Withdrawal Of Sympathetic Activity Research Articles

Optimizing Autonomic Function Analysis via Heart Rate Variability Associated With Motor Activity of the Human Colon.

The parameters of heart rate variability (HRV) can non-invasively assess some autonomic activities, and HRV is influenced by many bodily actions. Although parasympathetic activity is the primary driver of colonic propulsive activity, and sympathetic activity a major inhibitor of colonic motility, they are rarely measured and almost play no role in diagnosis of colon motor dysfunction or in standard treatments. Here we set out to optimize HRV analysis of autonomic nervous system changes related to human colon motility. The electrocardiogram and impedance were recorded in synchrony with colonic motor patterns by high-resolution manometry. Respiratory sinus arrhythmia (RSA), root mean square of successive differences of beat-to-beat intervals (RMSSD), the Baevsky Index or Sympathetic Index (SI), and the ratios of SI/RSA and SI/RMSSD were shown to indicate a marked increase in parasympathetic and withdrawal of sympathetic activity during the high-amplitude propagating pressure waves (HAPWs). Strong associations were seen with HAPWs evoked by a meal and rectal bisacodyl indicating a marked increase in parasympathetic and withdrawal of sympathetic activity during the gastrocolic reflex and the defecation reflex. When HAPWs occurred in quick succession, parasympathetic activation (RSA and RMSSD) occurred in a rhythmic fashion. Hence, during propulsive motor patterns, an overall shift in autonomic activity toward increased parasympathetic control was shown to be reflected in HRV. HRV assessment may therefore be valuable in the assessment of autonomic dysfunction related to colonic dysmotility.

Brugada syndrome and atrial fibrillation: pathophysiology and genetics

In 1992, the Brugada brothers described eight patients with a syndrome of ST segment elevation in electrocardiogram (ECG) leads V1–V3 accompanied by a right bundle branch block appearance and the risk of ventricular fibrillation and sudden cardiac death.1 One patient was an 8-year-old girl with an additional history of paroxysmal atrial fibrillation (AF). She had experienced her first paroxysm soon after birth while her first episode of syncope occurred at 8 years of age. Since this first description a dramatic variability in clinical presentation of the disease has transpired. A high prevalence of AF has, however, remained a feature.2 The first gene linked to the Brugada syndrome was SCN5A, which encodes the α-subunit of the NaV1.5 cardiac sodium channel responsible for the inward sodium current. A 20% yield of disease-associated variants has consistently been reported.2 More recently less common mutations in other genes have been associated with the Brugada syndrome including mutations in: GPD1L, involved in the transportation of cardiac sodium channels to the cell membrane; SCN1B and SCN3B, encoding β-subunits of NaV1.5; KCNE3 encoding a β-subunit of the channel responsible for the I (to) current; and CACNA1C and CACNB2b, which both encode subunits of the L-type calcium channel.3 Mutations in SCN5A have also been reported in association with familial AF.4 The prevalence of AF and atrial flutter in patients with Brugada syndrome is approximately 20%2 compared with 2.3% in the general population above the age of 40.5 Kusano et al . found that 70% of episodes of AF in their Brugada patients occurred at night, suggesting that nocturnal vagal activity and withdrawal of sympathetic activity may play an important role in arrhythmogenesis. Bradycardia …

Invited Commentary for: Predicting clinical physiology: A Markov chain model of heart rate recovery after spontaneous breathing trials in mechanically ventilated patients

This study proposes a Markov chain model study to assess heart rate recovery (HRR) in mechanically ventilated patients upon attempted weaning (spontaneous breathing trial, or SBT). It is known that postexercise HRR data can be plotted as an exponentially decreasing HR vs time curve, with an initial rapid decline (in the first 30 seconds), which can be curve fitted as a first-order decay curve with an exponential time constant. This initial rapid decline has been previously attributed to parasympathetic blockade, with minimal dependence on the sympathetic system and exercise intensity. The second slow HR decay phase supposedly reflects sympathetic activity withdrawal and the clearance of stress metabolites [1]. In fact, the interactions are quite complex, and it has been difficult to establish a clear correlation between HRR and HRV. What is established is that attenuated HRR after exercise is a reflection of the parasympathetic tone and is an independent predictor of mortality among patients undergoing stress testing [2]. The presence of autonomic dysfunction, as assessed by HRVor baroreceptor insensitivity, is likewise predictive of increased mortality. Can these alterations be extended to patients with pulmonary abnormalities? Seshadri et al [3] have similarly shown that during stress testing, in patients with a worsening FEV1 and FEV/ FVC, these spirometry abnormalities are associated with abnormal HRR. Finally, it has been demonstrated in healthy children and adolescents that there is an inverse correlation between HRR and metabolic risks (waist circumference,

Autonomic diseases: clinical features and laboratory evaluation

The autonomic nervous system has a craniosacral parasympathetic and a thoracolumbar sympathetic pathway (fig 1) and supplies every organ in the body. It influences localised organ function and also integrated...

Cephalic tetanus: report of case

Tetanus is an acute, often fatal, neurological disease that is characterised by increased muscle tone and spasms caused by tetanospasmin, which is a protein toxin elaborated by Clostridium tetani; this is an obligate anaerobic, motile Gram-positive rod found in the soil, in animal and occasionally in human faeces, and in house dust, hospitals, and operating theatres.1–3 The incubation period is about seven days and the mortality is high.1 Spores may survive for years and are resistant to various disinfectants and to boiling for 20 minutes.1 Muscles of the jaw, face, and head are involved first because the toxin has to travel along shorter axonal pathways.2 Infection is independent of the size of the wound provided that the blood supply and the oxygenation are compromised.2 Clinical tetanus comprises four symptomatic types: generalised, local, cephalic, and neonatal.2,4,5 Local tetanus is uncommon with a reasonable prognosis.3 Cephalic tetanus is a rare variant of local tetanus that involves 1–3% of all reported cases and several cranial nerves are involved.5 It may follow an injury such as laceration, abrasion, or puncture wound.1 It may be associated with a head injury or middle ear infection. It may follow traditional practices like ear piercing, circumcision, and tattooing, or the mouth may be the point of entry.6 Two-thirds of cases of cephalic tetanus progress to generalised disease that can involve the limb muscles and trunk progressively.3,7 The commonest presenting symptom is trismus. Other manifestations include dysfunction of one or more cranial nerves (often the seventh nerve), facial pain, dysphagia, dysarthria, risus sardonicus (spasms of the face and jaw), stiffness of the neck and back (opisthotonos – an arched back with the body resting on the heels and occiput), spasms, voiding difficulties, abdominal pain and gastrointestinal problems, and mental and emotional problems.5,7 Other presenting symptoms may be fever, nystagmus, diplopia, cardiac disorders and malaise.1,2,7 Episodes of hypotension and bradycardia have been attributed to either withdrawal of sympathetic activity or increased parasympathetic activity. Episodes of hypertension and tachycardia have also been recorded and are thought to be the result of sympathetic stimulation. Spasms may be mild, infrequent and brief, or severe, painful, and exhausting. They can cause cyanosis that threatens ventilation, occur repetitively, and may be spontaneous or provoked by even the slightest auditory, visual or emotional stimulation. They may also be protracted, the patient seeming to be in a state of perpetual convulsion. Spasm of the pharyngeal muscles prevents swallowing of saliva that may be aspirated and cause atelectasis and aspiration pneumonia. Laryngeal spasm may lead to sudden death from asphyxia. The diagnosis of tetanus is based entirely on clinical findings.1,2 The activity of creatine phosphokinase (CPK) may be increased in some cases, but it is not pathognomonic.1 It is of interest that C. tetani can be isolated from wounds of patients without tetanus and often cannot be recovered from wounds of those with tetanus.

SYMPATHETIC NERVOUS SYSTEM AND CHRONIC RENAL FAILURE

The aim of this work was to review evidence on the role of the sympathetic nervous system (SNS) in chronic renal failure (CRF). Three main points are discussed: 1) SNS and pathogenesis of arterial hypertension; 2) SNS and cardiovascular risk; 3) implication of SNS in arterial hypotension during hemodialysis. Several lines of evidence indicate the presence of a sympathetic hyperactivity in CRF, and its relationship with arterial hypertension. It is suggested that diseased kidneys send afferent nervous signals to central integrative sympathetic nuclei, thus contributing to the development and maintenance of arterial hypertension.The elimination of these impulses with nephrectomy could explain the concomitant reduction of blood pressure. Several experiments confirmed this hypothesis. Regarding SNS and cardiovascular risk, some data suggest that reduced heart rate variability identifies an increased risk for both all causes and sudden death, independently from other recognized risk factors. Symptomatic hypotension is a common problem during hemodialysis treatment, occurring in approximately 20–30% of all hemodialysis sessions and is accompanied by acute withdrawal of sympathetic activity, vasodilation and relative bradicardia. This reflex is thought to be evoked by vigorous contraction of a progressively empty left ventricle, activating cardiac mechanoceptors. This inhibits cardiovascular centers through vagal afferents, and overrides the stimulation by baroreceptor deactivation. Alternative explanations include cerebral ischemia and increased production of nitric oxide, which inhibit central sympathetic activity. It is hoped that therapies aimed at modulating sympathetic nerve activity in patients with CRF will ameliorate their prognosis and quality of life.

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)

Sympathectomy exaggerates antihypertensive effect of vasopressin withdrawal

The role of sympathetic function in the mechanism of the decrease in arterial pressure that follows withdrawal of an intravenous infusion of arginine vasopressin (AVP) in spontaneously hypertensive rats (SHR) was studied by comparing this withdrawal-induced antihypertensive phenomenon (WAP) in rats with intact sympathetic function to those subjected to sympathectomy. Sympathectomy with guanethidine did not lower blood pressure significantly in either SHR or normotensive Wistar-Kyoto (WKY) rats despite a marked impairment of sympathetic function as judged by a dramatic attenuation of blood pressure responses to tyramine and by evidence of denervation supersensitivity to phenylephrine. Cessation of a 3-h intravenous infusion of AVP (20 ng.kg-1.min-1) was associated with large and prolonged decrease in pressure below preinfusion levels in SHR with intact sympathetic function: 5 h after stopping the infusion, pressure was 27 +/- 3 mmHg below preinfusion levels. In sympathectomized SHR, the decrease in pressure after cessation of the AVP infusion was much larger: 5 h after the infusion, pressure was 44 +/- 2 mmHg below preinfusion levels. In contrast to SHR, pressure returned to control levels in WKY with intact sympathetic function after withdrawal of AVP. A small but significant decrease in pressure occurred after withdrawal of AVP in sympathectomized WKY. The results are consistent with the hypothesis that withdrawal of sympathetic activity is a contributing factor or a prerequisite condition for development of a WAP.

Neurogenic histaminergic vasodilation in canine skeletal muscle: mediation by alpha 2-adrenoceptor stimulation.

This study examines the neurogenic effect of alpha 2-adrenoceptor stimulation on skeletal muscle vascular resistance and its relation to the level of background sympathetic activity. The isolated, separately perfused, neurally intact canine gracilis muscle preparation was used since it permits deliberate and quantifiable alterations in background sympathetic activity, as measured by skeletal muscle vascular resistance. Systemic intravenous UK-14304, a highly selective alpha 2-adrenoceptor agonist, produced a precipitous, neurogenic vasodilation that lowered vascular resistance below the subsequently denervated resistance, thus indicating that an active vasodilation was involved. The overall magnitude of the vasodilation was much greater in animals that had been hemorrhaged to elevate background sympathetic activity than in animals that had been transfused to lower background activity. The neurogenic vasodilation was unaffected by baroreceptor and cardiopulmonary receptor denervation and by prior cholinergic-receptor blockade of the gracilis muscle. Prior H1- and H2-histaminergic-receptor blockade, on the other hand, eliminated the active vasodilation but not a vasodilation down to the subsequently denervated resistance. Prior alpha 1-adrenoceptor blockade lowered resistance down to the subsequently denervated resistance and greatly attenuated the active vasodilation. The present study demonstrates that withdrawal of sympathetic activity by alpha 2-adrenoceptor stimulation produces an active vasodilation resulting from histamine release in skeletal muscle as well as a passive vasodilation resulting from lysis of peripheral vasoconstrictor tone.

Effect of intracarotid administration of ouabain in dogs.

Recent work has documented both centrally mediated vasoconstriction and, paradoxically, a withdrawal of sympathetic activity in response to cardiac glycosides. In the present study the possibility that these different neurogenic responses might be dose related was investigated by infusing ouabain (5, 10, and 20 micrograms) for 5 min into the right common carotid artery of 51 anesthetized mongrel dogs. Effects on vascular resistance in the isolated, separately perfused but innervated gracilis muscle were measured. A 5-microgram infusion of ouabain (n = 6) produced a prolonged decrease in gracilis vascular resistance (GVR) of 19.4 +/- 5.4% (SE) from 43.4 +/- 6.7 (SE) to 33.7 +/- 4.2 mmHg.ml-1.100 g muscle.min (resistance units, RU). This vasodilatory response was not present in nine additional dogs following denervation of the carotid bifurcation. A 10-microgram infusion had no significant effect on GVR (n = 5), but the 20-microgram infusion of ouabain (n = 8) caused a rapid increase in GVR from 42.1 +/- 5.0 to 47.6 +/- 5.7 RU, an increase of 14.4 +/- 5.6%, which was not influenced by denervation of the carotid bifurcation (n = 8). This vasoconstriction was transient returning toward the control levels by 20 min following the infusion. These data indicate important dose-related differences in vascular responses to ouabain that are directionally opposite and mediated by separate neurogenic mechanisms. At high doses a centrally mediated vasoconstriction dominates, whereas at low doses carotid bifurcation mediated vascular dilatation occurs.

Neurohumoral response to hospitalization in hypertensive patients.

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day. 2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day. 3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively. 4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin--angiotensin--aldosterone system rose, but more conspicuously in group 1. 5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin--angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.