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N Montano

Publications and source records attributed to N Montano.

50 records · Page 3Linked to original sources
PubMed1996

Classification of coupling patterns among spontaneous rhythms and ventilation in the sympathetic discharge of decerebrate cats.

The spontaneous low- and high-frequency rhythms in the sympathetic discharge of decerebrate artificially ventilated cats are affected by external ventilation. Two graphical methods (i.e. the space-time separation plot and the frequency tracking locus) are used to classify the non-linear interactions. The observed behaviours in the sympathetic discharge consist of phase-locked periodic dynamics (at various frequency ratios with ventilation), quasiperiodic and aperiodic patterns. They depend on the experimental condition. In control condition the sympathetic discharge appears more frequently locked to each ventilatory cycle (1:1 dynamics). However, some cases of quasiperiodic dynamics are found. A sympathetic activation stimulus, such as inferior vena cava occlusion, is able to synchronize slow rhythms in the sympathetic discharge to a subharmonic of ventilation. During a sympathetic inhibition stimulus, such as aortic constriction, 1:1 dynamics is detected but the amplitude of the sympathetic responses can be modulated by unlocked slow rhythms. Moreover some cases of aperiodic dynamics are observed. Vagotomy reduces the 1:1 coupling between sympathetic outflow and ventilation. Vagotomy plus spinalisation disrupts periodic dynamics in the sympathetic discharge so that irregular and complex patterns are found.

Animals↗
PubMed1995

Adenosine activates cardiac sympathetic afferent fibers and potentiates the excitation induced by coronary occlusion.

Adenosine is a possible mediator of cardiac pain during myocardial ischemia; however, little is known about the influence of adenosine on cardiac sympathetic afferent activity and thereby on its algogenic mechanism. In 20 anaesthetized, decerebrated, curarized and artificially ventilated cats, we studied the impulse activity of 20 single afferent sympathetic fibers with a left ventricular receptive field in relation to epicardial applications of adenosine, coronary artery occlusions and arterial pressure rises. All fibers increased their impulse activity (from 1.2 +/- 0.2 to 2.6 +/- 0.5 imp/s; P < 0.001) during slight (20 +/- 8%) rises in aortic pressure, thus exhibiting low-threshold receptor characteristics. In 10 cats, epicardial applications of three different doses of adenosine (0.1, 1 and 10 mg/ml) caused a brief increase in neural activity with dose-related responses. This response was abolished by aminophylline, a P1 purinergic inhibitor. In the other group of 10 cats, four subsequent 30-s occlusions of the coronary arterial vessel supplying the receptive fields of the fibers were performed, in control conditions and 30 s, 3 and 7 min, respectively, after the end of excitation induced by adenosine (1 mg/ml) application. During the control coronary occlusion the impulse activity increased from 1.1 +/- 0.1 to 5.5 +/- 0.7 imp/s (P < 0.0001). A similar activation was present during the second occlusion initiated 30 s after the end of adenosine-induced activation. In contrast, a significant potentiation of the response was observed (8.8 +/- 1.2 vs. 5.3 +/- 0.9 imp/s; P < 0.001) during the occlusion initiated 3 min after the end of excitation by adenosine. This effect was no longer present during the last occlusion performed after 7 min. When the protocol was repeated substituting adenosine with saline (n = 5) or after i.v. administration of aminophylline (n = 5), no potentiation was observed, even though the excitatory response to coronary occlusion was preserved. These data show that adenosine can activate cardiac sympathetic afferent fibers in a dose-related manner, and potentiate their responses to coronary occlusion, while leaving unaffected the responsiveness to a hemodynamic stimulus. The excitatory effects are likely to involve the P1 purinergic receptors. The potentiation phenomenon might play a role in the genesis of an algogenic code.

Adenosine↗
PubMed1995

Sympathovagal effects of spinal anesthesia assessed by heart rate variability analysis.

Heart rate variations (HRV) result from moment-to-moment changes in sympathetic and parasympathetic activity in response to many conditions. These two neural inputs to the heart can be identified by analyzing power spectra of HRV for frequency components at the vasomotor (low-frequency [LF]) and the respiratory (high-frequency [HF]) rhythms. HRV analysis has been used successfully in humans to noninvasively evaluate the autonomic responses to specific maneuvers and drugs, as well as responses to more chronic preexisting pathologic conditions. The effects of an isolated "acute" withdrawal of sympathetic activity in humans, however, have not as yet been evaluated using an autoregressive (AR) technique. We examined HRV using this technique in a group of patients receiving subarachnoid block for abdominal surgery. The sensory levels achieved were within the range of those reported to interrupt sympathetic outflow to the heart. Electrocardiograms were recorded and subjected to AR analysis. AR analysis of HRV after spinal anesthesia revealed significant decreases in both dominant frequency components (LF and HF) that occur between 0.03 Hz and 0.5 Hz. These reductions coincided with blockade of cardiac sympathetic outflow after cephalad spread of the spinal block. The power spectra were almost abolished in patients with sensory blocks reaching T1-2. The decreases in amplitude of the LF and HF components, therefore, act as markers of diminished sympathetic and parasympathetic activity to the heart, while the ratio of LF:HF indicated that sympathovagal balance was predominantly maintained during most of the block.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Spinal↗
PubMed1995

[Role of low-frequency neuronal activity in the medulla in the regulation of the cardiovascular system].

We recorded discharge activity of 45 single neurons located in the rostral ventrolateral medulla (n = 21), lateral tegmental field (n = 10) and caudal raphe (n = 14) nuclei in baroreceptor-denervated decerebrate cats (n = 27). Autoregressive spectral analysis was performed on neuronal activity and systolic arterial pressure (SAP). The discharges of the recorded neurons were correlated to 2- to 6 Hz oscillations or 10 Hz rhythm present in sympathetic neural discharge. A low frequency (LF) oscillation (0.12 +/- 0.02 Hz) was observed in 25 (55%) units. The same rhythmicity was found in SAP variability in 25 of 45 (55%) recordings. In 21 of these cases the LF in SAP variability was highly correlated to LF in neural activity. Moreover, 32 out of 45 (71%) neurons showed a higher rhythm (HF; 0.34 +/- 0.06 Hz) related to the ventilation rate. These data demonstrate the presence of an LF oscillation in the discharge of single medullary neurons, involved in the regulation of cardiovascular system. This LF component was similar to that detectable in the spectral analysis of SAP variability, thus supporting the hypothesis of a central origin of this rhythm, largely independent of baroreceptor input.

Analysis of Variance↗
PubMed1995

A circadian perspective on myocardial ischaemia.

The non-uniform occurrence of myocardial ischaemia, with a trough at night and a peak in the morning, is at the base of the concept of a circadian distribution of coronary events. Cardiovascular variables known to influence the occurrence of ischaemia have similar rhythms, and a likely culprit could be hidden among them. Nevertheless, in many cases an identifiable trigger is lacking and the prediction of ischaemia is still elusive.

Autonomic Nervous System↗
PubMed1994

Morning and Monday: critical periods for the onset of acute myocardial infarction. The GISSI 2 Study experience.

The onset of acute myocardial infarction (AMI) is unevenly distributed over the 24 h and the week. While presence of a morning peak is generally agreed upon, contrasting results had been obtained regarding other periods of the day, probably due to differences of origin, size and composition of the populations. The 24 h and weekly distributions were studied within 6 h from the beginning of the symptoms in a population following a Latin life-style, who were enrolled in the GISSI 2 Study (n = 11472). Subgroups (smokers, the elderly (> 65 years), diabetics, hypertensives) were also considered. Six hour periods starting at midnight were tested for uniformity. Circadian non-uniformity was found. Events increased in the morning hours and reduced during the night regardless of the day of the week. The night and day difference was attenuated in smokers and diabetics. Non-uniformity of the events was also found among the days of the week. AMI significantly increased in non-smokers on Monday. We suggest that there is a night-day gradient (characterized by the short time interval between the two frequency extremes) in the time of onset of AMI. The different distribution in smokers stresses the possible unfavourable and masking effect of a heightened sympathetic tone during the day while the general protective role of the night hours is preserved. Moreover, the increased incidence of events on Monday may suggest the importance of the shift from a period of non-scheduled to scheduled activity.

Aged↗
PubMed1994

Power spectrum analysis of heart rate variability to assess the changes in sympathovagal balance during graded orthostatic tilt.

BACKGROUND: The powers of the low-frequency (LF) and high-frequency (HF) oscillations characterizing heart rate variability (HRV) appear to reflect, in their reciprocal relationship, changes in the state of the sympathovagal balance occurring during numerous physiological and pathophysiological conditions. However, no adequate information is available on the quantitative resolution of this methodology. METHODS AND RESULTS: We studied 22 healthy volunteers (median age, 46.5 years) who were subjected after a rest period to a series of passive head-up tilt steps randomly chosen from the following angles: 15 degrees, 30 degrees, 45 degrees, 60 degrees, and 90 degrees. From the continuous ECG, after appropriate analog-to-digital conversion, a personal computer was used to compute, with an autoregressive methodology, time and frequency domain indexes of RR interval variability. Spectral and cross-spectral analysis with the simultaneously recorded respiratory signal excluded its contribution to LF. Age was significantly correlated to variance and to the absolute values in milliseconds squared of very-low-frequency (VLF), LF, and HF components. The tilt angle was correlated to both LF and HF (expressed in normalized units [nu]) and to the LF-to-HF ratio (r = .78, -.72, and .68; respectively). Lower levels of correlation were found with HF (in ms2) and RR interval. No correlation was present between tilt angle and variance, VLF, or LF (in ms2). Individual analysis confirmed that the use of nu provided the greatest consistency of results. CONCLUSIONS: Spectral analysis of HRV, using nu or LF-to-HF ratio, appears to be capable of providing a noninvasive quantitative evaluation of graded changes in the state of the sympathovagal balance.

Adult↗
PubMed1994

Non-linear dynamics in the beat-to-beat variability of sympathetic activity in decerebrate cats.

Non-linear interactions between low-frequency rhythms (0.1 Hz) of beat-to-beat variability series of sympathetic discharge and respiratory rhythm (0.3 Hz) are observed in decerebrate artificially ventilated cats. Simple graphical tools as Poincaré and recurrence maps are used to detect, in a qualitative way, phase-locking phenomena. Non-parametric bispectral analysis is also carried out to quantify the degree of second-order coupling between oscillations at different frequencies.

Animals↗
PubMed1993

Effect of captopril on sympathetic preganglionic efferent activity in cats.

In 13 decerebrate cats, we studied the effects of captopril (10 mg/kg iv bolus) on the background discharge of thoracic preganglionic sympathetic fibers. After drug administration there was an initial reduction in systolic arterial pressure (SAP), which was followed by a later inhibition of sympathetic discharge (from 2.7 +/- 0.5 to 0.79 +/- 0.1 imp/0.1 s; P < 0.01). Captopril significantly reduced the excitatory response of sympathetic fibers to premature ventricular contraction (70 +/- 17 vs. 257 +/- 30%), inferior vena cava obstruction (176 +/- 56 vs. 315 +/- 85%) and asphyxia (143 +/- 20 vs. 245 +/- 51%). Vice versa the sympathetic response to aortic occlusion was unaffected (-58 +/- 8 vs. -62 +/- 6%). A similar reduction in sympathetic discharge was observed after captopril administration in anesthetized cats (n = 3). On the contrary, no changes in background neural discharge were noticed in decerebrate-spinalized cats (n = 5), despite comparable hemodynamic effects. These data indicate that captopril reduces sympathetic efferent activity and its responsiveness to excitatory stimuli. The lack of neural effects in decerebrate-spinalized cats is consistent with a brain stem site of action of captopril.

Animals↗
PubMed1992

Spectral analysis of sympathetic discharge, R-R interval and systolic arterial pressure in decerebrate cats.

In 19 decerebrate and artificially ventilated cats, we analyzed, with a power spectral methodology, the variability simultaneously present in R-R interval and in thoracic preganglionic sympathetic outflow. R-R interval was characterized, as already described in humans and other experimental preparations, by two rhythmic components occurring at a frequency of about 0.1 Hz (low-frequency, LF) and at one corresponding to respiratory rate (high-frequency, HF) which, in these experiments, was set at 0.32 Hz. Two similar rhythmic components were also present in the sympathetic discharge. Arterial pressure changes were produced by aorta or vena cava flow obstruction in order to produce reflex responses in sympathetic activity. Reflex sympathetic excitations induced an increase in the LF component of both R-R interval and sympathetic discharge variabilities, while the HF components were simultaneously reduced. In contrast, reflex sympathetic inhibitions were accompanied by a decrease in LF components of both variability signals, while the HF components were simultaneously increased. A significant and positive correlation was found between changes in impulse activity and the amplitude of LF component of either R-R interval or sympathetic discharge variabilities. These data support the hypothesis that the low-frequency component of R-R variability can be used as a marker of sympathetic modulation.

Animals↗
PubMed1991

[The excitatory effect of adenosine on the discharge activity of the afferent cardiac sympathetic fibers].

Recent clinical observations suggest that adenosine may produce cardiac pain; even though the mechanisms involved still need defining, one of the most convincing hypotheses seems to be a direct adenosine stimulation of the sympathetic nerve endings present in the myocardium. In 10 decerebrate and artificially ventilated cats, single sympathetic afferent fibres innervating the left ventricle were isolated from the third white thoracic ramus communicans of the left sympathetic chain. After locations of the fibre receptor field on the cardiac surface, we evaluated the effects of the local epicardial application of adenosine (0.1, 1 and 10 mg/ml) on the nervous discharge activity. These results were compared with those obtained by application of bradykinin, a potent natural algogenic substance which activates sympathetic afferents, and by a mechanical stimulus such as a slight increase of systolic arterial pressure (46 +/- 6% from 113 +/- 18 mmHg) induced by partial occlusion of the thoracic aorta. In particular, adenosine (1 mg/ml) elicited a significant increase in impulse activity (from 0.11 +/- 0.02 to 0.36 +/- 0.06 imp/0.1 s) with a latency of 16 +/- 2 s. Bradykinin application (20 micrograms/ml), in the same way, produced a significant increase in impulse activity (from 0.11 +/- 0.01 to 0.86 +/- 0.16 imp/0.1 s) with a latency of 8 +/- 1 s. Neither situation showed significant hemodynamic changes. An increased neural discharge (from 0.11 +/- 0.02 to 0.26 +/- 0.04 imp/0.1 s) was also observed during aortic occlusion. After purinergic receptor blockade by aminophylline (5 mg/kg, iv), the response to adenosine was no longer observed, while responses to bradykinin and aortic occlusion were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1990

Spectral analysis of sympathetic discharge in decerebrate cats.

To evaluate if the 0.1-Hz low-frequency oscillations of R-R interval are a reflection of rhythmical pattern of discharge of the sympathetic outflow, we analysed in 10 decerebrate cats heart rate and cardiac sympathetic efferent discharge variability. A predominant low-frequency component was present in both signals, thus suggesting that the 0.1-Hz rhythm indeed reflects a rhythmical pattern of discharge of sympathetic outflow.

Animals↗
PubMed1989

Restraining effect of captopril on cardiovascular sympathetic efferent neural activity.

In 13 decerebrate cats we studied the effects of captopril (10 mg/kg, intravenous bolus) on the background cardiac preganglionic sympathetic discharge and on its responsiveness to brief baroreceptor deactivations induced by premature ventricular contractions. Captopril caused a significant reduction of 57 +/- 7% (from 2.4 +/- 0.4 impulses/0.1s) in sympathetic discharge, with a mean latency of 35 +/- 3 min from the time of drug administration. In addition, the increase in cardiac sympathetic firing during premature ventricular contractions was markedly reduced, from 257 +/- 30% to 70 +/- 17%, before and after administration of captopril. These data indicate that captopril is not only likely to inhibit sympathetic discharge to the heart, but is also likely to restrain the excitatory sympathetic responses to baroreceptor deactivation.

Animals↗