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Plasma catecholamine concentrations are a reliable index of sympathetic vascular tone in patients with cirrhosis.

In patients with cirrhosis, the significance of elevated plasma catecholamine concentrations is unclear. Thus we investigated the relationship between plasma catecholamine concentrations and the hemodynamic effect of pindolol (an index of sympathetic vascular tone) in 10 patients with cirrhosis. Systemic and splanchnic hemodynamics and plasma catecholamine concentrations in the pulmonary artery and the splanchnic veins (hepatic and azygos veins) were studied before and after the oral administration of pindolol (20 mg). In basal conditions patients exhibited a hyperkinetic circulatory syndrome and elevated plasma catecholamine concentrations. Alterations in basal hemodynamics were correlated with plasma epinephrine concentrations but not with norepinephrine. Pindolol administration significantly decreased heart rate and increased right atrial pressure. After pindolol administration, individual hemodynamic changes (cardiac index, systemic vascular resistance, wedged hepatic venous pressure) were significantly correlated with plasma catecholamine concentrations. In conclusion, this study shows that in cirrhotic patients epinephrine may play a role in hemodynamic alterations, and plasma catecholamine concentrations are an index of sympathetic vascular tone.

Epinephrine↗

An adrenergic component of the nervous apparatus of the aortic reflexogenic zone.

The structural organization of the adrenergic (sympathetic) component of the autonomic innervation of the depressor zone of the cat aortic arch was studied by luminescence microscopy of the catecholamines. A terminal adrenergic plexus, branching extensively in the connective-tissue basis of the depressor area of the aortic arch, was discovered. The participation of vessels supplying blood to the depressor area was established. Adrenergic neurons were found in the territory of the depressor zone of the aortic arch. It is postulated that the adrenergic component of the depressor zone of the aortic arch participates in the peripheral mechanism of the regulatory effects of the sympathetic nervous system on the baroreceptor apparatus.

Animals↗

[Kidney in heart failure (author's transl)].

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Blood Proteins↗

Relation of efferent impulse activity in splenic nerve to reflexly induced reactions of resistance and capacitance vessels to spleen.

Constrictory responses of splenic resistance vessels arising under pressor reflexes were abolished by hexonium (2 mg/kg) as well as the high amplitude (above 15 muV) impulses in sympathetic splenic nerves. Constrictory and dilatory responses of splenic capacitance vessels were preserved after administration of the same dose of hexonium and correlated as to the directivity with the changes of the low amplitude (15 muV and lower) impulsation in the splenic nerve.

Animals↗

Vasospasm and adrenergic innervation of circle of Willis.

Cerebral vasospasm following the rupture of intracranial aneurysm presents perplexing situation, i.e. prolonged vasospasm results in cerebral infarct and too early relief causes recurrence of the bleeding. To understand mechanism underlying the cerebral vasospasm, catecholamine-containing sympathetic nerve plexus was examined in the arterial walls of the circle of Willis using rat, cat, dog and monkey using Falck-Hillarp's fluorescence method. The distribution of fluorescing nerve plexus was found to be essentially the same in the examination of all species. The distribution of the fluorescing fibers decreases in the following order; proximal anterior cerebral, internal carotid, distal anterior or proximal middle cerebral, and distal middle cerebral artery. The origin of the nerve plexus accompanying the basal cerebral arteries and the relation to the experimental cerebral vasospasm was investigated as detailed as they could.

Animals↗

Mechanisms of depressor effect of norepinephrine injected into subnucleus commissuriu of nucleus solitarius tractus in rabbits.

This experiment aimed to investigate the effect of adrenergic system in the subnucleus commissuriu of nucleus solitrius tractus (CNTS) on renal nerve discharges. Norepinephrine (NE) was microinjected into the CNTS of rabbits and mean arterial blood pressure (MAP) and renal nerve discharges (FRND) were synchronously recorded. The results indicated that (1) microinjection of norepinephine into the CNTS of rabbit could significantly attenuate the frequency of renal nerve discharge, and at the same time decrease markedly the mean arterial pressure. (2) Microinjection of 0.3 nmol yohimbin into CNTS had no significant influence on FRND and MAP, but could attenuate and even reverse the effects of NE on FRND and MAP. These results suggest that microinjection of NE into CNTS may activate the alpha-adrenorecptor located in CNTS and secondarily produce a depressor effect by attenuating the activity of periphenal sympathetic nervous system.

Animals↗

Sympathetic mediated vasomotion and skin capillary permeability in diabetic patients with peripheral neuropathy.

AIMS/HYPOTHESIS: A loss of sympathetic function could lead to changes in capillary fluid filtration in diabetic patients. We investigated whether a decreased sympathetically mediated vasomotion in the skin in diabetic patients with peripheral neuropathy is associated with an abnormal capillary leakage. METHODS: Three matched groups were studied: 18 diabetic patients with documented peripheral neuropathy (DN), 18 diabetic patients without peripheral neuropathy (D), and 18 healthy control subjects (C). Sensory and motor nerve function of the distal extremities were assessed by standard neurography, and expressed in a sensory-motor nerve function score. Sympathetic vasomotion of the skin microcirculation was assessed by determining the power of blood flow variability in the low-frequency (0.02-0.14 Hz) band by spectral analysis of laser Doppler flowmetry at the median ankle. Skin capillary leakage was evaluated by sodium fluorescein videodensitometry at the same site of the foot. RESULTS: Sympathetically mediated vasomotion of the foot skin microcirculation was lower in diabetic patients with documented peripheral neuropathy compared with diabetic patients without peripheral neuropathy and control subjects (p<0.001). Capillary sodium fluorescein leakage was larger in 18 diabetic patients with documented peripheral neuropathy than in diabetic patients without peripheral neuropathy (p<0.02) and C (p<0.005). Multiple regression analysis disclosed that a reduced sympathetically mediated vasomotion, together with a lower sensory-motor nerve function score, independently contributed to the variance in sodium fluorescein leakage, for 30% (p<0.001) and 17% (p<0.01), respectively. CONCLUSIONS: A loss of sympathetic tone, apart from sensory-motor nerve dysfunction, seems to be a major determinant of an increased capillary permeability in diabetic patients with neuropathy.

Capillary Permeability↗