Alterations In Local Blood Flow Research Articles

Individual variations in platelet reactivity towards ADP, epinephrine, collagen and nitric oxide, and the association to arterial function in young, healthy adults

IntroductionPlatelet aggregation and secretion can be induced by a large number of endogenous activators, such as collagen, adenosine diphosphate (ADP) and epinephrine. Conversely, the blood vessel endothelium constitutively release platelet inhibitors including nitric oxide (NO) and prostacyclin. NO and prostacyclin are also well-known vasodilators and contribute to alterations in local blood flow and systemic blood pressure. Materials and methodsIn this study we investigated individual variations in platelet reactivity and arterial functions including blood pressure and flow-mediated vasodilation (FMD) in 43 young, healthy individuals participating in the Lifestyle, Biomarkers and Atherosclerosis (LBA) study. Platelet aggregation and dense granule secretion were measured simultaneously by light transmission and luminescence. FMD was measured with ultrasound. ResultsThe platelet function assay showed inter-individual differences in platelet reactivity. Specifically, a sub-group of individuals had platelets with an increased response to low concentrations of ADP and epinephrine, but not collagen. When the NO-donor S-nitroso-N-acetyl-DL-penicillamine (SNAP) was combined with high doses of these platelet activators, the results indicated for sub-groups of NO-sensitive and NO-insensitive platelets. The individuals with NO-sensitive platelets in response to SNAP in combination with collagen had a higher capacity of FMD of the arteria brachialis. ConclusionsPlatelet reactivity towards ADP, epinephrine and NO differs between young, healthy individuals. Some individuals have a more effective response towards NO, both in the aspect of platelet inhibition ex vivo, as well as vasodilation in vivo.

Flap Perfusion after Free Musculocutaneous Tissue Transfer: The Impact of Postoperative Complications

In a previous study, the authors found persistence of pedicle blood flow up to 10 years after uncomplicated free latissimus dorsi transfer. In this study, the impact of postoperative complications (hematoma, thrombosis, infection) and successful surgical revision was tested. Since 1982, more than 1200 free tissue transfers have been performed at the authors' institution (Hannover Medical School). Of these, the authors selected two groups of 30 patients each who had received a free latissimus dorsi transfer to the lower leg without microsurgical nerve coaptation for wound coverage. All patients included in this study were carefully selected for clinical homogeneity, with one difference: group I comprised patients who had no postoperative complications after free latissimus dorsi transfer. Group II included only patients with major postoperative complications after the procedure. All flaps in group II survived after successful surgical revision. The arteries, which nourished the lower leg, were visualized and documented by means of a duplex scanner in both groups. Three different time intervals were chosen for measurements of blood flow: 4 to 6 months (groups I.I and II.I), 4 to 6 years (groups I.II and II.II), and 8 to 10 years (groups I.III and II.III). Quantitative measurements of local flap perfusion in milliliters per minute per 100 g tissue were performed by means of the hydrogen clearance technique. In each patient, a total of nine measurements was performed in three phases: phase A, before closing the vascular pedicle by manual compression (n = 3); phase B, with a closed pedicle (n = 3); and phase C, after releasing the vascular pedicle from manual compression (n = 3). Each measurement took approximately 10 minutes. One hundred percent closure of each pedicle in phase B was confirmed by the duplex scanner. Furthermore, all patients were monitored both clinically and by means of the hydrogen clearance technique during phase B for adequate blood supply to the lower leg. Lower leg perfusion showed no statistical differences for phases A, B, and C in all groups of patients. In group I, no statistical differences in local flap perfusion were encountered for phases A and C. In phase B, however, a statistically significant (p < 0.01) complete extinction of local flap perfusion was registered in all patients of group I at the site of the flap's skin paddle. In group II, however, persistent flap perfusion was registered during phase B in up to 50 percent of cases in one subgroup (II.III). No statistically significant alterations of local blood flow were registered in the surrounding tissue of group II during phases A, B, and C. Patients with thrombosis of the venous anastomosis (n = 7) seemed to have the highest incidence of loss of autonomous blood supply through the vascular pedicle (5 out of 11 cases). No inconstant results were found during the repetitive measurements (n = 3) for each patient in each phase. After uncomplicated free tissue transfer, the flap's intact vascular pedicle seems to play an important role in permanent flap survival up to 10 years after the procedure. Postoperative complications after free tissue transfer with successful surgical revision, especially venous thrombosis of the vascular anastomosis, may lead to loss of vascular flap autonomy over time.

Microcirculatory hemodynamics in oral tissues with reference to neurogenic response and reactive oxygen species interaction

The primary purpose of the microcirculation is to transport nutrients and oxygen and to remove metabolic waste products from tissues. It is also well known that the fundamental mechanism for vascular control is the local regulation of the basal vascular tone, which is reinforced by blood pressure and counteracted by tissue metabolites. Thus, the well-being of the tissue depends on the circulatory transport process, which is governed by many functional parameters of the microcirculation such as blood flow, blood volume, intravascular and extravascular pressures, and capillary permeability. Inflammatory reactions in oral tissues can be initiated by many different insults to the tissues, and the reaction itself can be expressed in various ways. In addition, the tissues seem to have many "backup" systems, so that any one response can be produced in several ways, which is important for a reaction that has a survival value. A recent concept is that repeated stimulation of sensitive teeth may induce pulpal changes; this could occur through induction of neurogenic inflammation and alteration of pulpal blood flow. One possibility is that production of reactive oxygen species, as well as release of the sensory neuropeptides, at sites of inflammation contributes to alterations in local blood flow. In addition to the part played by the neurogenic mediators, nitric oxide participation and its interaction with oxygen-derived free radicals in oral tissue hemodynamics are also discussed.

Endogenous vasoactive substances and oxygen-derived free radicals in pulpal haemodynamics

An adequate blood supply to the dental pulp is essential to the health of the tooth. A recent concept is that repeated stimulation of sensitive teeth may induce pulpal changes; this could occur through induction of neurogenic inflammation and alteration of pulpal blood flow. One possibility is that production of oxygen-derived free radicals at sites of inflammation contributes to alterations in local blood flow. The first target of free radicals, generated in several pathological processes, is the vascular system (essentially the endothelium). Although the exact mechanism by which free radicals induce changes in vascular conductance is still uncertain, they may act directly on vascular smooth muscle or modify vascular tone by interacting with the production and/or biological activity of endogenous vasoactive mediators. Recent data indicate that the oxygen-derived, free radical-generating system can decrease pulpal blood flow in the dog via endothelial dysfunction when applied locally in deep dentinal cavities. In addition to the part played by oxygen-derived free radicals, the measurement of pulpal blood flow and the effects of endogenous vasoactive substances on flow are discussed.

Antagonism of a specific dopaminergic receptor agonist with metoclopramide in horses

SUMMARY Changes in lateral cecal arterial blood flow, mean internal carotid arterial pressure, and heart rate caused by nasogastric administration of fenoldopam (3, 6, and 9 mg/kg of body weight), a selective agonist of dopaminergic receptors, were recorded in 7 healthy horses. Cecal arterial blood flow was significantly increased within 30 minutes after administration of fenoldopam at all 3 dosages, with the peak increases from baseline (67.8 ± 17.5 ml/min) being 125 ± 28, 120 ± 22, and 153 ± 32 ml/min for 3, 6, and 9 mg/kg, respectively. Although carotid arterial pressure did not change significantly after administration of fenoldopam at the dosage of 3 mg/kg, administration of fenoldopam at the dosages of 6 and 9 mg/kg significantly reduced carotid arterial pressure from 113 ± 10 to 88 ± 3 and 81 ± 5 mm of Hg, respectively. Intravenous infusion of metoclopramide, a dopaminergic receptor antagonist, at the rate of 0.125 mg/kg/h, blocked the effect of fenoldopam on cecal arterial blood flow and carotid arterial pressure. It was concluded that dopaminergic receptors mediate alterations in local blood flow and systemic pressure in horses.

Alterations in local blood flow and tissue-gas tension caused by epinephrine.

Subcutaneous injection of epinephrine markedly reduced local tissue pO2 levels and blood flow while increasing tissue pCO2 in a rat model. The duration and magnitude of these effects were correlated with prolonged elevation of tissue levels of epinephrine and were proportional to the amount of epinephrine injected.