitivity to the antiadrenergic actions of adenosine in hypertrophied hearts. Finally, isolated myocytes from hypertrophied hearts demonstrated a decreased ability to suppress isoproterenol-elicited increases in [Ca(2+)](i) transients in the presence of adenosine and the A(2A) receptor antagonist compared with myocytes from control hearts. Myocardial adenosine concentrations increase during the compensated phase of pressure overload hypertrophy but then decrease when there is evidence of decompensation. The antiadrenergic actions of adenosine transduced via the myocardial A(1) receptor are diminished in pressure overload hypertrophied hearts. These factors may render these hearts more vulnerable to the detrimental effects of chronically increased sympathetic activity.

Adenosine↗

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

Mechanism of binocular interaction in refraction errors: study using pattern-reversal visual evoked potentials.

In this study we sought to determine whether a natural condition involving fine discrimination, for example moderately severe myopia, might yield interesting information regarding the binocular interaction expressed by visual evoked potentials (VEPs). We studied ten normal subjects with a mild refraction deficits. Transient VEPs were elicited by monocular and binocular stimulation under conditions of natural and lens-corrected vision. The visual stimulus was a pattern-reversal checkerboard consisting of 15' and 40' checks. VEPs in response to binocular stimulation were compared with monocular VEPs. We plotted the monocular 'better-VEP' and 'worse-VEP' response, since significant differences between individual eye stimulations were present. We found no significant difference between the mean N75 and P100 latencies of the binocular VEP and the better monocular VEP, regardless of the check size used and of natural or corrected vision. Under all stimulus conditions, the mean amplitude of the N75-P100 of the binocular VEPs was also larger than the better monocular VEP response. The difference proved more significant when we stimulated our subjects with smaller squares and left vision uncorrected. The mean P100-N145 amplitude obtained with binocular stimulation was larger than the better monocular VEP response only when using small checks (15') and uncorrected vision. Overlapping latencies are consistent with an earlier hypothesis that monocular and binocular VEPs originate postsynaptically from the binocular neurons in the primary visual cortex. The gain in amplitude achieved by binocular stimulation may depend upon the removal of 'tonic interocular inhibition' and/or on a cortical modulatory mechanism.

Adult↗

PubMed1999

Nonischemic end-systolic performance. Effect of alterations in regional and global left ventricular contractility.

Nonischemic end-systolic performance decreases during ischemia. These changes in performance are likely to be dependent on the size and site of the ischemic zone, as well as the prevailing loading conditions. This study was designed to examine the effect of regional and generalized changes in inotropy on nonischemic end-systolic performance, independent of the ischemic zone size. Twenty dogs were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure-thickness relationship data were obained during vena-caval balloon inflation. Measurements were obtained before and 90 s after left circumflex (LC) artery occlusion. Then, simultaneous with the occlusion of the LC artery, isoproterenol (0.04 microg/ml) was infused into the left anterior descending artery. After recovery, the same protocol was repeated before and after propranolol (0.5 mg/kg). In a separate set of animals, the same measurements were made following 2.5 and 5 microg/kg/min dobutamine. The effect of ischemia on the nonischemic end-systolic pressure-thickness relationship was expressed as the extent to which the relationship is shifted to the left. Infusion of intracoronary isoproterenol into the perfusion bed of the nonischemic zone produced a significant increase in the slope of the end-systolic pressure-thickness relationship. During ischemia, however, the extent of leftward shift of this relationship was less than that following beta-blockade. Intravenous dobutamine resulted in a dose-dependent increase in the slope of the nonischemic end-systolic pressure thickness relationship, but the extent of leftward displacement of the relationship in response to regional ischemia was less than that following the control occlusion. The nonischemic segment is coupled with the nonfunctioning ischemic zone in such a way that it is required of the nonischemic segment to operate at decreased end-systolic thickness for any end-systolic pressure, the extent of which is to be determined, in part, by the size of the ischemic zone and the contractile state of the nonischemic myocardium. The lower the contractile state prior to coronary occlusion the greater extent of leftward shift of the pressure-thickness relationship.

Animals↗

PubMed1998

Adenosine mediates sustained adrenergic desensitization in the rat heart via activation of protein kinase C.

Adenosine attenuates the myocardial metabolic and contractile responses induced by ss-adrenergic stimulation. Our study was conducted to investigate the longevity of this antiadrenergic action after adenosine exposure. Adenosine (33 micromol/L) was infused into isolated perfused rat hearts for 1, 5, 30, or 60 minutes, and the adrenergic responsiveness (AR) to isoproterenol (10(-8) mol/L) was determined at the end of each infusion period and during a 45-minute adenosine washout period. Interstitial levels of adenosine, as determined from epicardial surface transudates, returned to preinfusion levels within 10 minutes of washout. The duration of adenosine infusion had no effect on the extent of attenuation of AR at the end of the infusion. Whereas AR returned to preadenosine levels with washout of shorter adenosine infusions (1 and 5 minutes), there was a slow and incomplete recovery of AR after the longer exposures (30 and 60 minutes) to adenosine. The magnitude of this persistent antiadrenergic effect (PAE) of adenosine at 15 minutes of washout was proportional to the epicardial concentration of adenosine during infusion of the nucleoside. Infusion of adenosine either with the nonselective adenosine receptor antagonist 8-p-sulfophenyl theophylline or with the selective A1-receptor antagonist 1,3-dipropyl, 8-cyclopentylxanthine, abolished the PAE during the washout period. In addition, the PAE could be demonstrated only with the selective A1-receptor agonist 2-chloro-N6-cyclopentyladenosine and not with the selective A3-receptor agonist 4-aminobenzyl-5'-N methylcarboxamido-adenosine. When the protein kinase C (PKC) inhibitor chelerythrine was coadministered with adenosine, the PAE of adenosine was not apparent during adenosine washout. A 30-minute infusion of phenylephrine, an alpha-adrenergic agonist that enhances PKC activity, produced a PAE that lasted for up to 30 minutes of washout. This effect was prevented by the coinfusion of chelerythrine. Thus, it is concluded that the PAE of adenosine is determined by the myocardial concentration of this nucleoside and is manifested when myocardial concentrations of adenosine returned to baseline levels. Moreover, a 5-minute duration of adenosine exposure is required for the expression of the PAE. This latter effect seems to be dependent on adenosine-induced PKC activation via A1-receptors.

Adenosine↗

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

Effects of chronic adenosine uptake blockade on adrenergic responsiveness and left ventricular chamber function in pressure overload hypertrophy in the rat.

BACKGROUND: Increased sympathetic activity contributes to the progression of heart failure. Adenosine counteracts sympathetic activity by inhibition of presynaptic norepinephrine release and attenuation of the metabolic and contractile responses to beta-adrenergic stimulation. In this study, we tested the hypothesis that the adenosinergic effects (uptake blockade) of dipyridamole may retard the progression of pressure overload hypertrophy in the rat. METHODS AND RESULTS: To verify that the administration of dipyridamole increases myocardial adenosine levels in the rat, epicardial adenosine concentrations were measured from 12 isolated, perfused rat hearts exposed to 10(-7) and 10(-6) mol/l dipyridamole. Adenosine concentrations were increased with both doses of dipyridamole. Also, 9 weeks of dipyridamole treatment resulted in decreased sensitivity to the adenosine A1-receptor agonist, 2-chloro-N6-cyclopentyl adenosine, suggesting that dipyridamole increases adenosine levels in the intact rat. In the second part of the study, rats were divided into either abdominal aortic-banded or sham-operated groups and were treated with either dipyridamole or saline. After 9 weeks of treatment, two-dimensional Doppler echocardiographic studies were performed and the adrenergic responsiveness to 10(-8) mol/l isoproterenol was assessed in vitro. The saline-treated banded group demonstrated concentric left ventricular hypertrophy, abnormal diastolic filling, increased wet lung weights and attenuation of adrenergic responsiveness. In contrast, the dipyridamole-treated banded rats exhibited more concentric geometry (higher relative wall thickness with similar left ventricular mass), normal left ventricular filling characteristics and preserved adrenergic responsiveness. Systolic left ventricular chamber and myocardial function, as assessed by stress-endocardial and midwall shortening relationships, were not significantly altered by banding or dipyridamole treatment. CONCLUSIONS: Dipyridamole treatment prevented the development of abnormal left ventricular chamber filling, preserved adrenergic responsiveness and appeared to attenuate detrimental chamber remodeling in rats with pressure overload hypertrophy.

Adenosine↗

PubMed1997

Effects of preload, afterload and inotropy on dynamics of ischemic segmental wall motion.

OBJECTIVES: This study sought to explore the separate and combined effects of changes in preload, afterload and contractility on the dynamics of systolic bulging. BACKGROUND: The extent of ischemic systolic bulging has been shown to be mechanically disadvantageous to left ventricular pump performance. The factors that determine ischemic segmental wall motion have not been systematically studied. METHODS: Fourteen beagles were instrumented with sonomicrometers, micromanometer pressure gauges and a balloon in the inferior vena cava. Regional function was evaluated before and after 90 s of proximal left circumflex coronary artery occlusion. Occlusions were repeated after increasing systolic pressure by 5 to 10 (afterload I) and 15 to 20 mm Hg (afterload II) with graded aortic occlusion during inotropic stimulation with dobutamine (2.5 and 5 micrograms/kg body weight per min intravenously), with simultaneous 5 micrograms/kg per min dobutamine infusion and afterload II and during 2.5% halothane (negative inotrope) concentration. A 20-min recovery period was allowed between each stage of the experiment so that regional function returned to its preocclusion level. Ischemic wall motion was characterized by percent systolic bulging and its peak positive systolic lengthening rate (+dL/dt). RESULTS: Because bulging is markedly influenced by regional preload, systolic bulging was characterized over a wide range of end-diastolic lengths of the ischemic segment during caval balloon occlusion. During each intervention, a decrease in regional preload increased the extent of percent systolic bulging. This preload dependency was more pronounced with dobutamine infusions. An increase in afterload was not associated with increased percent systolic bulging at any given preload. At a predetermined preload, bulging was not appreciably altered when an increase in left ventricular systolic pressure was not associated with a change in peak positive first derivative of left ventricular pressure (+dP/dt) but was significantly worse when peak +dP/dt increased. Dobutamine caused a dose-dependent increase in percent systolic bulging and peak +dL/dt that was positively correlated with peak +dP/dt. CONCLUSIONS: By using different loading and inotropic interventions and analyzing the regional wall motion behavior over a range of regional preloads, we can conclude that preload and rate of pressure (tension) development are the principal determinants of systolic bulging. Increases in left ventricular pressure alone had a minimal effect on systolic bulging.

Animals↗

PubMed1997

Influence of residual ischaemia on heart rate variability after myocardial infarction.

Despite the growing evidence for the positive predictive value of depressed baroreflex sensitivity and/or reduced heart rate variability after myocardial infarction, the mechanisms involved in these autonomic alterations are not fully understood. Specifically, the possible influence of residual ischaemia has not been assessed. To address this problem we studied the spectral analysis of heart rate variability in 21 patients with a first myocardial infarction in whom the only clinical correlate was the presence of residual ischaemia, as documented by the positive response to both an exercise stress test and an echocardiographic stress test. Data from these patients were compared with those obtained in a group of postmyocardial infarction patients similar for several risk factors, age, site of myocardial infarction, but without residual ischaemia. Patients positive for residual ischaemia had lower power in the whole spectrum (1146 +/- 158 vs 1631 +/- 159 ms2, P = 0.032) as well as in the low and high frequency bands of heart rate variability. A nocturnal increase in high frequency was observed in those without residual ischaemia (from 167 +/- 35 to 242 +/- 51 ms2, +45%, P = 0.034), but not in those with residual ischaemia (from 111 +/- 19 to 141 +/- 29 ms2, +27%, ns). Thus, residual ischaemia reduces heart rate variability after myocardial infarction. The autonomic effects of residual ischaemia probably contribute to its negative prognostic value after myocardial infarction.

Adult↗

PubMed1996

Dynamic right and left ventricular interactions in the rabbit: simultaneous measurement of ventricular pressure-volume loops.

PURPOSE: This study was performed to characterize the dynamic factors determining ventricular interdependence in an open-pericardium intact animal model. MATERIALS AND METHODS: Simultaneous measures of right ventricular (RV) and left ventricular (LV) pressures and volumes in 6 urethane-anesthetized open-chested, open-pericardium rabbits. RV and LV V were calculated every 2 milliseconds. Measurements were made at initial baseline blood volume, and again after two infusions of 20 mL/kg isoconductive colloid solution. At each blood volume level, partial aortic (AO), pulmonary artery (PAO), and inferior vena caval (IVC) occlusions were performed. Biventricular diastolic compliance and end-systolic elastance were calculated from these data. RESULTS: Baseline end-diastolic (ED) and end-systolic (ES) V were 3.29 +/- 0.55 and 2.43 +/- 0.33 mL (mean +/- SD) for the LV, and 3.38 +/- 1.56 and 2.84 +/- 1.36 mL for the RV, respectively. AO increased all LV pressure and volume (P < .05) but did not alter RV ED volume (2.85 +/- 1.20 mL) or ED pressure (3.3 +/- 2.0 to 3.6 +/- 2.1 mm Hg). PAO increased RV ES pressure (P < .05) but did not alter RV ED volume, ED pressure, or ES volume, although it decreased LV ED volume (2.82 +/- 0.59, P < .05). AO also immediately increased end-systolic RV elastance to a value greater than that defined by IVC (7.9 +/- 4.4 to 10.9 +/- 6.6 mm Hg/mL, P < .05). Intravascular volume expansion though increasing baseline pressure and volume, did not alter qualitatively biventricular responses to AO, PA, or IVC. CONCLUSION: Ventricular interdependence has both systolic and diastolic components that have differing directional effects. In the pericardectomized rabbit, increases in RV ED volume decrease LV ED volume by decreasing LV diastolic compliance, but do not alter LV systolic function. Whereas, increases in LV ED volume decrease RV ES volume resulting in an increase in RV maximal elastance, but minimally alter RV diastolic function.

Animals↗

PubMed1996

Effects of preload on regional nonischemic end-systolic performance.

BACKGROUND: Nonischemic segmental performance, assessed by end-systolic measures of shortening and thickening, decreases during ischemia. These changes in performance are likely to be dependent on the size, and, possibly, the site of the ischemic zone. This study was designed to examine the effect of preload, independently from ischemic zone size, on nonischemic end-systolic performance. METHODS: Twelve beagles were instrumented with sonomicrometers and micromanometer pressure gauges. End-systolic pressure length and thickness relationship data were obtained during vena caval balloon inflation. Control data were obtained both in left anterior descending and in left circumflex regions at left ventricular end-diastolic pressures of 5, 10 and 15 mmHg. The left circumflex artery was occluded for 90 s and nonischemic end-systolic pressure length and thickness data were obtained at each diastolic pressure. A 20 min recovery period was allowed between coronary occlusions. RESULTS: The isovolumic bulge in the ischemic area was more pronounced at an end-diastolic pressure of 5 mmHg than it was at an end-diastolic pressure of 15 mmHg. The slope of the nonischemic end-systolic pressure length and thickness relationships decreased at an end-diastolic pressure of 5 mmHg, whereas at 10 and 15 mmHg the slope of these relationships did not change significantly. The shift in the nonischemic end-systolic pressure-length relationship to the right was more pronounced at a low end-diastolic pressure (5 mmHg) than it was at a high end-diastolic pressure (15 mmHg). Similarly, the extent of the shift in the end-systolic pressure-thickness relationship to the left was more marked at a low end-diastolic pressure than it was at the higher end-diastolic pressure. CONCLUSION: Regional ischemia decreases the end-systolic performance of the nonischemic region. The extent of the shift and the degree to which the slopes of the nonischemic end-systolic relations decrease are influenced by loading conditions.

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

Effect of pharmacologically induced mydriasis on the normal variability of retinal oscillatory potentials in man.

In this study we describe certain aspects of normal variability of oscillatory potentials, with particular reference to interaction between pupil size and stimulus intensity. The mean latencies of the earlier oscillatory potentials, O1 and O2, were significantly shorter when adopting the dilated pupil condition than when stimulating with a normal pupil. This occurred at various light intensities, although the difference was more significant at the highest intensity. O1 and O2 latencies became significantly longer as the stimulus intensity was progressively reduced. The latencies of the later components O3 and O4 were unaffected. The O1 and O2 amplitudes were not influenced by pupil size, but a significant reduction occurred with the progressive decrease in stimulus intensity. The later components O3 and O4 are greatly reduced in amplitude after pupil dilatation using higher stimulus intensities; the O4 potential may even disappear in 10% of the cases. These data provide further support for the existence of two distinct behavior patterns for earlier and later oscillatory potentials. Although light adaptation may affect oscillatory potentials, we suggest that in our experimental conditions, oscillatory potential changes may occur as a result of the activity of the neural modulating system, not only as a result of photoreceptor interaction.

Adult↗

PubMed1995

Determinants of respiratory sinus arrhythmia in the vagotomized rabbit.

After cardiac denervation, a small-amplitude respiratory sinus arrhythmia (RSA) has been described in animals and humans. Its mechanical and chemical determinants were investigated in 19 urethan-anesthetized, vagotomized, and mechanically ventilated rabbits. We measured the influence on RSA of arterial blood gases, beta-adrenergic blockade, and phasic and steady changes in right atrial pressure (RAP) induced by changes in tidal volume (VT, 20, 40, 60 ml), respiratory frequency (RF, 10, 20, 30 cycles/min), and dextran-induced RAP increases. Phasic changes in RAP during each recording were quantified as standard deviation of the first derivative of the RAP signal (dRAP) as a measure of magnitude of variations of the rate of change due to respiration. RSA was assessed by combined autoregressive power spectral analysis of R-R interval and respiration on sequences of 256 heart-beats. Despite vagotomy, RSA was present in all recordings in all animals. During room air breathing, RSA changes were dependent on RF and VT (P < 0.025 and P < 0.001, respectively) and correlated with dRAP (P < 0.001) and arterial PO2 (P < 0.001). beta-Adrenergic blockade did not change the amplitude of this residual RSA or its dependence on ventilatory mechanics. Dextran-induced increase in mean RAP from 2.9 to 11.9 mmHg did not modify RSA or dRAP. During 100% O2 inhalation, RSA changes were no longer significantly linked to RF and VT, and also the correlation of RSA with dRAP was reduced (P < 0.05). Changing the arterial PCO2 from 28 to 79 mmHg (induced by increasing dead space at fixed ventilation) did not modify RSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗

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

[Acute myocardial infarction in young age and drug dependence. Review of the literature and personal experience].

UNLABELLED: The authors' personal experience in drug abuse-related acute myocardial infarction (AMI) is reported. STUDY POPULATION: Between January 1991 and May 1994, 6 drug-addict (5 occasional) male patients (pts.) aged 37 +/-3 yrs (Group A) were admitted to our CCU for AMI. Just before hospital admission 4 pts. had inhaled cocaine and 1 had assumed ¿ecstasy¿ tablets; one patient had been heroine-dependent for 5 years and was in an attack of abstinence. The clinical features were compared to those of 17 not drug-addict pts. (Group B) aged <45 years (15 males). DEMOGRAPHIC DATA: In Group A 3/6 pts. were graduated (vs 29.4% in Group B pts.), and nobody belonged to the working class (vs 29.4%); 5/6 pts. (83.3%) were admitted during the week-end (vs 29.4%, p<0.03) and presented a longer time delay between symptoms' onset and hospital admission (7.1 +/- 6.9 hrs in Group A pts. vs 4.7 +/- 4.2 hrs. in Group B pts.). RISK FACTORS: All Group A pts. were smokers (37 +/- 12 cigarettes/day vs 21 +/- 14, p<0.02); 4/6 were heavy alcohol drinkers (vs 29.4%); 1/6 had a family history of ischemic heart disease (vs 35%); nobody was hypertensive(vs 29.4%) or diabetic (vs 5.8%). CLINICAL AND INSTRUMENTAL FINDINGS: On admission, Group A pts. (83.3%) were in Killip class I (vs 82.3%) infarct location was anterior in 3/6 pts. (vs 47%); all pts. were given thrombolitic agents. No significant coronary artery stenosis was found in 3/5 (60%) Group A pts. (vs 23.5% in Group B pts.), where 1 had one-vessel disease (vs 64%%) and 1 had two-vessel disease (vs 11.8%). Ejection fraction was similar in the two groups. No death was observed during follow-up (mean 14.4 +/- 9.6 months, range 3-39 months), 1 patient (Group A) had post AMI angina and reinfarction during coronary angioplasty and 2 pts. continued drug abuse. CONCLUSIONS: AMI in drug addict subjects has to be taken into consideration in particular when the patient is young, male, alcohol consumer, heavy cigarette smoker, and is admitted during the week-end. Further study are warranted to better define therapeutic guidelines.

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