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At least 19 recordsLinked to original sources

PubMed1977

Reactive hyperemia in capillaries of red and white skeletal muscle.

Reactive hyperemia was examined in individual capillaries of the red anterior (ALD) and white posterior (PLD) latissimus dorsi muscles of the anesthetized chicken following total blood flow occlusion of 3.5-180 s in length. Capillary red cell velocities were measured by the dual-slit photometric technique. The control capillary velocities in the ALD and PLD were 0.56 +/- .03 (SE) and 0.34 +/- .03 mm/s, respectively. With increasing occlusion lengths, the reactive hyperemia peak velocity, hyperemia duration, and excess flow were found to increase progressively in both muscles suggesting a metabolic origin for the response. The ALD showed a greater peak reactive hyperemia flow than the PLD following occlusion lengths of 7-60 s and a greater excess flow following occlusion lengths of 15 s and longer. However, when these data were normalized to control velocities by calculating the peak-to-control velocity ratio and percent flow debt repayment, no significant differences were found between the two muscles. Furthermore, the reactive hyperemia durations were similar in the two muscles at each occlusion length. These data demonstrate that reactive hyperemia is similar in two muscle types which are known to differ considerably in resting metabolism and anaerobic capacity.

Animals↗

PubMed1978

Reactive hyperemia vs treadmill exercise testing in arterial disease.

We compared the ankle pressure response during reactive hyperemia to the response to treadmill exercise in 28 limbs of 14 normal individuals and 26 legs of 15 patients with arterial occlusive disease. The mean percent maximum drop in ankle blood pressure during reactive hyperemia in normal limbs, 17% +/- 11% (+/- 1 SD) was significantly less than that of legs with arterial disease, 54% +/- 15% (P less than .001). Abnormal values were recorded in all but three diseased limbs. There was good correlation between the ankle pressure responses to reactive hyperemia and treadmill exercise (r = 0.71, P less than .001). This study suggests that measurement of ankle pressure during reactive hyperemia may be a useful substitute for treadmill testing to determine the functional capacity of the circulation during stress in patients with arterial occlusive disease. Reactive hyperemia testing requires less time and equipment and may be performed in patients who might be at risk or unable to carry out treadmill exercise.

Adult↗

PubMed1978

Adenosine metabolism in canine myocardial reactive hyperemia.

In pentobrabital-anesthetized open chest dogs, myocardial adenosine content is elevated by 5 or 15 seconds of left coronary artery occlusion and falls exponentially to control levels during reactive hyperemia. The rate constants for adenosine dissipation are (mean +/- SEM): -0.08 +/- 0.01 and -0.034 +/- 0.007 sec-1 after 5- and 15-second occlusion, respectively. Kinetic analysis of the reactive hyperemia flow curves (Circ Res 14/15 (suppl I): 81-85, 1963) predicts rates of -0.069 +/- 0.009 sec-1 and -0.04 +/- 0.009 sec-1, indicating that changes in adenosine levels can account for the way coronary flow changes during this response. The log (dose-) response curve relating reactive hyperemia flow to tissue adenosine concentration has a steeper slope and is half-maximal at a lower adenosine concentration than the dose-response curve obtained by intracoronary infusions of adenosine in oxygenated hearts, indicating that the coronary vasoactivity of adenosine is enhanced during reactive hyperemia. This could explain why theophylline antagonizes the coronary vasocilatory effect of adenosine in oxygenated hearts but has relatively little effect on reactive hyperemia.

Adenosine↗

PubMed1979

Comparison between reactive and exercise hyperemia in normal subjects and patients with peripheral arterial disease.

Reactive and exercise hyperemia were compared in healthy men and in patients with PAD. In both patients and normals the calf blood flow of reactive hyperemia was recorded after a 5-minute ischemia. Exercise hyperemia was measured in normals after variable work loads (30 and 50 kg) and immediately after the occurrence of pain in patients with PAD. In healthy limbs the first and peak flows of exercise and reactive hyperemia are similar. The recovery time for basal flow is prolonged after exercise. However, reactive and exercise hyperemia differ significantly when arterial obstruction due to arteriosclerosis obliterans is present. First flow and peak flow are higher and recovery time more prolonged after exercise. It is also likely that the control mechanisms of the two hyperemic reactions are different. Muscular exercise, when protracted until pain occurs, can produce a metabolic and circulatory adjustment other than that of ischemia. There is experimental evidence to support this hypothesis.

Arterial Occlusive Diseases↗

PubMed1979

Cigarette smoking, prostaglandins and reactive hyperemia.

The hypothesis was investigated that cigarette smoking obstructs the blood flow response that develops as a protection against tissue damage in an organ subjected to ischemia (reactive hyperemia). Forearm blood flow was recorded at rest and following forearm ischemia before and after cigarette smoking in healthy male and female volunteers. The experiments were also repeated after pre-treatment of the subjects with indomethacin, a prostaglandin synthesis inhibitor. Before pre-treatment with indomethacin, ischemia induced a reactive hyperemia amounting to 20 +/- 4 ml/100 ml tissue. This hyperemia was significantly (p less than 0.01) reduced by cigarette smoking, to 12 +/- 3 ml/100 ml tissue. After indomethacin, which in itself lowered the reactive hyperemia to 8 +/- 2 ml/100 ml tissue, smoking did not elicit any effect. It is suggested that smoking counteracts reactive hyperemia in tissues by interfering with the same physiological mechanism as indomethacin, i.e. with the vascular formation of PG. The possible significance of this observation in relation to cigarette smoking and ischemic heart disease is stressed.

Adult↗

PubMed1978

Poststress Doppler ankle pressures: a comparison of treadmill exercise with two other methods of induced hyperemia.

Postocclusion reactive hyperemia and isolated leg exercise were evaluated as techniques for functional evaluation of lower extremity arterial insufficiency by comparing them with treadmill exercise. Sixty patients with claudication and six normal subjects were evaluated. Changes in Doppler ankle pressures were measured after each form of stress. With substantial occlusive disease, there is a drop in pressure with gradual recovery. Postocclusion reactive hyperemia and isolated leg exercise are abnormal if the pressure does not return to resting levels within two minutes. There was good correlation between the three methods. Postocclusion reactive hyperemia avoids the problems of patient cooperation inherent in the other two methods. Postocclusion reactive hyperemia should probably replace treadmill exercise as the first method of stress testing lower extremities.

Aged↗

PubMed1976

Regional myocardial blood flow during hyperemia induced by contrast agent in patients with coronary artery disease.

Regional myocardial specific blood flow (regional specific flow) was measured at rest and during contrast hyperemia after the intracoronary injection of xenon-133. The changes in regional specific flow were transient, resulting in some compromise in one of the underlying restraints of the inert gas washout method, namely, the presence of a steady state. Therefore, to determine the clinical utility of this technique, regional specific flow values obtained with this method were correlated with the presence and severity of coronary artery disease as assessed from the coronary arteriogram and left ventriculogram. Regional specific flow during contrast hyperemia was 186+/- 11 (mean +/- 1 standard error of the mean) ml/min per 100 g in control patients and 115+/-5 in patients with coronary artery disease. There was an inverse relation between regional specific flow during contrast hyperemia and the percent coronary stenosis when the stenosis was 40 percent or greater (r = 0.70, P less than 0.001). Regional specific flow was significantly less in patients with asynergy (77 +/- 10 ml/min per 100 g) than in patients with normal ventricular function (105 +/- 5) distal to coronary stenoses of greater than 75 percent. Thus regional specific flow measured during contrast hyperemia using the xenon washout technique and the Anger camera differentiated patients with normal coronary arteriograms from those with coronary artery disease. With this technique, good correlation was shown between regional specific flow and the percent coronary stenosis and presence of ventricular wall abnormalities. The information obtained with this method may provide prognostic information concerning suitability for surgical intervention.

Angiocardiography↗

PubMed1978

Decreased reactive hyperemia after coronary perfusion with nonoxygenated solution.

To gain more knowledge about the factors involved in reactive hyperemia in the coronary vessels, we performed comparative studies on the reactive hyperemia occurring after coronary occlusion and after coronary perfusion with nonoxygenated Tyrode solution. The peak coronary reactive hyperemic flow following 3 min of coronary perfusion with nonoxygenated Tyrode solution increased to only 142 +/- 16% of the control in contrast to 455 +/- 75% following 3 min of coronary occlusion alone. Myocardial oxygen uptake during reactive hyperemia was also much smaller after perfusion with Tyrode solution. First, the evidence suggests that the decreased reactive hyperemia after coronary perfusion with the nonoxygenated Tyrode solution is due to "washout" of the vasodilatory metabolites from the myocardium. Second, it suggests that there is a smaller "energy debt" during perfusion with Tyrode solution, so that deterioration of myocardial function due to oxygen deficiency is less severe than in coronary occlusion alone.

Animals↗

PubMed1977

Failure to abolish reactive hyperemia by indomethacin in denervated kidneys of rabbits.

The effect of indomethacin (10 mg/kg) on the distribution of cortical blood flow during postocclusive reactive hyperemia was evaluated in denervated kidneys of anesthetized rabbits by the radioactive microsphere technique. Renal denervation caused a slight but not significant increase in renal blood flow with no remarkable alteration in the distribution of cortical blood flow. After release of 1-min occlusion of the renal artery, hyperemic responses developed with a fractional flow redistribution toward the inner cortex. The absolute perfusion rate increased in the inner cortex but did not significantly change in the outer cortex. Indomethacin produced a decrease in renal blood flow despite elevated blood pressure. Even in the indomethacin-treated animals, postocclusive reactive hyperemia appeared concomitantly with the fractional flow redistribution to the inner cortex. The percentage repayment by reactive hyperemia of ischemia during the artery clamping was not significantly different before and after indomethacin administration. The findings indicate that indomethacin did not significantly affect the postocclusive vascular response in denervated kidneys of rabbits, thereby giving evidence against the role of prostaglandins as mediators of reactive hyperemia.

Animals↗

PubMed1976

Reduction of myocardial reactive hyperemia during oxygen breathing in dogs.

In 7 open-chest anesthetized mongrel dogs the left anterior descending coronary artery was occluded for 20 sec. Myocardial reactive hyperemia was recorded during air and oxygen breathings. The excess blood flow during the reactive hyperemia was smaller and the duration of the reactive hyperemia was shorter during oxygen breathing than during air breathing. It is suggested that the reduction of oxygen demand during oxygen breathing is a possible reason for the decreased reactive hyperemia and oxygen administration is beneficial in relieving myocardial ischemia.

Animals↗

PubMed1975

Role of vasoactive substances in active hyperemia in skeletal muscle (38520).

A prolonged, 2-hr period of exercise hyperemia in the canine gracilis muscle was associated with initial increases in the arteriovenous differences for potassium, hydrogen and osmolality. However, that for hydrogen decreased and those for potassium and osmolality became negligible by the 120th min while blood flow remained elevated. Thus, potassium and osmolality do not appear to participate importantly in the maintenance of exercise hyperemia in canine gracilis muscle. A bioassay muscle did not respond with comparable dilation when submaximal, graded levels of exercise hyperemia were induced in an upstream, donor muscle but did respond more comparably in terms of magnitude and time course when the exercise was more severe. Thus, stable vasoactive substances may not entirely account for exercise hyperemia and the study fails to provide evidence that the capillary acts as a significant barrier to the vasoactive substances.

Animals↗

PubMed1979

A study on the role of endogenous prostaglandins in the development of exercise-induced and post-occlusive hyperemia in human limbs.

The contribution of endogenous PGs to the development of functional (exercise-induced) and reactive (post-occlusive) hyperemia was investigated in healthy volunteers. Leg blood flow during dynamic leg exercise was estimated by an indicator dilution technique. Forearm blood flow during supine leg exercise and forearm and calf blood flow following 5 min of arterial occlusion were measured plethysmographically. All subjects were examined before and after pretreatment with indomethacin, a PG synthesis inhibitor. During leg exercise, and in the absence of indomethacin, a 10-fold rise in leg blood flow was observed. Forearm blood flow increased moderately. Both these blood flow effects of exercise were unaffected by indomethacin. Following arterial occlusion a marked hyperemia developed in the forearm and the calf. Indomethacin significantly reduced the magnitude of the reactive hyperemia both in the forearm and in the calf, decreasing both the peak value and the duration of the vasodilation. These data reveal differences between the mechanisms behind functional and reactive hyperemia in man, suggesting an appreciable contribution of endogenous PGs to post-occlusive vasodilation only.

Adult↗

PubMed1977

Dependence of reactive hyperemia in skeletal muscle on oxygen tension.

Red blood cell velocity was measured in capillaries of the rabbit tenuissimus muscle during exposure to a low-oxygen-tension (PO2 = 5 mmHg) and a high-oxygen-tension (room-air PO2 = 150 mmHg) suffusion solution. Control capillary red blood cell velocity was significantly reduced (44%) by elevating the suffusion solution PO2 from 5 to 150 mmHg. The reactive hyperemias that occurred after a 120-s aortic occlusion under these two conditions were compared. The mean RBC velocity during the hyperemia in the 1st min following the removal of occlusion was significantly reduced by increasing oxygen tension, as was the duration of the hyperemia. Peak capillary red blood cell velocities in the hyperemic phase during exposures to low and high PO2 were not significantly different. It can be concluded from this study that although oxygen tension does affect postocclusive reactive hyperemia, other factors such as myogenically induced vascular relaxation also contribute to the production of this phenomenon.

Animals↗

PubMed1979

Regional myocardial shortening in relation to graft-reactive hyperemia and flow after coronary bypass surgery.

Extent of regional shortening of myocardium in areas newly perfused by bypass grafting was determined in 56 patients by a new technique employing four to six radiopaque markers sutured in pairs to the epicardium near the coronary anastomosis. Paradoxical systolic expansion (PSE) was manifest in 16 regions (a 12% incidence) during the follow-up period, and six of these showed spontaneous remission. All cases of PSE were in the region of the left anterior descending artery. Correlation between graft flow measured during operation and regional shortening during the postoperative period revealed that the development of PSE could not be predicted from the hemodynamic measurements. In the majority of cases postoperative myocardial infarction could also be excluded as an explanation. At 1 year after operation most grafts were patent in PSE regions but collaterals, apparent preoperatively, could not be visualized. Excluding PSE, shortening fraction (ratio of shortening to maximum marker separation) for all graft regions at 1 week was 9.8%; 1 month, 12.8%; 3 months, 13.3%; and six months, 13.9%. Average graft flow was 56 ml. per minute and average reactive hyperemia was 25% with 37% of grafts showing no response. For those regions that did not develop PSE there was a positive correlation between shortening fraction and flow that became significant (null hypothesis: r = 0) when reactive hyperemia exceeded 20%. Correlation was greatest at 1 week and 1 month, but became nonsignificant at 6 months. These results are consistent with a simple interpretation of reactive hyperemia: Graft-reactive hyperemia is related to the dependence of viable tissue on the functioning of the graft.

Adult↗

PubMed1979

[Behavior of post-ischemic reactive hyperemia in increasing periods of circulatory arrest in healthy subjects and in patients with peripheral obliterating arteriopathy].

Reactive hyperemia was studied by plethysmographic measurement of the blood flow in the calf in normal subjects and in patients with peripheral arterial disease following circulatory arrest for periods ranging between 1 and 20 minutes. The duration of occlusion is an important factor in determining the behaviour of reactive hyperemia. Peak flow increases significantly when there is up to 10 minutes of circulatory arrest. Following release of an occlusion of 15 or 20 minutes, the further rise of peak flow is very moderate. The duration of subsequent hyperemia is greater in patients than in normal subjects, when the length of the occlusion is of 1 to 10 minutes. When circulatory arrest is prolonged for more than 10 minutes, the recovery time of basal flow is significantly greater in normal subjects. Several mechanisms are involved in reactive hyperemia; their relative importance may vary with the duration of occlusion. Circulatory arrest of 3--5 minutes is a useful clinical test to screen patients with arterial occlusive disease. It is not the best for a full evaluation of the blood flow in the lower limbs either in normal subjects or in partients.

Adult↗

PubMed1978

Constituents of chyme responsible for postprandial intestinal hyperemia.

While local venous outflow was measured in anesthetized dogs, various constituents of intestinal chyme were placed in the jejunal lumen to identify those responsible for postprandial intestinal hyperemia. Digested food and its supernatant increased local blood flow, whereas its precipitate, undigested food, and pancreatic enzymes did not. In the jejunum bile alone had no effect, but it markedly enhanced the hyperemic effect of digested food. Bile in the ileal lumen, however, increased local blood flow. At physiological postprandial concentrations in the jejunum, glucose, and micellar solutions of oleic acid and monoolein increased flow, but taurocholate and 16 common dietary amino acids did not. The hyperemic effect of lipids required the presence of taurocholate. Of the 16 amino acids, only Glu and Asp increased flow at 10 times the physiological concentrations (28 and 20 mM, respectively). The study indicates that the constituents of chyme responsible for postprandial intestinal hyperemia are the hydrolytic products of food, especially those of carbohydrates and fats and that bile plays an important role in the hyperemia.

Amino Acids↗

PubMed1978

Pyrogenic renal hyperemia: the role of prostaglandins.

The intravenous administration of triple typhoid vaccine to anesthetized dogs resulted in a significant increase in renal blood flow accompanied by a modest decline in systemic blood pressure. This renal hyperemia was associated with elevated renal secretory rates of renin and prostaglandin E and F. Measurements of the intracortical distribution of radiolabeled microspheres revealed a progressive decrease in outer cortical blood flow rates and a progressive increase in inner cortical flow rates. When meclofenamate, an inhibitor of prostaglandin synthetase, was administered concomitantly with triple typhoid vaccine renal hyperemia did not develop. The renal renin secretory rate increased modestly and intracortical renal blood flow was not redistributed. The increased renal blood flow after triple typhoid vaccine administration to unanesthetized dogs was also reversed by meclofenamate. The marked increase in prostaglandin secretion by the kidney during renal hyperemia following triple typhoid vaccine administration (pyrogen), and the effect of meclofenamate, is consonant with a role for increased renal synthesis and release of prostaglandins.

Animals↗

PubMed1978

The effects of short-term venous congestion on forearm venous volume and reactive hyperemia blood flow in human subjects.

Congestive heart failure is associated with a reduction in limb venous volume at an effective venous pressure of 30 mm Hg (VV[30]). Further, an attenuated arteriolar dilation in response to a metabolic stimulus has been demonstrated. It was the purpose of this study to determine to what extent the chronic elevation in venous pressure seen in heart failure might explain these abnormalities of the limb circulation. Ten normal human volunteers were subjected to venous congestion of one arm for three hours at 70 mm Hg. A mercury-in-rubber strain gauge plethysmograph was used to measure forearm VV [30] and forearm blood flow at rest after release of five minutes of arterial occlusion (the reactive hyperemia response). Congestion reduced VV [30] 22%, resting forearm blood flow 49% and peak reactive hyperemia blood flow 25%. Thus, chronic venous congestion per se may significantly reduce limb venous volume as well as resting and reactive hyperemia blood flow.

Adult↗