Lars Erik Lindblad

Is vibration white finger a primary sympathetic nerve injury

Changes in the sympathetic nerve system have been suggested as the pathophysiological mechanism underlying vibration white finger (VWF). The aim of the present study was to investigate if experimental support for such a mechanism could be found in VWF. Drugs with a known effect on sympathetic alpha receptors were administered into the finger skin by iontophoresis and their effects on blood flow in the same area evaluated using a laser Doppler technique. The effects of noradrenaline (stimulating alpha-1 and alpha-2 receptors), phenylephrine (an alpha-1 stimulator), and B-HT 933 (an alpha-2 stimulator) were studied in 12 patients with vibration white finger and 12 healthy controls. The reactions to noradrenaline and B-HT 933 were similar in both patients and controls, but the reaction of the patients to phenylephrine was significantly weaker than the controls. In additional experiments in six patients and six controls concentration effect curves to phenylephrine were derived. The curves for the patients were shifted to the right--that is, they reacted less strongly than the controls at all doses of the drug which induced an appreciable vasoconstriction. The results of this study are compatible with the hypothesis that the alpha-1 receptor mediated responses are weakened in VWF. The predominance of alpha-2 receptors in the digital arteries has, on the basis of animal experiments, been suggested as a possible mechanism for Raynauds phenomenon.

Neural regulation of vascular tone and cold induced vasoconstriction in human finger skin

Finger skin blood flow was measured by a laser Doppler during control conditions, after neural blockade at the finger base by prilocaine and after localized anaesthesia of the skin by lidocaine introduced iontophoretically into the finger skin. Vasoconstriction was achieved by local cooling of the finger and by iontophoretic administration of norepinephrine during the described three conditions. Compared to the control condition, blood flow increased after nerve block at the finger base but even more after local skin anaesthesia. This additional increase in blood flow after local application of lidocaine indicates that finger skin vascular tone is partly dependent on local reflexes. Vasoconstriction on local cooling was preserved after nerve blockade at the finger base but inhibited after local skin anaesthesia by iontophoresis of lidocaine. This inhibition was not due to paralysis of the vessel wall since vasoconstriction to norepinephrine was preserved. Thus, vasoconstriction in response to local cooling is mediated by local reflexes.

Adrenoceptors in Raynaud's disease.

Summary: Experiments were designed to study adrenoceptor function in subjects with Raynaud’s disease. Sympathetic agonists and antagonists were administered into the finger skin by iontophoresis, and the resulting change in local skin blood flow was evaluated by laser Doppler technique. The effects of norepinephrine (NE, stimulating α1-and α2-adrenoceptors), phenylephrine (stimulating α1-adrenoceptors), and B-HT 933 (stimulating α2-adrenoceptors) were studied in 12 women with Raynaud’s disease and in 12 healthy controls. Controls and cases showed a similar consistent vasoconstriction to NE and B-HT 933. All control subjects showed a vasoconstriction to phenylephrine. In contrast, the Raynaud subjects demonstrated a weaker vasoconstriction or even a vasodilation, especially to low concentrations of the drug. After blockade of the α1-adrenoceptors by doxazosin in the controls, phenylephrine mimicked the reaction in Raynaud subjects. β-Adrenoceptor agonists (isoprenaline and terbutaline) had no effect on finger blood flow in the examined finger skin area in either control or Raynaud subjects. We suggest that Raynaud’s disease is characterized by a defect in α1-adrenoceptor function.

Digital blood pressure after local cooling as a diagnostic tool in traumatic vasospastic disease.

Measurement of digital blood pressure before and after local cooling was performed in 10 men with traumatic vasospastic disease (TVD), 10 men who worked with vibrating tools but had no symptoms in arms or hands, and 10 men who had never worked with vibrating tools. The reduction in finger systolic pressure was significantly larger in the group with TVD than in either of the reference groups (p less than 0.001). There was no difference between the two reference groups. Nine of the 10 patients with TVD had a larger reduction in their finger systolic pressure after local cooling than anyone in either control group. The effects of two different room temperatures (17 degrees C and 23 degrees C) were evaluated. At the higher temperature the overlap between patients with TVD and controls was greater. The method described seems a feasible way to obtain an objective verification of TVD.

Afferent and efferent nerve injury in vibration white fingers

To study afferent pain and efferent sympathetic nerve function in vibration-induced Raynauds phenomenon, 10 patients and 11 healthy controls were examined. Thresholds for mechanically and thermally induced pain were determined on the left side of the tip of the second finger, on the skin fold between thumb and second finger and on the ear lobe. Superficial skin blood flow was simultaneously measured by laser Doppler technique on the right third finger. The patients had higher pain thresholds than controls on the vibration-exposed index finger but not on other stimulation areas. Thus receptors or pain-mediating nerve fibres in the fingers are affected by work with vibrating tools. The controls demonstrated vasoconstriction on pain stimulation, whereas the patients showed no or weak vasoconstriction in response to the stimulation. This was true also when areas not included in the disease process were stimulated, indicating that also sympathetic vasoconstrictor nerves or receptors are affected in vibration syndrome.

Circulatory effects of dihydroergotamine in patients with disturbed sympathetic vasomotor control with special reference to postural hypotension.

In five patients with postural hypotension (disturbed sympathetic vasomotor control) the effect of intravenous and oral administration of dihydroergotamin (DHE) has been studied. The therapeutic effect of oral administration of DHE has also been compared to the effect of treatment with an antigravity suit. Following intravenous administration of DHE, systemic and central venous pressure increased in all cases. The effect on cardiac output was negligible and consequently the calculated total peripheral vascular resistance increased. Orthostatic tolerance increased in all cases. During long-term oral administration the effect was comparable to that obtained with an antigravity suit. The increased orthostatic tolerance is explained by a constrictive effect on both capacitance and resistance vessels. In order to analyze the influence of a functional denervation on the effect of DHE on peripheral circulation, a study has also been performed during epidural anaesthesia of the lower body in 11 patients. In the legs which were deprived of sympathetic tone intravenous administration of DHE caused constriction of resistance vessels. In the intact forearm there was a decrease of tone in the resistance vessels. The results indicate that DHE - apart from its well-known venoconstrictive effect - also may constrict resistance vessels when they are subjected to a low sympathetic nervous outflow.