PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “VASOMOTOR SYSTEM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources
PubMed1999

[Biomechanical study of the vasomotor system of the arterial smooth muscle after long-term cryopreservation of a human arterial graft at two different temperatures -80 and -150C].

We conducted two parallel studies on cryopreserved arterial homografts: a biomechanical study based on traction tests and a functional study coupled with a histology examination. Twenty-four arterial segments from 6 donors (2 iliac and 2 superficial femoral segments per donor) were cryopreserved at -150 degrees C and -80 degrees C. Cryopreservation lasted at least 6 months. Lengthening at rupture, the Young elasticity module, and rupture stress were calculated from the traction test. Results were significantly different depending on the preservation temperature. The functional properties of the cryopreserved arterial grafts were evaluated by studying the vasomotricity capacity of the vascular smooth muscle (VSM) and the endothelium. The expected results (direct contracture of VSM induced by PHE and endothelial dependent relaxation of VSM induced by ACH) were measured on fresh arteries. Cryopreserved arteries showed no response to physiological doses of PHE and ACH, whatever the preservation temperature. In one-third of the cases, a lower amplitude vasoconstriction was obtained using nonphysiological doses of PHE; there was no relaxation with ACH.

Adult↗
PubMed1998

[Role of endothelial nitric oxide in the regulation of the vasomotor system].

The arterial wall is structurally and functionally compartmentalized. Each compartment is characterized by a specific cell type and by specific interactions. The endothelial compartment interacts with circulating blood, and the adventitial compartment with the surrounding tissue. The media, which contains the effector smooth muscle cells, perceives centrifugal messages from the endothelium and centripetal messages from metabolically active tissues, from adventitial nerve endings, and from peptides produced in the interstitium. The degree of contraction or relaxation of the vascular smooth muscle cells characterizes the general vasomotor tone, which governs the local blood pressure level and distributes the flow according to metabolic needs. The main physiologic vasoactive agent is nitric oxide (NO) and is produced by the endothelium. In disease states, other agents can become predominant in centrifugal parietal messages. NO is produced by type 3 NO synthase, an enzyme that is constitutively expressed by endothelial cells. The activity of this enzyme on its substrate, arginine, is regulated by the concentration of free calcium and by intracellular phosphorylations. Several peptides, including receptors, are coupled to the phospholipase C pathway in the endothelial cell; endothelial growth factors such as FGF and VEGF, enhance the activity of endothelial NO synthase. However, the main physiologic factor responsible for endothelial NO synthase activation is the shearing stress produced by friction of the flowing blood against the immobile vessel wall. This shearing stress constantly adjusts the diameter of conductance vessels to peripheral metabolic needs. Expression of endothelial NO synthase is modulated by the chronic effects of the same agents. NO has a vasodilating effect that is mediated by the generation of cyclic GMP. Cyclic GMP and cyclic AMP are the main second messengers in smooth muscle cell relaxation. NO binds to a heme-protein, soluble guanylate cyclase, that converts GMP to cyclic GMP. Kinase-G is the main target for cyclic GMP in the smooth muscle cell. Kinase-G phosphorylates phospholambans and releases the repumping activity of calcium ATPase. More importantly, kinase-G phosphorylates the protein G that links seven-domain membrane-spanning receptors to phospholipases, thus inhibiting coupling between the ligand-receptors interaction and the intracellular signaling process that leads to contraction. NO can relax the smooth muscle cell only in the presence of a preexisting contractile tone. Conversely, absence of NO enhances the preexisting contractile tone. All these notions can be analyzed via the experimental model of L-NAME-induced chronic NO synthase blockade in rats. The decrease in parietal cyclic GMP seen in this model is associated with an increase in contractile tone that translates into systemic arterial hypertension. The increase in contractile tone can be blocked by renin-angiotensin system inhibitors. Chronic blockade of NO production rapidly induces vascular wall phenotype changes that lead to renal failure, ischemic stroke, and fibrosis of target organs. These phenotype changes may be related to the increase in the oxidative potential of the various types of parietal cells, as suggested by the abnormal presence of inflammatory cells and by the increased expression of inflammation mediators including cyclooxygenase II, inducible NO synthase, and adhesion molecules such as ICAM and VCAM. This model therefore holds promise for elucidating interactions between NO and arteriosclerosis. NO system dysfunction is also seen in other cardiovascular disorders, including congestive heart failure.

Animals↗
PubMed1992

Systemic vasomotor interaction between nicardipine and hypocapnic alkalosis in man.

The effects of hypocapnic alkalosis on the vasodilating action of nicardipine were studied in 6 patients after cerebral arterial aneurysm surgery. Each patient served as his/her own control during the 6 steps of the study. T0: baseline; T1: hypocapnic alkalosis alone (PaCO2: 3.5 kPa); T2: hypocapnic alkalosis and bolus injection of nicardipine (30 micrograms.kg-1 i.v.); T3: hypocapnic alkalosis and continuous 60 min infusion of nicardipine (0.5 microgram.kg-1.min-1), T4: determination of the infusion rate required to neutralize the effect of hypocapnic alkalosis; T5: same continuous dose of nicardipine as in T4 but reversal of hypocapnic alkalosis. Hypocapnic alkalosis alone caused a significant increase in the systemic vascular resistance index by 20% (T1). The bolus injection of nicardipine reversed this first effect (T2). The continuous infusion of nicardipine in T3 was insufficient to cancel the haemodynamic effect of hypocapnic alkalosis. During T4 the plasma levels required to neutralize completely the effect of hypocapnic alkalosis were twice those at T3. Normalization of the PaCO2 in step T5 induced a significant fall in the systemic vascular resistance index by 27.5% as compared with T0. In this study hypocapnic alkalosis modified the relationship between plasma levels of nicardipine and its expected vasoactive effects. This interaction was reversible.

Aged↗