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S Cassarino

Publications and source records attributed to S Cassarino.

14 recordsLinked to original sources
PubMed1999

Investigating feed-forward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations.

BACKGROUND: Analysis of spontaneous fluctuations in systolic arterial pressure (SAP) and pulse interval (PI) reveals the occurrence of sequences of consecutive beats characterized by SAP and PI changing in the same (+PI/+SAP and -PI/-SAP) or opposite (-PI/+SAP and +PI/-SAP) direction. Although the former reflects baroreflex regulatory mechanisms, the physiological meaning of -PI/+SAP and +PI/-SAP is unclear. We tested the hypothesis that -PI/+SAP and +PI/-SAP "nonbaroreflex" sequences represent a phenomenon modulated by the autonomic nervous system reflecting a feed-forward mechanism of cardiovascular regulation. METHODS AND RESULTS: We studied anesthetized rabbits before and after (1) complete autonomic blockade (guanethidine+propranolol+atropine, n=13; CAB), (2) sympathetic blockade (guanethidine+propranolol, n=15; SB), (3) parasympathetic blockade (atropine, n=16), (4) sinoaortic denervation (n=10; SAD), and (5) controlled respiration (n=10; CR). Nonbaroreflex sequences were defined as >/=3 beats in which SAP and PI of the following beat changed in the opposite direction. CAB reduced the number of nonbaroreflex sequences (19. 1+/-12.3 versus 88.7+/-36.6, P<0.05), as did SB (25.3+/-11.7 versus 84.6+/-23.9, P<0.001) and atropine (11.2+/-6.8 versus 94.1+/-32.4, P<0.05). SB concomitantly increased baroreflex sensitivity (1.18+/-0. 11 versus 0.47+/-0.09 ms/mm Hg, P<0.01). SAD and CR did not significantly affect their occurrence. CONCLUSIONS: These results suggest that nonbaroreflex sequences represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the control of heart period.

Animals↗
PubMed1999

Effect of postural changes on cardiovascular responses to static exercise in hypertensive human beings.

OBJECTIVE: In hypertensive patients, exaggerated increases in vascular resistance and arterial blood pressure have been reported on changing posture from supine to upright. In this study we tested the hypothesis that in hypertensive subjects, upright posture induces an increase in the vasoconstrictor and pressor responses to physical exercise. SUBJECTS AND METHODS: We studied 17 males with mild hypertension and 10 sex- and age-matched normotensives. Each performed three bouts of static handgrip at 30% maximum voluntary contraction for 2 min after 10 min of supine rest and, in sequence, after 10 min of sitting and 10 min of standing. Arterial pressure, heart rate and forearm vascular resistance were measured by Finapres and plethysmography, respectively. RESULTS: Exercise posture did not affect the mean arterial pressure and heart rate responses to static handgrip. No significant differences in these responses were observed between the hypertensives and the normotensives in any posture. In the hypertensives (n = 12), forearm vascular resistance did not change significantly from resting values during supine and sitting static handgrip but increased significantly during standing static handgrip. In the normotensives, forearm vascular resistance did not change significantly from resting values during static handgrip in any posture. The forearm vascular resistance response to the standing static handgrip was significantly greater in the hypertensives than the normotensives. The algebraic sum of forearm vascular resistance responses to postural change from sitting to standing plus that induced by sitting static handgrip (i.e. additive reflexes) was significantly less than the forearm vascular resistance response to the standing static handgrip (i.e. combined relexes), indicating a facilitatory interaction between exercise and orthostatic stimuli in hypertensives. In contrast, the algebraic sum of the heart rate responses to postural change from sitting to standing plus that induced by sitting static handgrip was significantly greater than the response to standing static handgrip, indicating an inhibitory interaction. CONCLUSIONS: In hypertensive patients, physiological orthostasis causes an increased vasoconstrictor response to static exercise, but this is opposed by an inhibitory influence on the heart rate response, with the result that the pressor response to static exercise is unaffected by upright posture.

Baroreflex↗
PubMed1998

Peripheral vascular changes after short-term simulated microgravity.

Cardiovascular deconditioning and orthostatic intolerance are the main symptoms experienced by astronauts after space flights. Alterations in the cardiovascular neural regulation have been implicated in the genesis of these disorders, but the mechanisms have not been clearly established. Alterations in the reflex control of circulation from the arterial and cardiopulmonary baroreceptive areas have been mainly hypothesized on the basis of long-term simulated microgravity studies. However, symptoms of orthostatic intolerance, and even fainting, are also observed after short-term exposure to simulated micro-G conditions. The possibility does exist that short-term exposure to micro-G conditions could affect the cardiovascular regulation differently from long-term exposure. Previous studies from this laboratory have shown that arterial baroreflex control of heart rate is not altered after 4 hours Head Down (HD) at -6 degrees, whereas it is significantly decreased after 28 days. Again, the role played by possible disturbances of the vasomotor regulation in the genesis of orthostatic intolerance after short term exposure to simulated microgravity has not yet been clarified. The aim of this study was therefore to evaluate peripheral blood flow changes following 2 and 4 h HD -6 degrees in healthy volunteers.

Adult↗
PubMed1998

[Spontaneous baroreflex control of heart rate during chronic tandropril therapy].

Differently from other vasodilators, the antihypertensive effect of ACE-inhibitors is not accompanied by an increase in resting heart rate which suggests a modulatory action of these drugs on arterial baroreflex control of heart rate. It is debated whether this modulation involve, an increase in gain (or sensitivity) of baroreflex mechanisms controlling heart rate or is due to a baroreflex control resetting. In this study we investigated the arterial baroreflex control of heart rate both in supine rest and during active standing before and after 7 and 30 days of treatment with a new ACE-inhibitor, trandolapril (2 mg per os oid) in 15 mild hypertensive patients. Baroreflex control of heart rate has been dynamically and non-invasively assessed by analysis of the continuous relationship between beat-to-beat spontaneous fluctuations in systolic blood pressure and pulse interval. By this method, sequences of 3 or more consecutive beats in which systolic blood pressure and pulse interval change in the same direction (either increasing or decreasing) are identified and a linear regression is applied to each individual sequence. The mean individual slope of the systolic blood pressure/pulse interval ratio obtained by averaging all slopes computed within a given period, is calculated and taken as an estimate of the spontaneous baroreflex sensitivity for that period. Trandolapril reduced resting blood pressure significantly (from 147.5 +/- 3.3/95.3 +/- 1.5 to 129.5 +/- 3.7/83.6 +/- 1.6 and 126.6 +/- 3.9/84.5 +/- 1.7 mmHg after 7 e 30 days, respectively) without affecting heart rate. The treatment did not alter baroreflex sensitivity but resulted in an apparent leftward shift of the regression line relating systolic blood pressure to pulse interval along the pressure axis, reflecting the lower prevailing level of arterial pressure. The increases in heart rate and blood pressure induced by standing in control conditions were not significantly modified by trandolapril. Baroreflex sensitivity was significantly reduced by standing both in control conditions and, to the same extent, during treatment. These results suggest that ACE-inhibition does not alter the gain of the integrated baroreflex mechanisms controlling heart rate, but results in a baroreflex resetting that may explain the lack of tachycardia normally observed during antihypertensive therapy with ACE-inhibitors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit.

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Anesthesia↗
PubMed1996

Noxious stimuli do not determine reflex cardiorespiratory effects in anesthetized rabbits.

The main purpose of this study is to examine whether the stimulation of an exclusively pain-sensing receptive field (dental pulp) could determine cardiorespiratory effects in animals in which the cortical integration of the peripheral information is abolished by deep anesthesia. In 15 anesthetized (alpha-chloralose and urethan) rabbits, low (3-Hz)- and high-frequency (100-Hz) electrical dental pulp stimulation was performed. Because this stimulation caused dynamic and static reflex contractions of the digastric muscles leading to jaw opening jaw-opening reflex (JOR); an indirect sign of algoceptive fiber activation], experimentally induced direct dynamic and static contractions of the digastric muscle were also performed. The low- and high-frequency stimulation of the dental pulp determined cardiovascular [systolic arterial pressure (SAP): -21.7 +/- 4.6 and 10.8 +/- 4.7 mmHg, respectively] and respiratory [pulmonary ventilation (VE): 145.1 +/- 44.9 and 109.3 +/- 28.4 ml/min, respectively] reflex responses similar to those observed during experimentally induced dynamic (SAP: -17.5 +/- 4.2 mmHg; VE: 228.0 +/- 58.5 ml/min) and static (SAP: 5.8 +/- 1.5 mmHg; VE: 148.0 +/- 75.3 ml/min) muscular contractions. The elimination of digastric muscular contraction (JOR) obtained by muscular paralysis did away with the cardiovascular changes induced by dental pulp stimulation, the effectiveness of which in stimulating dental pulp receptors has been shown by recording trigeminal-evoked potentials in six additional rabbits. The main conclusion was that, in deeply anesthetized animals, an algesic stimulus is unable to determine cardiorespiratory effects, which appear to be exclusively linked to the stimulation of ergoreceptors induced by muscular contraction.

Anesthesia↗
PubMed1995

[Cardiodepressive effects of muscular exercise in spontaneously hypertensive rats].

Conflicting results have been reported on the differences in the cardiovascular reactivity to muscular exercise between normotensive and hypertensive subjects and normotensive subjects with family history of hypertension and normotensive subjects without familial hypertensive history. Also studies performed in spontaneously hypertensive in comparison with normotensive rats have not led to final conclusions. Therefore, the aim of the present study was twofold: to evaluate cardiorespiratory reactivity to different types of muscular exercise in normotensive (WKY) compared to spontaneously hypertensive rats (SHR) at pre-hypertensive and hypertensive stages; to verify the role played by the "muscular reflex drive" in mediating the cardiorespiratory responses in rats. We utilized four groups of anesthetized rats: 8 young WKY, 8 SHR in pre-hypertensive stage, 6 adult WKY and 6 SHR in hypertensive stage. We evaluated the cardiorespiratory responses to (rhythmic) dynamic and (static) isometric contractions of gastrocnemius muscles induced by electrical stimulation of the tibial nerve. Cardiorespiratory responses during the initial phase of dynamic and static contractions of hindlimb muscles were studied. Muscle contractions were elicited by stimulating the tibial nerves at 3 and 100 Hz. We measured: mean arterial pressure (MAP), heart rate (HR), and pulmonary ventilation (VE). Both types of exercise caused a significant decrease in MAP and a significant increase in VE while HR did not change significantly. The four groups of rats did not show significant differences in the pattern of cardiorespiratory responses to muscular exercise. The cardiorespiratory reflexes initiated by activation of muscle receptors, verified by interrupting the afferents from the contracting muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1991

On the role of neural mechanisms in the cardiocirculatory inhibitory action of alpha-human atrial natriuretic peptide in the anesthetized rabbit.

The effects induced by alpha-human 28-amino acid residue atrial natriuretic peptide (alpha-hANP) on arterial pressure, heart rate and vascular resistance, measured as hindlimb perfusion pressure (HPP), were examined in anesthetized rabbits. In particular, the involvement of the autonomic nervous system in mediating the cardiocirculatory effects of alpha-hANP was investigated. Intravenous alpha-hANP (8 micrograms/kg, bolus injection) in anesthetized rabbits caused a sustained decrease in atrial pressure, a transient decrease in HPP and no significant changes in heart rate. After sinoaortic denervation, alpha-hANP produced a greater decrease in arterial pressure and in hindlimb vascular resistance and also a consistent decrease in heart rate. Bilateral vagotomy did not significantly alter the cardiocirculatory responses to alpha-hANP in either normal or in sinoaortic denervated rabbits. Intravenous infusion of alpha-hANP (2 micrograms/kg bolus + 0.2 micrograms/kg per min) did not substantially change the baroreflex cardiocirculatory responses to loading and unloading carotid and aortic baroreceptors with bilateral carotid occlusion and phenylephrine or nitroglycerin bolus injection. In addition, alpha-hANP infusion did not modify the cardiovascular reflex responses to chemical stimulation of neural receptors (sensory endings of group III and IV somatic afferents) in the hindlimb muscles which are primarily mediated by sympathetic nerves in the anesthetized rabbit. Pharmacological blockade of the autonomic nervous system with atropine and guanethidine did not reduce the hypotensive and bradycardic effects caused by alpha-hANP in sinoaortic denervated animals. The results indicate that in anesthetized rabbits: (1) alpha-hANP can induce inhibitory cardiocirculatory responses (hypotension, bradycardia, musculocutaneous vasodilation) which are consistently offset by the sinoaortic baroreceptor system; (2) alpha-hANP does not alter the reflex control of arterial pressure and heart rate by arterial baroreceptors and muscle chemosensitive receptors; (3) activation of cardiopulmonary vagally-mediated depressor reflexes does not contribute to the inhibitory cardiovascular action of alpha-hANP; and (4) inhibitory effects on sympathetic activity do not constitute a significant component of the cardiocirculatory action of alpha-hANP.

Anesthesia↗
PubMed1990

[Integrated cardiorespiratory changes induced by chemical stimulation of muscular receptors].

Muscular exercise is accompanied by evident and perfectly matched cardiovascular and respiratory adjustments to avoid changes in arterial blood gases. The mechanisms responsible for this perfect regulation have not yet been defined. Our previous experimental investigations have shown that a consistent rate of cardiorespiratory reflex responses to exercise is caused by chemosensitive muscular receptors activation. The 2 different types of classical muscular exercise (rhythmic and isometric exercise) are joined with the 2 different patterns of cardiorespiratory reflex responses attributed in our opinion to the activation of 2 different kinds of muscle receptors (K and P). It has been observed that the increase in ventilation (VE), elicited by activation of both types of chemoreceptors during muscular experimental exercise is not accompanied by significant variations of partial pressure of CO2 (PaCO2) in the arterial blood (isocapnic hyperpnea). This suggest that muscular chemoreceptor activation during physical exercise determines an adequate cardiopulmonary matching. The main purpose of the present study has been to verify, in anesthetized rabbits, if also the chemical activation of muscular receptors was able to evoke reflexly an adequate degree of cardiopulmonary matching. The ventilation reflex changes and the concomitant variations of PaCO2 induced by injection of bradikinin (BK 250 ng) and hypertonic solutions (NaCl 10% 1 ml) in femoral artery have been evaluated in 10 anesthetized rabbits. The PaCO2 modifications observed during reflex hyperpnea have been compared with those recorded during hyperpnea induced by artificial ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Study of the interactions of atrial natriuretic peptides with the autonomic nervous system. Effects on cardiocirculatory and respiratory reflexes caused by activation of chemosensitive muscle receptors].

In order to verify the hypothesis that possible interactions with the autonomic nervous system may contribute to the cardiovascular effects of atrial natriuretic factor (ANF), 9 rabbits were anesthetized to study the effect of the infusion of synthetic human ANP (2 mcg/kg in bolus followed by 0.2 mcg/kg/min for 20 min iv) on the reflex responses induced by intra-arterially injected BK (250 ng) and hypertonic NaCl (10%) or glucose (40%). The infusion of ANP provoked a decrease in systolic (SBP, 14%) and diastolic (DBP, 8%) pressure without any significant changes in heart rate (HR). The injection of BK and hypertonic NaCl into femoral arteries carried out during ANP infusion produced cardiorespiratory response patterns similar to those observed in control conditions. After injecting BK, a fall in SBP (25%), DBP (50%) and HR (16%), and an increase in breathing frequency were observed. After injecting NaCl, an increase occurred in SBP (20%), DBP (25%), HR (10%) and in depth of breathing. In the present experimental conditions, ANP has not been found to be capable of significantly interfering with the reflex pattern of cardiorespiratory responses either from the inhibition or activation of the sympathetic nervous system induced by chemical stimulation of muscle receptors.

Animals↗
PubMed1989

[Cardiocirculatory and respiratory reflexes of muscular origin during prolonged experimental dynamic exercise. Effects of sectioning of the sino-carotid and aortic nerves and bilateral vagotomy].

In anesthetized rabbits we have evaluated the effects of denervation of sino-aortic areas and vagotomy on the reflex cardiorespiratory responses during 2 min of contractions of gastrocnemius muscle induced by electrical stimulation of tibial nerve. The following parameters were examined: blood pressure (BP), heart rate (HR), respiratory frequency (f), tidal volume (Vt) and pulmonary ventilation (Ve) while arterial pH, pCO2 and pO2 and end-tidal CO2 (petCO2) were monitored. During steady state of rhythmic contractions we observed a decrease of BP, a slight decrease in HR and marked rise of Ve due to an increase of f with a slight increase of Vt. The sectioning of carotid-sinus, aortic and vagus nerves does not substantially modify the cardiorespiratory responses to muscular exercise; all the responses are abolished from the sectioning of somatic nerves in exercising limbs. The importance of the role of the peripheral nervous control by muscles (peripheral drive) is confirmed in the regulation of cardiorespiratory participation in motory activity, also in the steady state phase of muscular exercise in which components of a chemometabolic or hemodynamic nature could be more effective.

Animals↗
PubMedDate not supplied

Cardiorespiratory effects evoked by electrical stimulation of somatic afferent fibers.

Several neurophysiological studies have shown that electrical activation of afferent fibers of somatic nerves can evoke inhibitory or excitatory cardiovascular responses. The present investigation was undertaken to examine the effects induced by electrical stimulation of somatic nerves on cardiocirculatory and respiratory functions in anesthetized rabbits. Both low frequency stimulation and high frequency stimulation of afferent fibers of somatic nerves caused two distinct patterns of cardiocirculatory and respiratory reflex responses absolutely similar to those observed in our previous experiments on rabbits with dynamic and static exercise. The present findings do not support the existence in the somatic nerves of afferent fibers with cardiorespiratory effect having physiological functions different from that of producing cardiopulmonary adjustments to muscular activity.

Afferent Pathways↗