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Biomedical subjects

G Peruzzi

Publications and source records attributed to G Peruzzi.

At least 19 recordsLinked to original sources

A new autologous venous valve by intimal flap. One case report.

Various surgical techniques have been proposed for the treatment of chronic venous insufficiency of post-thrombotic recanalized deep veins of the lower limbs. The preferable method seems to be represented by intravenous valvuloplasty except for the cases affected by extensive valvular damage. For this reason some experimental autologous, heterologous and prosthetic venous valves have been proposed. Such a problem emerged for 1 patient (male, aged 78 years, right limb, leg dystrophy, multiple ulcerations at the ankle) which was selected by duplex, Doppler venous pressure index, photoplethysmography and ascending phlebography. An iliac-femoral and popliteal post-thrombotic, recanalized, decompensated venous insufficiency and one Cockett's perforator incompetence were diagnosed (CEAP classification: C6s Es As2d14 Pr). A bicuspid apparently repairable popliteal valve was detected by phlebography. A traditional intravenous valvuloplasty was planned but the valve was not found at surgical exploration. A monocuspid valve reconstruction by intimal flap vein was performed. The following results were obtained and controlled after one year: stable ulceration healing, dystrophy reduction, improvement in the quality of life, normalization of the hemodynamic parameters and of the radiological morphology of the new valve. It can be concluded that monocuspid valvular repair by intimal flap can be successfully performed in cases affected by secondary valveless deep venous insufficiency of the lower limbs.

Aged↗

Group III muscle afferents evoke reflex depressor responses to repetitive muscle contractions in rabbits.

Repetitive-twitch contraction of the hindlimb muscles in anesthetized rabbits consistently evokes a reflex depressor response, whereas this type of contraction in anesthetized cats evokes a reflex pressor response in about one-half of the preparations tested. Rapidly conducting group III fibers appear to comprise the afferent arm of the reflex arc, evoking the depressor response to twitch contraction in rabbits because electrical stimulation of their axons reflexly decreases arterial pressure. In contrast, electrical stimulation of the axons of slowly conducting group III and group IV afferents reflexly increases arterial pressure in rabbits. In the present study, we examined the discharge properties of group III and IV muscle afferents and found that the former (i.e., 13 of 20), but not the latter (i.e., 0 of 10), were stimulated by 5 min of repetitive-twitch contraction (1 Hz) of the rabbit triceps surae muscles. Moreover, most of the group III afferents responding to contraction appeared to be mechanically sensitive, discharging in synchrony with the muscle twitch. On average, rapidly conducting group III afferents responded for the 5-min duration of 1-Hz repetitive-twitch contraction, whereas slowly conducting group III afferents responded only for the first 2 min of contraction. We conclude that rapidly conducting group III afferents, which are mechanically sensitive, are primarily responsible for evoking the reflex depressor response to repetitive-twitch contractions in anesthetized rabbits.

Afferent Pathways↗

Muscle metaboreflex contribution to sinus node regulation during static exercise: insights from spectral analysis of heart rate variability.

BACKGROUND: It is currently assumed that during static exercise, central command increases heart rate (HR) through a decrease in parasympathetic activity, whereas the muscle metaboreflex raises blood pressure (BP) only through an increase in sympathetic outflow to blood vessels, because when the metaboreflex activation is maintained during postexercise muscle ischemia, BP remains elevated while HR recovers. We tested the hypotheses that the muscle metaboreflex contributes to HR regulation during static exercise via sympathetic activation and that the arterial baroreflex is involved in the HR recovery of postexercise muscle ischemia. METHODS AND RESULTS: Eleven healthy male volunteers performed 4-minute static leg extension (SLE) at 30% of maximal voluntary contraction, followed by 4-minute arrested leg circulation (ALC). Autonomic regulation of HR was investigated by spectral analysis of HR variability (HRV), and baroreflex control of heart period was assessed by the spontaneous baroreflex method. SLE resulted in a significant increase in the low-frequency component of HRV that remained elevated during ALC. The normalized high-frequency component of HRV was reduced during SLE and returned to control levels during ALC. Baroreflex sensitivity was significantly reduced during SLE and returned to control levels during ALC when BP was kept elevated above the resting level while HR recovered. CONCLUSIONS: The muscle metaboreflex contributes to HR regulation during static exercise via a sympathetic activation. The bradycardia that occurs during postexercise muscle ischemia despite the maintained sympathetic stimulus may be explained by a baroreflex-mediated increase in parasympathetic outflow to the sinoatrial node that overpowers the metaboreflex-induced cardiac sympathetic activation.

Adult↗

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↗

The cardiomyopathic hamster as model of early myocardial aging.

Few experimental studies are available on aging, because of the lack of suitable experimental models to test specific pathophysiologic mechanisms. In the present study, the cardiomyopathic Syrian hamster is proposed as experimental model of the aging myocardium. In fact, the hamster myocardium develops an early alpha to beta myosin isoform shifting in ventricles that is independent of hemodynamic overload and repeats the phenomenon physiologically occurring in healthy hamsters during the entire lifespan. At the same time, in atria there is a progressive decline of ANF production that is independent of intracavitary pressure. Conversely, ANF production in ventricles is enhanced before the onset of hemodynamic overload, but parallel to the increase in the fibrotic proportion of the ventricular wall. These characteristics mimic the modifications occurring in otherwise healthy aged mammals and candidate the cardiomyopathic hamster as a model of early myocardial aging.

Animals↗

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↗

Role of muscular factors in cardiorespiratory responses to static exercise: contribution of reflex mechanisms.

We investigated the effects of muscle mass and contraction intensity on the cardiorespiratory responses to static exercise and on the contribution afforded by muscle metaboreflex and arterial baroreflex mechanisms. Ten subjects performed static handgrip at 30% maximal voluntary contraction (MVC) (SHG-30) and one-leg extension at 15% (SLE-15) and 30% (SLE-30) MVC, followed by postexercise circulatory occlusion (PECO). Mean arterial pressure (MAP) and heart rate (HR) responses were greater during SLE-30 than during SHG-30. The difference in MAP was maintained by PECO, and the part of the pressor response maintained by PECO was greater after SLE-30 than after SHG-30 (88.3 +/- 10.6 and 67.8 +/- 12.7%, respectively, P = 0. 02). There were no differences in MAP and HR responses between SHG-30 and SLE-15 trials. Baroreflex sensitivity was maintained during SHG-30 and SLE-15, whereas it was significantly reduced during SLE-30 and recovered back to the resting level during PECO. Minute ventilation and oxygen uptake increased more during SLE-30 than during both SHG-30 and SLE-15 trials. Minute ventilation remained significantly elevated above rest only during PECO following SLE-30. These data suggest that during static exercise the muscle mass and contraction intensity affect 1) the magnitude of the cardiorespiratory responses, 2) the contribution of muscle metaboreflex to the cardiorespiratory responses, and 3) the arterial baroreflex contribution to HR control.

Adult↗

Effect of aging on responses to autonomic cardiovascular tests.

Cardiovascular deconditioning (CD) and orthostatic intolerance represent some of the major disturbances experienced by astronauts returning on Earth after micro-G exposure. The orthostatic intolerance observed in crew members after space missions has been hypothesized to be related to a disorder of the autonomic control of the cardiovascular system. There is evidence that advanced acing itself may alter the cardiovascular mechanism that underlie the CD. Due to involvement of elderly subjects in space flights it is mandatory to verify how age affects the cardiovascular autonomic neural regulation. In order to assess age-related differences in autonomic cardiovascular regulation our aim is to analyze the cardiovascular responses to 3 different autonomic tests that explore baroreceptor (tilt and deep breathing) and non-baroreceptor (isometric exercise) afferent pathways, in two goups of normal subjects characterized by significant different age.

Adolescent↗

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↗

[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↗

Effects of isokinetic, isotonic and isometric submaximal exercise on heart rate and blood pressure.

The purpose of the present study was to compare arterial pressure (AP) and heart rate (HR) responses to submaximal isokinetic, isotonic and isometric exercises currently employed in physical rehabilitation therapy in terms of both magnitude and time-course. To this aim AP and HR were continuously and noninvasively measured in ten healthy subjects performing isokinetic, isotonic and isometric exercises at the same relative intensity. Isokinetic and isotonic exercises consisted of 30 knee extension/flexion repetitions at 40% of maximal effort. Isokinetic speed was set at 180 degrees s(-1). Isometric exercise consisted of a 60-s knee extension at 40% maximal voluntary contraction. The AP showed a rapid and marked increase from the onset of all types of exercise progressing throughout the exercises. Peak systolic (SAP) and diastolic (DAP) arterial pressure were 190.7 (SEM 8.9) and 121.6 (SEM 7.8) mmHg during isokinetic and 197.6 (SEM 11.2) and 128.3 (SEM 7.7) mmHg during isotonic exercise, respectively. During isometric exercise peak SAP and DAP were 168.1 (SEM 6.3) and 102.1 (SEM 3.7) mmHg, respectively [both lower compared to isokinetic and isotonic exercise (P < 0.05)]. The HR rose abruptly and after five isokinetic and isotonic repetitions it had already increased by about 30 beats min(-1), continuing to rise throughout the exercises. The HR response to isometric exercise was significantly less (P < 0.05) at all times. An immediate fall in AP, undershooting resting levels, was observed at the cessation of all types of exercise, being more marked after isokinetic and isotonic exercise. These results indicate that submaximal exercise of a dynamic type induces greater AP responses than intensity-matched isometric exercise and that even submaximal endurance-type rehabilitation exercise yields an elevated functional stress on the cardiovascular system which could precipitate hazardous events particularly in subjects with unrecognized cardiac diseases.

Adult↗

Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes.

This study evaluated the influence of central command and muscle afferent stimulation (mechanical and chemical) on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Twenty-two healthy men performed voluntary knee extension and electrically induced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) were measured continuously and noninvasively. The arterial baroreflex was evaluated by analyzing the slopes of sequences of three or more consecutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, both voluntary exercise and electrically induced exercise under arrested-flow conditions resulted in a maintained baroreflex sensitivity (BRS; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmHg, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest that the central command and muscle chemoreflex act to preserve the BRS, possibly "resetting" the baroreceptor-cardiac response relationship, whereas stimulation of mechanosensitive receptors appears capable of modifying the integrated baroreflex control of sinus node function in humans. The first two mechanisms seem, however, to overwhelm the latter to maintain BRS, thus permitting a concomitant increase in arterial pressure and heart rate.

Adult↗

Embryonic gene expression in nonoverloaded ventricles of hereditary hypertrophic cardiomyopathic hamsters.

Current information regarding the molecular and biochemical mechanisms of myocardial hypertrophy, as obtained from isolated cardiomyocytes and/or healthy animals with aortic banding, does not permit dissection of the hierarchical relationship among different steps and triggers of the pathogenic process in vivo. The aim of the present study was to depict the temporal relationship among myocardial structural and functional characteristics, the embryonic gene program, and transforming growth factor (TGF) beta 1 expression in euthyroid hereditary hypertrophic cardiomyopathic hamsters (CMPH). This investigation was performed using Western and Northern blot and in situ hybridization techniques. The results show that in CMPH, the severity of the hemodynamic overload is not related to any modification in structural myocardial characteristics (cardiac mass, cardiomyocyte dimensions, total RNA, and protein content), whereas an early activation of the embryonic gene program occurs in not yet overloaded 90-day-old CMPH (left ventricular end diastolic pressure < 15 mm Hg). In these animals, a 30% to 90% decrease in the alpha myosin heavy chain (alpha MHC) relative content was found in ventricles, whereas beta MHC increased 5-fold. In addition, the alpha skeletal actin expression was enhanced 2-fold versus age-matched controls. No modifications were observed in myosin function evaluated by in vitro motility assay, whereas the administration of L-thyroxine (100 micrograms/kg intraperitoneally daily) to CMPH was able to reinduce the ventricular expression of the alpha MHC isoform (5-fold increase). Conversely, no changes were found in alpha cardiac actin and myosin light chain 2 (MLC2) expression. A close temporal relationship occurred in CMPH ventricles between the re-expression of the embryonic gene program and a 3-fold enhancement of the expression of TGF beta 1. These results indicate that the CMPH provides a useful model for investigating the expression of embryonic genes in hypertrophic ventricles in the absence of mechanical and hormonal stimuli, and that TGF beta 1 is involved in regulating in vivo the "embryonic step" of myocardial hypertrophy. Furthermore, the study offers new insights into the pathophysiologic mechanisms leading to heart failure.

Actins↗

Evaluation of reproducibility of spontaneous baroreflex sensitivity at rest and during laboratory tests.

OBJECTIVE: The aim of the present study was to examine the reproducibility of arterial baroreflex sensitivity (BRS) provided by the spontaneous baroreflex method at rest and during laboratory tests. METHODS: Twenty healthy volunteers were studied 24 h apart, in the same laboratory and under the same environmental conditions, at rest, during active standing, while performing mental arithmetics and during static hand-gripping. Systolic blood pressure, mean arterial pressure and pulse interval were continuously and non-invasively measured by using a Finapres device. BRS was evaluated by analysing the slopes of spontaneously occurring sequences of three or more consecutive beats in which systolic blood pressure and pulse interval of the following beat both increased or decreased, in the same direction, in a linear fashion. Individual BRS were obtained by averaging all slopes computed within a given test. RESULTS: Under each test condition BRS did not differ significantly between the two consecutive days, showing strikingly similar values. The mean group coefficients of variation (CVAR), obtained by averaging individual CVAR, between the two experimental days were 15.0, 13.9 and 19.7% for resting, standing, static hand-gripping and mental arithmetic, respectively. No relationships were found between individual CVAR and individual mean arterial pressure, pulse interval and number of baroreflex sequences under any tested condition, on both experimental days. CONCLUSIONS: These results show that the spontaneous baroreflex method provides good BRS reproducibility under various stimuli that affect the neural control of circulation differently. They also suggest that BRS variability is dependent neither on haemodynamic modifications nor on the degree of baroreflex engagement, but it seems to reflect an inherent feature of the way in which arterial baroreflex modulate the heart period.

Adult↗

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↗

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↗

Sapheno-femoral valves. Histopathological observations and diagnostic approach before surgery.

BACKGROUND: Since the literature indicated that in the early stages of primary venous disease valves are simply dilated, some authors performed external valvuloplasty of deep and superficial venous valves with encouraging results, although some failures were observed without being sufficiently explained. OBJECTIVE: To obtain further interpretations of the natural history of venous valve pathology, clarify methods for a correct diagnostic approach, and provide indications for the external valvuloplasty procedure. METHODS: Forty-two proximal valves of the long saphenous vein removed for varicose veins of the lower limbs were studied with optical microscopy. The relationship between histologic alterations and age of varicose disease was investigated. Five valvuloplasties were explanted for recurrent reflux and submitted to histopathological observation. Preoperative echographic findings and histologic observations were compared. Nineteen limbs were subjected to external valvuloplasty under angioscopic control; preoperative echographic findings and angioscopic observations were compared. RESULTS: The histologic alterations observed in venous valves were mainly hypotrophy of cusps, which seemed to be the main cause of failure after external valvuloplasty. The frequency of such hypotrophic alterations increases with the age of varicose disease but no statistically significant relationship was found. Preoperative echographic imaging of venous valves does not appear sufficiently predictive when compared with histologic and angioscopic examinations. CONCLUSION: Hypotrophic valve damage seems to be prevalent in patients with varicose veins of the lower limbs. Valve cusp hypotrophy may be present in early disease though some normal cusps can be found in advanced disease. When preoperative echographic visualization of cusps is doubtful, intraoperative angioscopy plays the main role in the diagnosis of venous valve disease before and during external valvuloplasty.

Angioscopy↗