Reactive hyperemia

NO was indeed being detected in the subjects. The same group used a similar experimental design to monitor NO concentration, as well as SkBF, during reactive hyperemia under the human skin [126],... 

J.L. Zhao, P.E. Pergola, L.J. Roman, and D.L. Kellogg, Bioactive nitric oxide concentration does not increase during reactive hyperemia in human skin. J. Appl. Physiol. 96, 628-632 (2004). 

Vasoconstriction induced by an a-sympathomimetic is followed by a phase of enhanced blood flow (reactive hyperemia, A). This reaction can be observed after the application of a-sympa-thomimetics (naphazoline, tetrahydro-zoline, xylometazoline) to the nasal mucosa. Initially, vasoconstriction reduces mucosal blood flow and, hence, capillary pressure. Fluid exuded into the interstitial space is drained through the veins, thus shrinking the nasal mucosa. 

Due to the reduced supply of fluid, secretion of nasal mucus decreases. In coryza, nasal patency is restored. However, after vasoconstriction subsides, reactive hyperemia causes renewed exudation of plasma fluid into the interstitial space, the nose is stuffy again, and the patient feels a need to reapply decongestant. In this way, a vicious cycle threatens. Besides rebound congestion, persistent use of a decongestant entails the risk of atrophic damage caused by prolonged hypoxia of the nasal mucosa. 

A. Reactive hyperemia due to a-sympathomimetice, e.g., foiiowing decongestion of nasai mucosa... 

B. Authier, Reactive hyperemia monitored on rat muscle using perfluorocarbons and F-19 NMR, Magn. Reson. Med. 8 (1988) 80-83. 

Juhran W, Voss EM, Dietmann K, et al. Pharmacological effects on coronary reactive hyperemia in conscious dogs. Naunyn-Schmiedebergs Arch Exp Pathol Pharmakol 1971 269 32-47. 

Curnish RR, Berne RM, Rubio R. Effect of aminophylline on myocardial reactive hyperemia. Proc Soc Exp Biol Med 1972 141 593-598. 

In most cases of the thoracolumbar infarction, the swollen cord shows peripheral enhancement of the central gray matter. The concomitant enhancement of the cauda equina was reported first by Friedman and Flanders in 1992 (Fig. 17.8). This phenomenon is a characteristic finding in the course of spinal cord ischemia which might involve the cord itself and the ventral cauda equina as well, which is composed of motor fibre bundles (Amano et al. 1998). It indicates disruption of the blood-cord barrier as well as reactive hyperemia (Friedman and Flanders 1992 Amano et al. 1998). The differential diagnosis of contrast enhancement of the cauda equina includes transverse myelitis, bacterial or viral meningitis, and spinal metastasis. 

Damage of the vessel wall is produced by placing a hemostatic clamp on the coronary artery a fixed amount of stenosis is produced by an externally applied obstructive plastic cylinder upon the damaged part of the vessel. In dogs, the stenosis is critical, i.e. the reactive hyperemic response to a 10-second occlusion is abolished (protocol 1) in pigs, the stenosis is sub-critical, i.e. there is a partial reactive hyperemia left (Just et al. 1991a protocol 2). 

R. Kragelj, T. Jarm, and D. Miklavcic, Reproducibility of Parameters of Postocclusive Reactive Hyperemia Measured by Near-Infrared Spectroscopy and Transcutaneous Oximetry, Ann. Biomed. Eng., 28(2), 168-173 (2000). 

Coronary blood flow is closely tied to oxygen needs of the heart. Changes in oxygen balance lead to very rapid changes in coronary blood flow. Although a number of mediators may contribute to these changes, the most important ones are likely to be adenosine, other nucleotides, nitric oxide, prostaglandins, CO2, and H. Adenosine, which is formed from adenosine triphosphate (ATP) and adenosine monophosphate (AMP) under conditions of ischemia and stress, is a potent vasodilator that links decreased perfusion to metabolically induced vasodilation, or reactive hyperemia. The synthesis and release of adenosine into coronary sinus venous effluent occur within seconds of coronary artery occlusion, and about 30% of the hyperemic response can be blocked by metabolic blockers of adenosine. " ... 

Most patients with systemic sclerosis have Raynaud s phenomenon, where the digits tarn white, followed by a bluish color, which is then followed by reddening in response to an appropriate stimulus. Usually the precipitating event is cold temperatare or emotion. The pallor is due to vasospasm, the bluish color is from ischemia, and the reddish color is caused by a reactive hyperemia. Raynaud s phenomenon is a common manifestation of other syndromes, and most patients with Raynaud s phenomenon do not have systemic sclerosis. Approximately 50% to 80% of patients with systemic sclerosis have gastrointestinal symptoms, and 75% to 90% of patients have esophageal dysmotility. 

Reactive hyperemia is the increased blood flow over normal values that is seen following a period of interruption of flow. Reactive hyperemia is attenuated by glibenclamide in both coronary and skeletal muscle vascular beds, suggesting a role of K xp channels in this phenomenon (Clayton et al., 1992). Activation of K xp channels under these conditions may occur through a buildup of vasodilator metabolites (e.g., adenosine) during the period of occlusion. 

A. Berdeaux, Effects of antiaggregant and antiinflammatory doses of aspirin on coronary hemodynamics and myocardial reactive hyperemia in conscious dogs, J. Cardiovasc. Pharmacol. 1999, 33, 264-272. 

In the subacute phase, arterial vascular enhancement peaks at 1-3 days. Large infarcts will also demonstrate meningeal enhancement that may represent reactive hyperemia, which peaks at 2-6 days. Both arterial and meningeal enhancement typically resolve by 1 week [11]. Parenchymal enhancement also occurs during this phase gray matter enhancement can appear band-like or gyriform (Fig. 6.5). This is secondary to disruption of the BBB and restored tissue perfusion from a recanalized occlusion or collateral flow. 

Ruano, J., Lopez-Miranda, J., Puentes, F., Moreno, J.A., Bellido, C., Perez-Martinez, P, Lozano, A., Gomez, R, Jimenez, Y., and Perez Jimenez, F., Phenolic content of virgin olive oil improves ischemic reactive hyperemia in hypercholesterolemic patients, J. Am. Coll. Cardiol., 46, 1864-1868, 2005. 

Hyperthermia is a new treatment that is currently being evaluated in phase II and III studies in combination with radiotherapy or chemotherapy for treating locally advanced cervical cancer [106,107]. Hyperthermia exerts a direct cytotoxic effect by heating the tumor tissue but primarily aims at improving the tumor s response to radiotherapy or chemotherapy through reactive hyperemia. It is performed as deep regional hyperthermia by means of electromagnetic radiation with simultaneous control of temperature in special MRI scanners. 

The symptoms usually disappear when the hand and arm or, preferably, the whole body is warmed. The vasospasm is succeeded by a short period of reddened skin, evidence of reactive hyperemia elicited by the net vasodilatory action of metabolites and other substances that have accumulated in the vasculature during the attack. Case reports of other skin color changes have been published from time to time, but their relationship to vibration exposure is most often unsubstantiated. 

Several epidemiological studies have linked a protective effect against cardiovascular diseases and regular consumption of either red wine [7, 8, 98] or polyphenol-rich sources such as green tea [14,15,99], cocoa, or chocolate [16,17]. Since many cardiovascular diseases are associated with an impaired endothelial function, the evaluation of the endothelial function is of great importance. In humans, the endothelial function is often assessed by the flow-mediated dilatation (FMD). For this purpose, reactive hyperemia is induced after a transient ischemia in the upper arm using an inflatable cuff like that used for the measurement of blood pressure, while the diameter of the brachial artery is monitored continuously at the elbow level by ultrasound. The cuff is inflated tmtil the occlusion of the brachial artery, which is maintained for 5 min before the blood flow is released. The reperfusion then induces an endothelium-dependent dilatation of the brachial artery due to the increased shear stress, the most important physiological activator of eNOS. Impaired endothelial function, assessed by FMD, has been reported as an independent predictor of cardiovascular outcome in subjects with cardiovascular risk factors or established cardiovascular diseases [18]. 

Another observation that militates against a direct effect of PO2 on vascular smooth muscle is that within 1-2 s, after the onset of reactive hyperemia, the coronary venous blood becomes bright red (high POj). If POj directly affected coronary resistance one would expect a prompt return of CBF to control levels after release of a brief (10-60s) eoronary occlusion. Hence, it is evident that the decrease in coronary vascular resistance observed with hypoxemia is probably secondary to the release of a vasodilator substance triggered by an inadequate oxygen supply to the myocardium. 

Case RB, Felix A, Wachter M, Kyriakidis G, Castellana F (1978) Relative effect of CO2 on canine coronary vascular resistance. Circ Res 42 410-418 Dawes GS (1941) The vaso-dilator action of potassium. J Physiol London 99 224-238 Degenring FH, Curnish RR, Rubio R, Berne RM (1976 Effect of dipyridamole on myocardial adenosine metabolism and coronary flow in hypoxia and reactive hyperemia in the isolated perfused guinea pig heart. J Molec Cell Cardiol 8 877-888 Driscol TE, Berne RM (1957) Role of potassium in regulation of coronary blood flow. Proc Soc Exptl Biol Med 96 505-508... 

Rubio R, Berne RM, Katori M (1969) Release of adenosine in reactive hyperemia of the dog heart. Am J Physiol 216 56-62... 

Scott JB, Radawski D (1971) Role of hyperosmolarity in the genesis of active and reactive hyperemia. Circ Res 28 and 29 (Suppl. I) 26-32... 

The nonapeptide, bradykinin, has been reported to induce pulmonary vasodilatation in the foetal lamb. It was suggested that bradykinin might be responsible for the reactive hyperemia which ensues after ischemia in unventilated foetal lungs. The vasoactive polypeptide, substance P, reduced the pulmonary arterial pressure of anesthetized dogs, as measured by pulmonary artery catheterization S. The effect was transient in nature and thought to be the result of direct action on the pulmonary vasculature. 

Skeletal muscle perfusion in mouse leg was determined quantitatively, dynamically and noninvasively by NMR arterial spin-labeled(ASL) imaging. It was shown that despite the small size of the animal, mouse muscle perfusion may be measured, at rest and in conditions of reactive hyperemia, using saturation inversion recovery sequence, a pulsed ASL variant combined with NMR imaging. 

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