Biomedical subjects

S C Malpas

Publications and source records attributed to S C Malpas.

At least 37 records · Page 2Linked to original sources

PubMed1998

Contribution of renal nerves to renal blood flow variability during hemorrhage.

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml.min(-1).kg-1 for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 +/- 1 vs. 31 +/- 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of oscillations in each variable. Before hemorrhage, a rhythm at approximately 0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (< 0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies > 0.25 Hz was significantly less in intact than denervated rabbits (0.83 +/- 0.12 vs. 1.19 +/- 0.10 ml.min(-1).mmHg-1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These wer accompanied by increases in the spectral power of RBF at the same frequency. Arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

Animals↗

PubMed1998

Modelling of the dynamic relationship between arterial pressure, renal sympathetic nerve activity and renal blood flow in conscious rabbits.

A linear autoregressive/moving-average model was developed to describe the dynamic relationship between mean arterial pressure (MAP), renal sympathetic nerve activity (SNA) and renal blood flow (RBF) in conscious rabbits. The RBF and SNA to the same kidney were measured under resting conditions in a group of eight rabbits. Spectral analysis of the data sampled at 0.4 Hz showed that the low-pass bandwidth of the signal power for RBF was approximately 0. 05 Hz. An autoregressive/moving-average model with an exogenous input (ARMAX) was then derived (using the iterative Gauss-Newton algorithm provided by the MATLAB identification Toolbox), with MAP and SNA as inputs and RBF as output, to model the low-frequency fluctuations. The model step responses of RBF to changes in SNA and arterial pressure indicated an overdamped response with a settling time that was usually less than 2 s. Calculated residuals from the model indicated that 79 5 % (mean s.d., averaged over eight independent experiments) of the variation in RBF could be accounted for by the variations in arterial pressure and SNA. Two additional single-input models for each of the inputs were similarly obtained and showed conclusively that changes in RBF, in the conscious resting rabbit, are a function of both SNA and MAP and that the SNA signal has the predominant effect. These results indicate a strong reliance on SNA for the dynamic regulation of RBF. Such information is likely to be important in understanding the diminished renal function that occurs in a variety of disease conditions in which overactivity of the sympathetic nervous system occurs.

Algorithms↗

PubMed1997

24-hour recordings of blood pressure, heart rate and behavioural activity in rabbits by radio-telemetry: effects of feeding and hypertension.

We used radio-telemetry to measure 24-hour rhythms of systolic, diastolic and mean blood pressure, heart rate and behavioural activity in conscious rabbits, which were maintained under normal day/night rhythms and restricted feeding. Over three consecutive days, all variables showed little change between day-period and night-period, except for a pronounced rise in the afternoon, coinciding with the presentation of pellet food. Mean blood pressure increased during this period from baseline values between 78-82 mm Hg to a peak of 89-91 mm Hg. At the same time heart rate rose from baseline values of 147-161 b/min to a peak of 206-234 b/min and behavioural activity scores rose from 11-31 counts/h to a peak of 52-81 counts/h. Changing the time at which pellet food was presented to the rabbits from the early afternoon to the early morning, caused a complete and immediate shift of the peak of blood pressure and heart rate to the morning period. Chronic intravenous infusion of angiotensin II caused a significant increase in blood pressure (24-hour average: 80 +/- 1 vs. 114 +/- 7 mm Hg) but did not alter basal heart rate or behavioural activity. The increase in heart rate and blood pressure seen with food presentation was attenuated with angiotensin II infusion. These data show that in rabbits diurnal changes in blood pressure, heart rate and activity were determined to a large extent by timed feeding. In addition, in rabbits with angiotensin-induced hypertension the food-induced changes in blood pressure and heart rate were blunted.

Angiotensin II↗

PubMed1997

Chronic renal blood flow measurement in dogs by transit-time ultrasound flowmetry.

To test the validity of transit-time ultrasound flowmetry for chronic measurement of renal blood flow in dogs, we compared this method with the renal clearance of para-aminohippuric acid (CPAH) (corrected for hematocrit), and with direct volumetric measurements. When flow-probes were implanted without silastic sheeting to stabilize the implant, there was significant disparity between the (within-dog) mean levels of renal blood flow estimated by flow-probe and CPAH. In contrast, when the flow-probe implants were stabilized with silicone sheeting, there was close agreement in each dog between the flow rates measured by the two methods. When flow-probes were calibrated volumetrically in situ, there was a close linear relationship between flow derived from the flow-probe and that measured volumetrically (r = 0.98 +/- 0.02). We conclude that valid, chronic measurement of renal blood flow in dogs can be achieved using transit-time ultrasound flowmetry, provided the implant is stabilized with silicone sheeting.

Animals↗

PubMed1997

Renal effects of rilmenidine in volume-loaded anaesthetized dogs.

1. In anaesthetized, fluid expanded rats rilmenidine has diuretic and natriuretic effects. There is strong evidence that the natriuresis is mediated by putative imidazoline receptors. In contrast, in conscious euvolaemic dogs rilmenidine has a diuretic effect that is entirely attributable to activation of alpha 2-adrenoceptors, but no natriuretic effect. To determine whether the effects of rilmenidine are truly species dependent, or merely dependent upon the influences of anaesthesia and volume status, we tested the effects of rilmenidine in pentobarbitone anaesthetized, volume-loaded dogs. 2. The effects of rilmenidine in anaesthetized, volume-loaded dogs were similar to those found in conscious euvolaemic dogs. Compared with vehicle treatment, levels of glomerular filtration rate, urine flow and haematocrit were increased following rilmenidine treatment. No effect of rilmenidine on sodium excretion was observed. 3. We conclude that the renal responses to rilmenidine in dogs are largely unaffected by anaesthesia and plasma volume status. In particular, the natriuretic effect seen in rats was not observed. We conclude that putative imidazoline receptors do not have a major influence on sodium excretion in dogs.

Anesthesia↗

PubMed1997

Sympathetic burst activity: characteristics and significance.

1. The activity recorded from mammalian sympathetic nerves comes in bursts, which result from large numbers of fibres firing synchronously. 2. Human sympathetic nerve activity behaves similarly to that in animals, although burst rates may be lower. 3. Vasomotor, cardiac and sudomotor nerve fibres all fire in bursts. Whether other sympathetic pathways do so is unknown. 4. Sympathetic activity is intrinsically 'bursty' but not intrinsically regular. 5. Bursting is a population phenomenon, not usually evident in the firing of individual neurons. 6. Bursts in post-ganglionic nerves are driven by synchronously firing preganglionic neurons. 7. The origin of bursts remains controversial. Preganglionic neuron properties are likely to be important in at least shaping bursts. 8. Burst amplitude, which reflects the number of fibres firing together, and burst probability are controlled independently. 9. Baroreceptors affect burst probability over a wide range, but have less effect on mean burst amplitude. How they affect burst timing within the cardiac cycle is discussed. 10. Burst probability is determined 'downstream' of the rostral ventrolateral medulla, implicating either the spinal cord or recurrent brainstem connections in burst generation. 11. Neuroeffector responses are too slow to follow individual bursts. However, bursting will promote spatial facilitation at both ganglionic and effector levels, which may increase the dynamic range of neural control.

Animals↗

PubMed1997

Role of endogenous angiotensin II on sympathetic reflexes in conscious rabbits.

In the present study we sought to determine the contribution of endogenous brain stem angiotensin to renal sympathetic reflexes in conscious rabbits. Initial studies determined the subtype of receptor involved in the pressor response to angiotensin II (ANG II) administration into the fourth ventricle (4V). The AT1 antagonist losartan (0.001-10 micrograms 4V) had no effect on blood pressure alone but caused a dose-dependent blockade of the pressor effect of ANG II, with complete blockade produced by 10 micrograms, an effect that lasted for at least 3 h. The AT2 antagonist PD-123319 (0.1-1,000 micrograms) and vehicle had no effect on the ANG II pressor response. The effect of losartan (10 micrograms) on the baroreceptor, chemoreceptor, and trigeminal reflexes was examined in eight rabbits that had been implanted with 4V catheters and an electrode for recording renal sympathetic nerve activity (RSNA) 1 wk earlier. Baroreflex assessments were made during normoxia and two conditions of hypoxia (10% O2 and 10% O2 + 3% CO2) before and after 10 micrograms losartan or vehicle, on separate experimental days. During normoxia and hypoxia+CO2 losartan increased resting RSNA, the range, and upper plateau of the RSNA-MAP baroreflex curves. By contrast the marked increase in RSNA due to activation of trigeminal afferents was not affected by losartan. In conclusion the effect of losartan to increase RSNA activity in conscious rabbits, particularly during hypoxia and baroreceptor unloading, suggests that endogenous ANG II via AT1 receptors normally inhibits renal sympathetic baroreceptor and chemoreceptor reflexes.

Angiotensin II↗

PubMed1997

Frequency-dependent modulation of renal blood flow by renal nerve activity in conscious rabbits.

To examine the influence of the various frequency components of renal sympathetic nerve activity (RSNA) on renal blood flow (RBF) dynamics, a Doppler flow probe and renal nerve electrode were implanted on the left renal artery of 10 rabbits. Experiments were performed 4-9 days after surgery. Physiological changes in RSNA were induced by subjecting the rabbits to periods of breathing hypoxic gas mixtures. Signals were sampled at 1 kHz and analyzed by spectral analysis. During moderate hypoxia (arterial PO2 = 44 +/- 1 mmHg), arterial pressure and heart rate did not change, averaged RSNA increased by 90 +/- 7%, and RBF fell by 18 +/- 3%. In a separate group of renal-denervated rabbits (n = 6), no changes in RBF occurred during hypoxia. In intact rabbits, 53 +/- 4% of spectral density power of RSNA was found at the cardiac frequency and the remainder was predominantly coupled to respiration (approximately 0.9 Hz). During moderate hypoxia the amplitude of the RSNA oscillations increased 17 +/- 6 times at the cardiac frequency and 10 +/- 3 times at the respiration-related frequency. Modulation of RBF variability by the fluctuations of RSNA at the cardiac- and respiration-related frequency was, however, small. The normalized transfer gain between RSNA and RBF was approximately 0.1 at > 0.5 Hz. This means that, at > 0.5 Hz, maximally 10% of the amplitude of the RSNA oscillations is transmitted to corresponding RBF fluctuations. These transfer properties did not change during hypoxia. At < 0.5 Hz the transfer gain between RSNA and RBF increased. During moderate hypoxia, 0.3-Hz coherent oscillations of RSNA and RBF were found. In renal-denervated rabbits, 0.3-Hz oscillations in RBF were absent. Thus the renal vasculature was able to follow relatively low-frequency (< 0.5-Hz) fluctuations of RSNA and responded with corresponding oscillations in RBF. In contrast, the renal vasculature responded with increased constriction at the high-frequency (> 0.5-Hz) fluctuations of RSNA. These findings suggest that, in conscious rabbits, high-frequency oscillations of RSNA contribute to the vasoconstrictor tone, whereas the lower frequencies of RSNA contribute to the variability of RBF.

Animals↗

PubMed1997

Baroreflex control of heart rate and cardiac hypertrophy in angiotensin II-induced hypertension in rabbits.

The cardiac hypertrophy observed in hypertension is thought to be responsible for the accompanying deficiency in the baroreflex control of heart rate. In this study, we assessed the baroreflex relationship between heart rate and arterial pressure on a group of seven rabbits during a normotensive period, during the early phase of angiotensin II (Ang II)-induced hypertension II week) (50 ng/kg per minute i.v. via osmotic minipumps), after 7 weeks of continuous hypertension, then 2 days after Ang II was stopped, and finally 7 days after Ang II. Left ventricles were weighed for measurement of left ventricular weight-body weight ratio. One week of intravenous Ang II infusion produced hypertension (mean arterial pressure from 80 +/- 2 up to 115 +/- 8 mm Hg), with significantly increased heart rate and hematocrit. The heart rate-arterial pressure baroreflex curve was shifted to the right, with a significant 45% reduction in the gain of the reflex (-6.4 +/- 1.5 to -3.5 +/- 0.2 beats per minute/mm Hg). After 7 weeks of Ang II, arterial pressure was still elevated (112 +/- 4 mm Hg) and the gain of the baroreflex curve still somewhat attenuated, although it was no longer markedly different from normotensive levels (gain, -5.09 +/- 0.95, 20% reduction from normotensive level). Two days after the Ang II infusion was stopped, arterial pressure had returned to normotensive levels, although hematocrit and heart rate remained elevated. At this time, the baroreflex curve was similar to prehypertensive control levels, with no further changes when measured again 7 days after Ang II. Cardiac hypertrophy was present when measured at 7 days after angiotensin (left ventricular weight-body weight ratio: 1.78 +/- 0.05 versus 1.35 +/- 0.04 g/kg, hypertensive versus normotensive, P < .05). Thus, although Ang II infusion produced an initial deficit in the baroreflex control of heart rate, this effect became less as the hypertension continued. Furthermore, although cardiac hypertrophy developed, its presence did not appear to be sufficient to produce a decrease in barosensitivity independent of raised arterial pressure.

Angiotensin II↗

PubMed1996

Renal responses to increases in renal sympathetic nerve activity induced by brainstem stimulation in rabbits.

We have stimulated the rostral ventrolateral medulla of the central nervous system to increase renal sympathetic nerve activity (RSNA), and measured the effect on renal blood flow, glomerular filtration rate, and urinary excretion. Increases in RSNA were produced by infusion of 0.02 M glutamate at a rate of 30-50 nl/min into the subretrofacial nucleus for 40 min, in 10 urethane anaesthetized rabbits. Changes in RSNA were quantified as the mean nerve activity per 1 s period and as the frequency and amplitude of individual discharges (reflecting the number of activated nerve fibres). Glutamate infusion increased RSNA 59 +/- 11% over control levels. This was predominantly due to a 65 +/- 15% increase in the frequency of discharges (3.0 +/- 0.35 to 4.6 +/- 0.4 Hz), rather than the amplitude of the discharges (+9 +/- 3% over control). The effects of these changes on the kidney were made against data collected in the last 20 min of the infusion and the 40 min pre-and post-stimulation periods, when arterial pressure and heart rate were unchanged from control levels. Renal blood flow fell significantly from 31.3 +/- 4.5 to 17.7 +/- 5.1 ml/min (47% decrease) and filtration fraction significantly increased from 12.7 +/- 1.1 to 15.7 +/- 2.1% (24% increase) during glutamate infusion. Each of these variables returned to their pre-stimulus levels after ceasing the central stimulation. Fluid, sodium and potassium excretion were not changed by this stimulus. In conclusion, the results in this study suggest that a selective increase in sympathetic nerve activity to the kidney without change in renal perfusion pressure can cause constriction of the renal vasculature without alteration in sodium and water excretion.

Anesthesia↗

PubMed1996

Frequency and amplitude of sympathetic discharges by baroreflexes during hypoxia in conscious rabbits.

Sympathetic nerve activity (SNA) from multifiber preparations exhibits two distinct components: the frequency at which discharges occur and their relative amplitude (reflecting the number of activated nerve fibers within each burst). These two components may respond independently to various afferent inputs, indicating separate central controlling processes. We examined the response in the frequency and amplitude of renal SNA to changes in baroreceptor activity and the effect of two forms of hypoxia on this relationship in nine conscious rabbits. Rabbits breathed either room air or one of two hypoxic gas mixtures (10% O2 or 10% O2 + 3% CO2) for 20 min, during which baroreflexes were stimulated by ramp increases and then decreases in arterial pressure with phenylephrine (0.5 mg/ml iv) and nitroprusside (1 mg/ml) (total arterial pressure range induced was 80 mmHg). Hypoxia with 10% O2 significantly increased the resting frequency of SNA before baroreflex modifications from 2.15 +/- 0.18 to 2.82 +/- 0.25 discharges/s and with 10% O2 + 3% CO2 to 3.20 +/- 21 discharges/s. The amplitude of sympathetic discharges was increased 44 +/- 5% over control levels during 10% O2 but was not further increased by the addition of 3% CO2. The baroreflex curve for total SNA (1-s averages of the integrated neurogram) showed a graded response to the two hypoxic stimuli, with significant increases in the upper plateau, gain, and resting point on the curves. However, the baroreflex curve for the frequency or amplitude of sympathetic discharges did not show graded responses to each hypoxic treatment. The frequency baroreflex curve was sigmoidal and not changed from air during 10% O2. During 10% O2 + 3% CO2, the gain (responsiveness) of the curve was increased although the range of frequencies occurring was unaltered. The baroreflex curve for the amplitude showed similar responses to the two hypoxic stimuli, namely, increases in the upper plateau, gain, and resting point of the curve. We conclude that the frequency and amplitude of sympathetic discharges are able to respond differentially to changes in afferent stimuli. Given that alterations in the frequency and recruitment of sympathetic fibers (amplitude) to the kidney may have differing effects, this phenomenon may provide a previously unknown level of renal hemodynamic control through the interaction of specific afferent inputs to the central nervous system.

Animals↗

PubMed1996

Functional response to graded increases in renal nerve activity during hypoxia in conscious rabbits.

Changes in renal sympathetic nerve activity (SNA) are postulated to influence renal function in selective ways, such that different levels of activation produce particular renal responses, initially in renin release, then sodium excretion, with changes in renal hemodynamics occurring only with much greater stimulus intensities. The aim of this study was to determine the renal hemodynamic and excretory responses to graded physiological increases in renal SNA induced by breathing different hypoxic gas mixtures. Experiments were performed in seven conscious rabbits subjected to four gas mixtures (14% O2, 10% O2, 10% O2 + 3% CO2, and 10% O2 + 5% CO2) and instrumented for recording of renal nerve activity. After a 30-min control period, rabbits were subjected to one of the four gas mixtures for 30 min, and then room air was resumed for a further 30 min. The four gas mixtures increased renal SNA by 14, 38, 49, and 165% respectively, but arterial pressure (thus renal perfusion pressure) was not altered by any of the gas mixtures. The greatest level of sympathetic activation produced significant falls in glomerular filtration rate (GFR), renal blood flow, sodium and fluid excretion, and significant increases in plasma renin activity. These returned to levels not significantly different from control conditions in the 30-min period after the gas mixture. When the changes to the various gas mixtures were analyzed within each rabbit, a significant linear relationship was found with all variables to the increase in SNA. Renal denervation in a separate group of seven rabbits completely abolished all of the above responses to the different gas mixtures. Thus graded activation of renal nerves induced by changes in inspired gas mixtures resulted in graded decreases in renal blood flow, GFR, and sodium excretion and graded increases in renin activity, with the changes occurring across a similar range of nerve activities; there was no evidence for a selective change in any renal variable.

Animals↗

PubMed1995

A new model for the generation of sympathetic nerve activity.

1. Sympathetic discharges from multifibre nerve recordings vary in their frequency of occurrence which displays both slow and fast rhythms and in their amplitude which reflects the number of activated fibres. It has been shown that the frequency of occurrence of these rhythms varies according to baroreceptor activity (via blood pressure and heart rate) while the number of activated fibres is independently affected by chemoreceptor activity. 2. A new model is proposed for the generation of sympathetic nerve activity by the central nervous system to account for these results. The upper layer of the model comprises two oscillators, a fast and a slow cycle frequency oscillator, with the balance and occurrence maintained by afferent inputs such as the baroreceptors. 3. It is hypothesized that two central oscillators impinge on a lower layer of the model influencing the number of activated fibres within each postganglionic sympathetic burst. This is independent of the frequency control and affected by separate afferent inputs such a chemoreceptors.

Animals↗

PubMed1995

Pressure natriuresis and long-term blood pressure control.

The relationship between arterial pressure and the rate of Na+ excretion is regulated by a number of mechanisms- some well known, some newly discovered, and probably some yet to be discovered. These mechanisms affect either the amount of Na+ filtered at the glomerulus or its rate of reabsorption from the proximal or distal tubule. Other than physical factors (plasma protein concentration, glomerular capillary and tubular pressures) and glomerular ultrafiltration properties (Kr), important regulators of both filtration and reabsorption include the renin-angiotensin system, aldosterone, and renal nerves, although much remains to be learned about renal sympathetic innervation, especially neural control of renal tubular function. It has recently become evident that other factors may also be important, in particular, nitric oxide, endothelin, and medullipin. The latter is a vasodepressor hormone released from the renal medulla by increased arterial pressure, and its role in pressure-related Na+ excretion is only now being studied. Despite the central importance of this mechanism in the regulation of arterial pressure, there has been little study of many other potentially important mechanisms, especially those capable of affecting active Na+ transport across the tubule, including the imidazoline-preferring receptors. New techniques to study the relationship between arterial pressure and Na+ excretion are becoming available, and these will allow a better assessment of the potential of pharmacologic agents capable of modifying this relationship.

Animals↗

PubMed1994

Role of vasopressin in sympathetic response to paraventricular nucleus stimulation in anesthetized rats.

Vasopressin may play an extrahypothalamic role in the central control of the cardiovascular system, specifically acting as a spinal neurotransmitter in the pathway where the paraventricular nucleus (PVN) alters sympathetic outflow. In this study, the effect of stimulating neuronal cell bodies in the PVN on renal sympathetic nerve activity (RSNA) and the possible involvement of vasopressin in the pathway was investigated in anesthetized rats. The PVN was stimulated by microinjection with 0.2 M D,L-homocysteic acid via a glass micropipette, and the hemodynamic and sympathetic responses were recorded. A computerized sympathetic peak-detection algorithm was applied to recordings of sympathetic discharges to retrieve information about the characteristics of RSNA during PVN stimulation. The algorithm scanned the series of RSNA voltages for significant increases followed by significant decreases in a small cluster of voltage values. Once each synchronized RSNA peak had been detected, its corresponding amplitude and peak-to-peak interval were calculated. PVN stimulation consistently increased the amplitude of RSNA (mean 30 +/- 5.6% over control), arterial pressure, and the peak-to-peak interval of discharges. A V1 vasopressin antagonist intrathecally administered as a 500-pmol dose was subsequently able to completely block the hemodynamic response (blood pressure increase of 14 +/- 5%) and a 35 +/- 6% increase in RSNA in response to PVN stimulation and intrathecal vasopressin. Thus spinal vasopressin is likely to be a neurotransmitter involved in the cardiovascular regulation involving the PVN.

Animals↗

PubMed1993

The amplitude of synchronized cardiac sympathetic nerve activity reflects the number of activated pre- and postganglionic fibers in anesthetized cats.

In order to obtain information regarding the number of pre- and postganglionic fibers that are firing, we measured cardiac sympathetic nerve activity (CSNA) before and after the successive sectioning of T1-T5 thoracic rami in anesthetized cats. Total activity from the area was measured under the mean CSNA curve. Peak amplitude, width and periodicity of the synchronized discharge was analyzed from the CSNA curve by the method we developed. Total CSNA decreased to 91 +/- 6%, 63 +/- 6%, 27 +/- 10%, 8 +/- 6% and < 1% of the control due to successive section of the T5, T4, T3, T2 and T1 rami, respectively. The peak amplitude of synchronized CSNA decreased to 95 +/- 6%, 73 +/- 8%, 40 +/- 5% and < 10% of the control value, due to section of the T5, T4, T3 and T2 rami, respectively. The control width was 107 +/- 8 ms and decreased to 106 +/- 1 ms, 92 +/- 6 ms and 68 +/- 5 ms by successive section of the respective T5, T4 and T3 rami. However, periodicities of 80-120 ms (Tc rhythm) and 140-500 ms (Tb rhythm) of synchronized CSNA remained unchanged after section of the T3-T5 rami. The total CSNA decreased gradually due to decreases in the peak amplitude and width of synchronized CSNA with the successive section of preganglionic fibers. These results indicate that the peak amplitude of synchronized CSNA reflects the number of pre- and post-ganglionic fibers that are firing and suggest that the number of preganglionic neurons which activate the cardiac fibers naturally was largest in the T3 segment.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1992

Fundamental rhythm of renal sympathetic nerve activity in anesthetized cats.

To examine the fundamental rhythms of sympathetic discharges, the periodicity of synchronized renal nerve activity (RNA) was measured in anesthetized cats. After filtering the RNA between 50-3000 Hz, rectification and integration the periodicity was calculated by measuring the peak to peak intervals. Two major periodicities were detected, a Tc rhythm between 6 and 25 c/s with a 43% probability and a Tb rhythm between 2 and 6 c/s with a 57% probability. The mean periods of Tc and Tb were 95 +/- 2 ms and 297 +/- 4 ms (+/- SE) respectively. Another techniques which has previously been used to assess the periodicity was also applied, in which the original neurogram was filtered between 0.08-3000 Hz and measured by power spectral analysis. However, this technique only identified the 2-6 c/s frequency and the faster Tc rhythm was undetected. Baroreceptor stimulation induced by noradrenaline decreased the probability of Tc and Tb modal components. Baroreceptor denervation led to an increase in the probability of the Tc rhythm and reduction in the Tb rhythm. These results support our model that the Tc rhythm reflects a fundamental periodicity of central origin and that the Tb rhythm reflects a periodicity of cardiac-related RNA, which is produced by reflex inhibition of the fundamental rhythm by periodic baroreceptor input.

Anesthesia↗

PubMed1992

Effect of chemoreceptor stimulation on the periodicity of renal sympathetic nerve activity in anesthetized cats.

The effect of chemoreceptor stimulation, with asphyxia (1 min), hypoxia (2 min) or hypercapnia (2 min), on the periodicity of synchronized renal sympathetic nerve activity (RNA) was examined in anesthetized cats before and after peripheral chemoreceptor and baroreceptor denervation. RNA was filtered between 50-3000 Hz, rectified and integrated. Time intervals, less than 500 ms, between synchronized interburst intervals were measured and used to produce periodicity histograms. Under control normoxia two major periodicities were evident, a Tc rhythm between 6 and 17 c/s comprising 34 +/- 5% (+/- SE) of measured intervals and a Tb rhythm between 2 and 6 c/s with a 66% probability. The mean periods of Tc and Tb were 110 +/- 6 ms and 299 +/- 7 ms respectively. The periodicity distribution and mean Tc and Tb rhythms for RNA discharge under various chemoreceptor stimulations were not significantly changed despite significant increases in arterial blood pressure in all cases. The amplitude and overall number of synchronized RNA peaks were however increased with chemoreceptor stimulation. When asphyxia was applied under a constant arterial pressure the periodicity of synchronized RNA still was not significantly altered. Baroreceptor and peripheral chemoreceptor denervation led to an increase in the probability of the Tc mode and reduction in the Tb mode, once again the application of chemoreceptor stimulation did not significantly alter the frequency distribution of synchronized RNA. The results indicate that chemoreceptor stimulation does not affect the 10 c/s fundamental rhythm and the stability of gate operators altering Tc/Tb proportions, although it can alter the number of active fibres and interacts with the baroreflexes to maintain RNA at elevated blood pressures. The results support our model that the Tc mode reflects a fundamental periodicity of central origin and the Tb mode a periodicity of cardiac related RNA, which is produced by the opening and closing of gate operators to the fundamental rhythm.

Anesthesia↗