PubMed Health⌕ Search

Biomedical subjects

V Novak

Publications and source records attributed to V Novak.

At least 37 records · Page 2Linked to original sources

Alpha 2-adrenergic modulation of colonic tone during hyperventilation.

Our aims were to assess the role of adrenergic modulation in the hyperventilation-induced increase in colonic tone. Of 40 healthy volunteers, 12 received placebo (saline) and the remaining 28 received either clonidine, yohimbine, phenylephrine, or ritodrine. Time-frequency mapping of heart rate based on Wigner distribution assessed variations in parasympathetic and sympathetic activity during hyperventilation. Tone in the descending colon was recorded by a barostat balloon before, during, and after 5 min of hyperventilation. Heart rate spectral analysis suggested diminished sympathetic and vagal activity during hyperventilation and increased sympathetic and vagal activity after hyperventilation. Adrenergic agents influenced (P = 0.01) the tonic response after, but not during, hyperventilation. Yohimbine reduced the increment in colonic tone after hyperventilation compared with saline (P < 0.05) and clonidine (P = 0.002); phenylephrine and ritodrine had no effects. Different mechanisms modulate the increase in colonic tone during and after hyperventilation. Yohimbine attenuates the increase in colonic tone after hyperventilation probably by enhancing inhibitory sympathetic input to the colon.

Adrenergic alpha-Agonists↗

Postural tachycardia syndrome: time frequency mapping.

Orthostatic tachycardia is common but its specificity remains uncertain. Our preliminary work suggested that using autonomic function testing in conjunction with time-frequency mapping (TFM), it might be possible to characterize a subset of the postural tachycardia syndrome (POTS), that is due to a restricted autonomic neuropathy. We describe 20 patients (17 women and 3 men, aged 14-43 years) with florid POTS and 20 controls (14 women and 6 men, aged 20-41 years). Autonomic failure was quantified by its distribution (cardiovagal, adrenergic and sudomotor) and severity, a symptom profile was generated, and spectral indices, based on modified Wigner distribution during rest and head-up tilt (80 degrees) were evaluated. During tilt-up POTS patients differed from controls by an excessive heart rate (> 130 bpm) (P < 0.001), and higher diastolic pressure (P < 0.01). During rest, cardiovagal oscillations (at respiratory frequencies [RF]) and slow rhythms at nonrespiratory frequencies (NONRF) (from 0.01 to 0.07 Hz) in R-R intervals (RRI) (P < 0.01) were reduced. Both RF and NONRF rhythms in RRI were further blunted with tilt-up (P < 0.001). Slow adrenergic vasomotor rhythms in blood pressure (BP) (approximately 0.07 Hz) surged with tilt-up and returned to normal levels afterwards. The index of sympatho-vagal balance (NONRF-Systolic BP (SBP)/RF-RRI) was dramatically increased in POTS (P < 0.001). Distal postganglionic sudomotor failure was observed, and impairment of the BP responses to the Valsalva maneuver (phase II) suggested peripheral adrenergic dysfunction. Persistent orthostatic dizziness, tiredness, gastrointestinal symptoms and palpitations were common in POTS patients. It is possible to identify a subset of POTS patients who have a length-dependent autonomic neuropathy, affecting the peripheral adrenergic and cardiovagal fibers, with relative preservation of cardiac adrenergic fibers.

Adolescent↗

Is the heart "empty' at syncope?

Neurally-mediated syncope (NMS) is thought to be reflexly triggered by vagal cardiac ventricular afferents that are activated by impaired cardiac filling. If this hypothesis is true then maneuvers that increase venous pooling should progressively diminish cardiac volume triggering syncope once a threshold decrease in cardiac filling is reached. Beat-to-beat recordings of heart rate, blood pressure (Finapres) and stroke volume (impedance cardiograph) were made at rest and during head-up tilt (80 degrees) in twenty controls and in fourteen patients with recurrent NMS (group 1). Hemodynamic profiles of controls and group 1 were compared. In eleven additional patients with NMS (group 2) we measured cardiac chamber volume from apical two or four-chamber views or stroke volume from Doppler measurements of the left ventricular outflow tract at rest and during tilt. Baseline values and initial response to head-up tilt of controls and group 1 patients were similar. A small negative trend in blood pressure and total peripheral resistance was present for at least 250 s before the onset of syncope. Stroke volume remained stable during this presyncopal period and increased at syncope. The profile of stroke volume changes using impedance cardiography mirrored those obtained using Doppler (5 subjects). Reliable echocardiographic measurements of cardiac chamber size were obtained in five subjects and did not change during tilt, presyncope or syncope. These data show that there is no significant decrease in cardiac volume before syncope that could serve as a trigger of syncope.

Adult↗

Spontaneous blood pressure fluctuations and renal blood flow dynamics.

Two mechanisms operating at 0.03-0.05 and 0.1-0.2 Hz are involved in autoregulation of renal blood flow (RBF). To examine the behavior of the faster system, the response of RBF to spontaneous fluctuations of arterial pressure was assessed in Sprague-Dawley rats anesthetized by isoflurane or halothane. During halothane anesthesia, autonomous oscillation of total RBF was observed at 0.10-0.15 Hz, and normalized admittance gain became negative at 0.11 +/- 0.01 Hz. During isoflurane anesthesia, there was autonomous power in blood flow in a broad peak between 0.15 and 0.25 Hz, and gain became negative at 0.15 +/- 0.01 Hz. Increasing inspired isoflurane concentration from 1.4 +/- 0.1% to 2.2 +/- 0.1% reduced pressure by 22 +/- 2 mmHg but did not alter blood flow or the transfer function, indicating that the operating frequency was not changed. In another experiment, changing from isoflurane to halothane increased peak power in the autonomous blood flow oscillation fivefold and reduced its frequency from 0.18 +/- 0.01 to 0.14 +/- 0.01 Hz. Gain became negative at a higher frequency (0.16 +/- 0.01 Hz) during isoflurane than halothane anesthesia (0.12 +/- 0.01 Hz). The results show that the 0.1-0.2 Hz system is reliably detected under unforced conditions and provides modest attenuation of pressure fluctuations at < or = 0.1 Hz. Its operating frequency under isoflurane anesthesia is consistent with previous estimates from barbiturate-anesthetized rats, whereas it operates significantly slower under halothane anesthesia.

Administration, Inhalation↗

The effect of severe brainstem injury on heart rate and blood pressure oscillations.

To determine whether an intact brainstem is essential for the generation of neurogenically mediated fluctuations of R-R intervals and blood pressure, three patients with cerebellar lesions causing severe brainstem compression or death, one patient with a large pontine infarct and one patient with a pontine haemorrhage, were studied. Time-frequency maps (based on a modified Wigner distribution) were constructed from blood pressure and R-R interval signals in these patients with brainstem injury and were compared with maps of normal control subjects. Low frequency sympathetically mediated rhythms (0.01-0.12 Hz) in systolic and diastolic pressure remained detectable but attenuated in patients with brainstem injury whereas there was an almost complete loss of normal R-R intervals rhythmicity over 0.01 to 0.5 Hz range. These data suggest that fluctuations in R-R intervals require an intact brainstem, whereas low frequency approximately 0.06 +/- 0.02 Hz blood pressure rhythms may be preserved by spinal sympathetic circuitry.

Aged↗

Slow cardiovascular rhythms in tilt and syncope.

The cardiovascular oscillations during orthostasis were analyzed by time-frequency mapping in 23 patients with history of vasodepressor (VD) syncope and in 10 control subjects. Syncope was induced by head-up tilt (80 degrees, 25 min) alone in 11 patients (VD-1). Twelve patients remained asymptomatic (VD-2) during this tilt, but presented VD syncope or presyncope during tilt with an isoproterenol infusion. Data from the first tilt without isoproterenol infusion are presented here. Amplitude of sympathetically-mediated nonrespiratory fluctuations [0.01 Hz-respiratory frequency (Rf)] in blood pressure was greater at the beginning of the tilt in both (VD-1 and VD-2) groups compared to controls. Nonrespiratory oscillations were present throughout the tilt and their amplitude increased toward its end (p < 0.001) in VD-2 and control groups. In contrast, in the VD-1 group, the amplitude of 0.01-0.05 Hz rhythm in blood pressure diminished shortly after the beginning of tilt and continued to decline toward the syncope. Nonrespiratory fluctuations in R-R intervals were greatest in VD-1 group. The slow blood pressure rhythms reflect an integrity of feedback loops, and their disappearance is an early sign of an impending syncope.

Adult↗

Time-frequency analysis of slow cortical activity and cardiovascular fluctuations in a case of Alzheimer's disease.

The dynamics and relationship of slow cortical activity (amplitude modulation of electroencephalograph at 0.02-0.05 Hz) and cardiovascular fluctuations (0.01-0.05 Hz range) was studied by time-frequency mapping (modified Wigner distribution) in a patient with Alzheimer's disease. The amplitude modulating at rest basal alpha and theta activity (lead Oz) was exaggerated compared with control subjects. Fluctuations at respiratory and nonrespiratory (0.01-0.05 Hz) frequencies in R-R intervals and blood pressure were present and within normal range. Spontaneous hypotension (by 20 to 80 mmHg lasting 15-20 s) accompanied by cardioacceleration occurred repeatedly in the supine position and during hyperventilation. Slow cortical activity and nonrespiratory fluctuations (0.01-0.05 Hz) in blood pressure increased concurrently with hypotensions. No signs of peripheral autonomic dysfunction or malfunction of baroreceptors were observed and the vasomotor instability appeared to be of central origin. The results suggested that slow cortical activity was functionally related to the central autonomic nervous system and reflected cortico-thalamo-brainstem interaction.

Alpha Rhythm↗

Accuracy of beat-to-beat noninvasive measurement of finger arterial pressure using the Finapres: a spectral analysis approach.

OBJECTIVE: Our objective was to test the accuracy of noninvasive recordings of finger arterial pressure (FAP) using the Ohmeda Finapres (Ohmeda Monitoring Systems, Englewood, CO). METHODS: Twenty patients, aged 20 to 78 years, requiring admission to the intensive care unit and placement of intraarterial catheters participated in the study. Systolic and diastolic pressures were derived from 1-hr recordings of beat-to-beat FAP and from ipsilaterally recorded intraarterial pressure (IAP) signals. In all 20 cases, we analyzed beat-to-beat discrepancies between the actual magnitude of FAP and IAP, as well as the distribution of the consecutive differences within each of the two signals. In 10 cases, spectral analysis of the frequency content of both signals was performed. RESULTS: The average systolic FAP (128.1 +/- 22.4 mm Hg) did not differ from IAP (127.1 +/- 19.7 mm Hg), whereas diastolic FAP (78.1 +/- 11.9 mm Hg) was greater (71.5 +/- 10.3 mm Hg) (p < 0.001). No differences in the linear trends of FAP and IAP were observed. Overall, systolic FAP and IAP were discrepant by 0.84 +/- 13.3 mm Hg (-21.82 to 25.8 mm Hg); diastolic FAP and IAP were discrepant by 6.67 +/- 5.23 mm Hg (2.68 to 13.05 mm Hg). Despite discrepancies in the magnitude of the two signals, the contour of IAP approximated that of FAP. Spectral analysis demonstrated good reproducibility and coherence between diastolic IAP and FAP fluctuations in both low-frequency (0.01 to 0.15 Hz) and high-frequency (0.15 to 0.33 Hz) bands. The low-frequency fluctuations in FAP systolic pressure were significantly amplified (p < 0.001) (gain 1.75), whereas the high-frequency fluctuations were not. CONCLUSIONS: Over the course of 1 hr, FAP followed the contour and frequency content of IAP.

Adult↗

Time-frequency mapping of the QRS complex in normal subjects and in postmyocardial infarction patients.

The effect of myocardial infarction upon the frequency content of the QRS complex was analyzed. Three bipolar signal-averaged surface electrograms, recorded during the early (10-15 days) and late (6 months) chronic phases of myocardial infarction, were analyzed in 61 patients and 11 healthy subjects. All patients were free of ventricular arrhythmia during 6 months of follow-up examinations. Time-frequency analysis of the QRS complex was based on the modified Wigner distribution, which is well suited to examine nonstationary character of data. Standard time-domain analysis for the presence of late potentials was used for comparison. High-frequency (> or = 90 Hz) components, separable from the dominant low-frequency components (< 90 Hz), were found in all groups. They were present throughout the QRS complex and were peaking in its middle portion. The high-frequency components were found significantly higher in postinfarction patients in both early (P < .007) and late chronic stage myocardial infarction (P < .05) compared to healthy subjects. Patients who tested positive for late potentials (24%) also had elevated high-frequency components; however, a comparable increase was also observed in late potential negative patients. Furthermore, the high-frequency component increase occurred in all patients earlier in the QRS than in its terminal 40 ms, where late potentials are traditionally evaluated. It is concluded that high-frequency components are an integral part of the QRS complex under physiologic conditions and persist in variable amount throughout its duration. The high-frequency components are increased in patients after myocardial infarction not associated with ventricular arrhythmia, and their elevation is not limited to the terminal QRS complex.

Adult↗

Altered cardiorespiratory transfer in hypertension.

The effect of continuously slowing respiration (from 0.46 to 0.05 Hz, eg, from 30 to 3 breaths per minute) on cardiovascular variables was studied in 14 hypertensive patients and 16 normotensive subjects. Beat-to-beat time-frequency (Wigner) distributions were used for dynamic analysis of RR interval and systolic and diastolic pressures. Dominant breathing frequency at rest did not differ in hypertensive patients from the control group (0.21 versus 0.19 Hz). However, in the hypertensive group it was disturbed 34.4% of the time by slow breathing and apneas, which evoked transient blood pressure instability and increased spectral powers at low frequencies (range, 0.01 to 0.1 Hz). The nonrespiratory fluctuations (NONRFs) and respiratory fluctuations (RFs) in RR interval and NONRFs in systolic pressure were smaller in hypertensive patients (P < .001). In both groups, slowing of respiratory frequency from 0.46 to 0.05 Hz entrained RFs in the RR interval and systolic and diastolic pressures. RFs in the RR interval remained diminished in hypertensive patients (P < .001), but RFs in systolic pressure increased higher at maximum, corresponding to breathing frequencies from 0.07 to 0.09 Hz (P < .001). A dynamic cardiorespiratory index (ratio of RFs in RR interval and systolic pressure) was smaller (P < .01) in hypertensive patients than in normotensive subjects. Irregular breathing at rest was found in hypertensive patients. The transfer from respiration into RR interval was diminished, suggesting an impaired parasympathetic responsiveness in mild hypertension.

Adult↗

Time/frequency mapping of the heart rate, blood pressure and respiratory signals.

The discrete Wigner distribution (DWD) was implemented for the time/frequency mapping of variations of R-R interval, blood pressure and respiratory signals. The smoothed cross-DWD was defined and the modified algorithm for the smoothed auto- and cross-DWD was proposed. Spurious cross-terms were suppressed using a smoothing data window and a Gauss frequency window. The DWD is easy to implement using the FFT algorithm. Examples show that the DWD follows well the instantaneous changes of spectral content of cardiovascular and respiratory signals which characterise the dynamics of autonomic nervous system responses.

Blood Pressure↗

Influence of respiration on heart rate and blood pressure fluctuations.

The dynamics of the respiratory and cardiovascular systems were studied by continuously slowing respiration from 0.46 to 0.05 Hz. The time-frequency distribution and global spectral analysis were used to assess the R-R interval (R-R) and the systolic and diastolic blood pressure fluctuations in 16 healthy subjects. During rest, the nonrespiratory-to-respiratory frequency ratios were not affected by occasional slow breathing, whereas the low- (0.01-0.15 Hz) to high- (0.15-0.3 Hz) frequency indexes for blood pressure were increased (P < 0.05). The respiratory fluctuations in R-R and the systolic and diastolic pressures were paced over the 0.46- to 0.05-Hz range. As respiration slowed to 0.07-0.09 Hz, the frequency content of the respiration and cardiovascular variables increased sharply and nonlinearly to a maximum that exceeded values at higher frequencies (P < 0.001). The nonrespiratory frequency content remained stable in the 0.01- to 0.05-Hz range and did not significantly differ from that at rest. In contrast, the nonstable 0.05- to 0.1-Hz component was suppressed. A slow 0.012- to 0.017-Hz rhythm modulated respiration and hemodynamic fluctuations at both respiratory and nonrespiratory frequencies. The study indicated that respiration input should be considered in the interpretation of global spectra. Furthermore the time-frequency distributions demonstrated that a close nonlinear coupling exists between the respiratory and cardiovascular systems.

Adult↗

Bush's and Clinton's fat cats.

As the 1992 presidential race went into full swing, Republican and Democratic fundraisers were busy soliciting $100,000 donations from corporations, labor unions and wealthy individuals. This kind of money is supposedly illegal in presidential campaigns, but both parties have found a way to launder it: by channeling it through their state affiliates and calling it "soft money." Whatever its name, it is compromising the integrity of the system.

Economics↗

The other drug lords.

To gain an understanding of how hard it will be to control skyrocketing health care costs in the United States, consider one small part of the health care system: the pharmaceutical industry. Every time Congress threatens to crack down on drug costs or reduce government support for the industry, the pharmaceutical firms crank out PAC contributions and deploy their lobbyists. The upshot: drug companies get to charge what they want while holding onto millions of dollars' worth of government giveaways, including tax breaks and generous patent protection.

Aged↗