Search

Background: Retinal vessel diameter assessment is complicated by various components among them dynamic changes due to vasomotoric effects. Measurement of these diameters was usually obtained from fundus photographs. Functional diameter changes induced by external stimuli were difficult to evaluate because of their dynamic nature. The Retinal Vessel Analyzer (RVA) allows continuous on-line measurement of those dynamic changes. Whether functional changes due to 100% O2 breathing can be assessed by RVA is investigated in this study., Materials and Methods: Continuous on-line registration of retinal arterial and venous branch vessels was obtained in 10 healthy volunteers. A baseline was taken during the first minute. Then for 5 minutes 100% O2 was delivered by mask. Further recording ensued for 4 minutes, while breathing room air. Vessel diameter change in percent to baseline was calculated for each individual and for a mean of the group., Results: Each individual demonstrated vasoconstriction. The mean diameter reduction for the group was 6.5% for arteries and 15% for veins., Conclusions: RVA allows assessment of functional retinal branch vessel reactions. Retinal branch vessels diameters are denominators for capillary perfusion. RVA might be able to demonstrate an individual vessel's regulation potential by purposeful stimulation to constrict and dilate. This property could be helpful in understanding pathophysiologic processes as well as improving diagnosis and therapeutic effects in diseases influencing ocular perfusion such as diabetes, retinal vessel occlusion or even glaucoma. Further evaluation of effects of systemic diseases might be an additional application of functional retinal vessel diameter assessment by RVA.

By measuring pulse rate (PR), blood pressure (BP), electrical integral skin resistance (SR), and skin surface temperature in different areas, the activity of the sympathetic nerves in spinal anaesthetics of different levels was evaluated. It was found that the sympathetic subsystems for vasomotor and sudomotor activity have their own innervation and that the functionally different effectors also manifest different deficiency reactions in low- and medium-level spinal anaesthesia. Functional sympathetic innervation, however, is unimportant after high sensory spread of spinal anaesthesia. The sympathetic nerves show similar signs of deficiency during administration of centrally acting general anaesthetics. In contrast to these, however, high spinal anaesthesia does not block the vagal component of the autonomic nervous system. The unopposed parasympathetic nerves directly affect the heart and other effectors, which may result in life-threatening cardiovascular reactions with decreases in BP and bradycardia. If high sympathetic blockade is recognized early, such life-threatening situations can be managed successfully. Suitable means of measuring sympathetic activity are the observation of BP, HR, temperature, and particularly SR at the hand. Sympathetic nerve blockade due to spinal anaesthesia first causes a reduction of SR in the lower extremity. In high spinal anaesthesia there is also a loss of sympathetic activity at the hands. Subsequently, hand temperature increases, and finally bradycardia and hypotension occur. The functional reaction of sympathetic activity is indicated by correlation of the vasomotor and sudomotor activities in high and low spinal anaesthesia. Failure of sudomotor activity can be observed on average at least 3 min prior to an increase in acral temperature and 9 min at the hands in cases of high spinal anaesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

The beneficial cardiovascular effects of ACE inhibitors are thought to be based primarily on a reduction in vascular angiotensin II formation. However, since ACE also degrades the potent endothelium-dependent vasodilator bradykinin, it has been proposed that the local accumulation of this peptide in the vascular wall represents an additional mechanism by which ACE inhibitors exert their cardiovascular effects. In this context it has been demonstrated that incubation of cultured endothelial cells with ACE inhibitors leads to an enhanced formation of nitric oxide (NO) and prostacyclin (PGI2). This effect is believed to be the consequence of an accumulation of endothelium-derived bradykinin in the vicinity of the endothelial cells. Moreover, by virtue of an as yet unidentified mechanism, ACE inhibitors may also enhance the potency of bradykinin at the receptor level and/or activate the B2-kinin receptor following pre-exposure to bradykinin. Both of these effects may enhance or sustain the bradykinin-induced formation of NO and PGI2 by the endothelium. ACE inhibition also leads to the accumulation of angiotensin I which can be metabolized to angiotensin-(1-7) by another endothelial enzyme, the neutral endopeptidase 24.11. Activating an as yet unidentified receptor, angiotensin-(1-7) (but not other known angiotensin peptides) stimulates endothelial NO release in coronary arteries from different species as well as in the isolated perfused rat heart. This effect also seems to involve the release of vasoactive kinins from the endothelium. The shift in angiotensin I metabolism towards an enhanced formation of angiotensin-(1-7) in the presence of an ACE inhibitor may thus also contribute to the hypotensive action of this class of compounds.

Synonyms like "paralysie á frigore" and "rheumatic palsy" imply a dysfunction of the vasa nervorum during coldness application. Cooling the nerve, however, only reduces perfusion by 18%. Cooling of the facial nerve with pure ice to 0 degrees C leads to a functional loss due to a blockade of the temperature-controlled Na-K-channels. The vasomotor regulation of the nerve vessels under these conditions seems to be relatively unimportant.

In anesthetized cats massive doses of methylprednisolon (40 mg/kg body wt.) induce a blood pressure decrease with bradycardia, which is not transmitted through vagal efferents. These effects are due to an inhibition of sympathetic outflow to heart and vessels.