Objectives To investigate whether prior exposure to hand-transmitted vibration on the day of a cold provocation test affects the cold
response of digital arteries.
Methods Each of ten healthy men attended two experimental sessions in which their right hands were exposed for 60 min to either contact
force alone (5 N) or a combination of contact force (5 N) and 125-Hz vertical vibration with an acceleration magnitude of
64 m s−2 r.m.s. (unweighted). Finger systolic blood pressure (FSBP) during local cooling to 10°C was measured in the second right
finger (exposed hand) and the second left finger (unexposed hand) before exposure and at 30 and 70 min after the end of both
exposure conditions.
Results Analysis of repeated measures of FSBP during local cooling by means of an autoregressive model revealed no significant difference
in cold-induced vasoconstriction of the digital arteries between exposure to contact force alone and combined exposure to
contact force and vibration. There were no significant changes in the cold response of digital arteries over time in either
the right or the left hand after exposure of the right hand to either the contact force alone or the combined contact force
and vibration.
Conclusions The results of this experimental study of the influence of prior vibration exposure on the cold test results suggest that
in healthy men recent exposure to contact force and moderate levels of hand-transmitted vibration does not affect the response
of finger circulation to cold provocation. These findings may be of practical importance for the definition of test conditions
in the field, especially the length of time required between the last occupational exposure to tool vibration and the commencement
of objective vascular testing. 相似文献
First pass radionuclide ventriculography was performed withgold 195m in a sequential evaluation of left ventricular ejectionfraction during cold pressor stimulation. We studied 10 normalcontrols, 10 patients with angina pectoris who had proven coronaryartery disease and normal left ventricular function during contrastangiography and 10 patients with dilated cardiomyopathy withnormal coronary arteries and impaired left ventricular functionat contrast angiography. Mean resting ejection fraction was similar in controls and patientswith coronary heart disease (57 ± 2 vs 58 ± 3)but was significantly lower in the cardiomyopathic subjects(27 ± 4, P < 0.001). After 30 seconds cold pressorstimulation, mean left ventricular ejection fraction fell inthe normal controls (57 ± 2 to 52 ± 2, P <0.05)but was unchanged in those with coronary heart disease and dilatedcardiomyopathy (58 ± 3 to 55 ± 3 and 27 ±4 to 24 ± 4, both NS). No further significant changeoccurred after 2.5 minutes stimulation (53 ± 1, 58 ±3 and 23 ± 3, respectively). There was no differencein the pattern of left ventricular ejection fraction responsebetween the groups. Six controls, 4 patients with coronary heartdisease and 4 patients with dilated cardiomyopathy had a significantfall in left ventricular ejection fraction and 4, 5 and 6, respectively,developed a new or further deterioration in regional wall motion.Thus neither changes in regional wall motion nor left ventricularejection fraction response distinguished either patient groupfrom the normal controls. We do not recommend cold pressor stimulationas a diagnostic test for coronary heart disease. 相似文献
Whiplash injury and chronic whiplash syndrome represent major health problems in certain western communities, pain being the main symptom. Sensitization of the nociceptive system may play a role for non-recovery after whiplash injury. AIMS: This study examined if tolerance to endure pain stimuli may predict outcome in whiplash injury. In a prospective fashion, 141 acute whiplash patients exposed to rear-end car collision (WAD grade 1-3) and 40 ankle-injured controls were followed and exposed to a cold pressor test, respectively, 1 week, 1, 3, 6 and 12 months after the injury. VAS score of pain and discomfort was obtained before, during and after immersion of the dominant hand into cold water for 2 min. The McGill Pain Questionnaire showed that ankle-injured controls had higher initial pain scores than the corresponding whiplash group, while whiplash-injured subjects had higher scores at 6 months; pain scores being similar at other time points. No difference was found in cold pressor pain between recovered whiplash patients and ankle-injured subjects. Non-recovery was only encountered in whiplash injury. Eleven non-recovered whiplash patients (defined as: handicap after 1 year) showed reduced time to peak pain from 1 week to 3 months (P<0.001), 6 months (P<0.01), but not 12 months after the injury. A larger pain area was seen in non-recovered vs. recovered whiplash-injured subjects during the entire observation period (P<0.001). Non-recovery after whiplash was associated with initially reduced cold pressor pain endurance and increased peak pain, suggesting that dysfunction of central pain modulating control systems plays a role in chronic pain after acute whiplash injury. 相似文献
Clinical findings and recent non-invasive functional imaging studies pinpoint the insular cortex as the crucial brain area involved in cold sensation. By contrast, the role of primary (SI) and secondary (SII) somatosensory cortices in central processing of cold is controversial. So far, temporal activation patterns of cortical areas involved in cold processing have not been examined. Using magnetoencephalography, we studied, in seven healthy subjects, the temporo-spatial dynamics of brain processes evoked by innocuous and noxious cold stimulation as compared to tactile stimuli. For this purpose, a newly designed and magnetically silent cold-stimulator was employed. In separate runs, cold and painful cold stimuli were delivered to the dorsum of the right hand. Tactile afferents were stimulated by pneumatic tactile stimulation.
Following innocuous cold stimulation (ΔT=5±0.3°C in 50±2 ms), magnetic source imaging revealed an exclusive activation of the contra- and ipsilateral posterior insular cortex. The mean peak latencies were 194.3±38.1 and 241.0±31.7 ms for the response in the ipsi- and contralateral insular cortex, respectively. Based on the measurement of onset latencies, the estimated conduction velocity of peripheral nerve fibres mediating cold fell in the range of Aδ-fibres (7.4±0.8 m/s).
Noxious cold stimulation (ΔT=35±5°C in 70±12 ms) initially activated the contra- and ipsilateral insular cortices in the same latency ranges as innocuous cold stimuli. Additionally, we found an activation of the contra- and ipsilateral SII areas (peak latencies 304±22.7 and 310.1±19.4 ms, respectively) and a variable activation of the cingulate cortex. Notably, neither cold- nor painful cold stimulation produced an activation of SI. By contrast, the evoked cortical responses following tactile stimulation could be located to the contralateral SI cortex and bilateral SII.
In conclusion, this study strongly corroborates the posterior insular cortex as the primary somatosensory area for cortical processing of cold sensation. Furthermore, it supports the role of SII and the cingulate cortex in mediating freeze-pain. Therefore, these results suggest different processing of cold, freeze-pain and touch in the human brain. 相似文献
The effects of repeated local exposure to cold on the integrity of the subcutaneous microcirculation were studied in a model
using a transparent tissue chamber implanted into a dorsal skin fold of Syrian hamsters. A detailed study of the vascular
ultrastructure within the chamber revealed the following features: Endothelial damage was prominent in true capillaries and
venous vessels, while arterioles remained unaffected. The endothelial lining appeared extremely attenuated around the entire
vascular perimeter causing the development of “gaps”, some of which contained leukocytes or platelets. Smaller vessels were
often completely filled with blood cells with leukocytes integrated into the endothelial wall. Fibrin was never observed within
these occluded vessels. Finally, only veil-like remnants of the endothelium persisted, and compressed erythrocytes were still
mimicking the original vascular outline. It is concluded that the ultrastructural changes observed after a repeated non-freezing
cold injury closely resemble those observed during ischemia/reperfusion injury. 相似文献