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PubMedDate not supplied

Reactive hyperemia vs. pharmacologic hyperemia in the canine iliac circulation. A comparison.

Different methods of selective vasodilation have been described. One method is reactive hyperemia, which occurs when an arterial occlusion is released, and another method involves injection of vasodilator drugs. Since both arteriography and pressure measurements are often performed during hyperemia, it is important to know whether these two methods differ in the degree or duration of hyperemia achieved. We measured reactive hyperemia in the hind limb of five anesthetized mongrel dogs after arterial occlusion times between 20 seconds' and 20 minutes' duration and after selective intra-arterial injection of 5, 10, and 20 cc of Renografin-76. Only 5 cc of Renografin-76 created greater and longer lasting hyperemia than the maximum reactive hyperemia achieved after 10 minutes of arterial occlusion. For this reason, contrast material-induced hyperemia appears to be preferable to reactive hyperemia as an aid to peripheral arteriography and as an aid to the evaluation of aortoiliac stenoses.

Angiography↗
PubMed2005

Hyaluronidase treatment of coronary glycocalyx increases reactive hyperemia but not adenosine hyperemia in dog hearts.

Because adenosine is commonly used for inducing maximal coronary hyperemia in the clinic, it is imperative that adenosine-induced hyperemia (AH) resembles coronary hyperemia that can be attained by endogenous stimuli. In the present study we hypothesized that coronary reactive hyperemia (RH) is limited compared with AH due to the presence of the glycocalyx and that the AH response is therefore unable to detect glycocalyx modifications. In anesthetized open-chest dogs, blood flow and pressure were measured in the left circumflex artery. RH after 15-s occlusion was compared with an intracoronary infusion of adenosine (650 microg; AH) during control conditions and after intracoronary treatment of the glycocalyx with hyaluronidase (20.000 U, 2 x 20 min; n = 6) or heat-inactivated hyaluronidase (n = 5). During control, coronary conductance during RH was 1.49 +/- 0.15 ml.mmHg(-1).min(-1) and 76 +/- 7% of coronary conductance during AH (P < 0.05). After hyaluronidase, RH conductance increased (P < 0.01) by 43 +/- 13% and became 93 +/- 4% of AH conductance (P = NS). Heat-inactivated hyaluronidase had no effect on RH and AH conductance. Our results demonstrate that adenosine-induced coronary hyperemia profoundly exceeds RH and that the difference is virtually abolished on selective removal of the glycocalyx. It is concluded that, compared with RH, adenosine-induced coronary hyperemia is not affected by modification of the glycocalyx. This glycocalyx insensitivity should be taken into account when using adenosine-induced coronary hyperemia as a marker for vasodilating capacity to an ischemic stimulus.

Adenosine↗
PubMed2003

Reactive hyperemia following coronary balloon angioplasty, but not dipyridamole-induced hyperemia, predicts resolution of exercise-induced ST-segment depression.

OBJECTIVES: To characterize delayed restoration of coronary blood flow following successful percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Delayed restoration of coronary blood flow following successful PTCA is common and likely the result of multiple factors. Temporary myocardial ischemia and dipyridamole administration both result in increased coronary blood flow, but by different mechanisms. The relationship between these phenomena and exercise-induced ST-segment depression after PTCA was investigated to determine if any correlation existed. METHODS: Forty consecutive patients with single-vessel coronary artery disease underwent treadmill exercise testing before and after PTCA. The percentage change in coronary blood flow before and after 90 s balloon inflation was assessed. After a new steady state had been reached, dipyridamole was infused and changes in coronary blood flow were again determined. The relationship between changes in coronary blood flow and the presence of ST-segment depression during exercise testing after PTCA was determined. RESULTS: Peak coronary blood flow induced by reactive hyperemia was significantly greater than that in the steady state after balloon inflation (48.5+/-38.8 compared with 15.1+/-13.2 ml/min, P<0.0001). Dipyridamole administration also resulted in significant increases in coronary blood flow (15.1+/-13.2 ml/min compared with 31.0+/-24.9 ml/min, P<0.0001). ST-segment depression after PTCA was significantly less than before (0.10+/-0.07 mV compared with 0.19+/-0.08 mV, P<0.001). Further, reactive hyperemia, but not dipyridamole-induced hyperemia, correlated with attenuation of exercise-induced ST-segment depression after PTCA (r=0.62, P<0.0001). CONCLUSIONS: Reactive hyperemia following temporary coronary occlusion recreates local conditions associated with delayed resolution of myocardial ischemia following successful PTCA. Further, this phenomenon appears to be distinct from changes in coronary blood flow induced by dipyridamole.

Adult↗
PubMed1984

Characteristics of reactive hyperemia in the cerebral circulation.

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.

Animals↗
PubMed1996

Hyperemia following traumatic brain injury: relationship to intracranial hypertension and outcome.

The role of posttraumatic hyperemia in the development of raised intracranial pressure (ICP) has important pathophysiological and therapeutic implications. To determine the relationship between hyperemia (cerebral blood flow (CBF) > 55 ml/100 g/minute), intracranial hypertension (ICP > 20 mm Hg), and neurological outcome, 193 simultaneous measurements of ICP and CBF (xenon-133 method) were obtained in 59 patients with moderate and severe head injury. Hyperemia was associated with an increased incidence of simultaneous intracranial hypertension compared to nonhyperemic CBF measurements (32.2% vs. 21.6%, respectively; p < 0.059). However, in 78% of blood flow studies in which ICP was greater than 20 mm Hg, CBF was less than or equal to 55 ml/100 g/minute. At least one episode of hyperemia was documented in 34% of patients, all of whom had a Glasgow Coma Scale (GCS) score of 9 or below. In 12 individuals with hyperemia without simultaneous intracranial hypertension, ICP was greater than 20 mm Hg for an average of 11 +/- 16 hours and favorable outcomes were seen in 75% of patients. In contrast, in eight individuals with hyperemia and at least one episode of hyperemia-associated intracranial hypertension, ICP was greater than 20 mm Hg for an average of 148 +/- 84 hours (p < 0.001), and a favorable outcome was seen in only one patient (p < 0.001). Compared to the remainder of the cohort, patients with hyperemia-associated intracranial hypertension were distinctive in being the youngest, exhibiting the lowest GCS scores (all < or = 6), and having the highest incidence of effaced basilar cisterns and intractable intracranial hypertension. In the majority of individuals with hyperemia-associated intracranial hypertension, their clinical profile suggests the occurrence of a severe initial insult with resultant gross impairment of metabolic vasoreactivity and pressure autoregulation. In a minority of these patients, however, high CBF may be coupled to a hypermetabolic state, given their responsiveness to metabolic suppressive therapy. In patients with hyperemia but without intracranial hypertension, elevated CBF is also likely to be a manifestation of appropriate coupling to increased metabolic demand consistent with a generally favorable outcome. This study supports the concept that there are multiple etiologies of both elevated blood flow and intracranial hypertension after head injury.

Adult↗
PubMed2003

Conjunctival hyperemia in healthy subjects after short-term dosing with latanoprost, bimatoprost, and travoprost.

PURPOSE: To evaluate conjunctival hyperemia after short-term use of latanoprost 0.005%, bimatoprost 0.03% and travoprost 0.004% in normal adults. DESIGN: Prospective, randomized, double-masked crossover active controlled comparison. METHODS: We evaluated conjunctival hyperemia by a standard photographic measure at the slit lamp and by anterior segment photographs in healthy subjects after dosing for 5 days with latanoprost, bimatoprost, or travoprost. Conjunctival hyperemia was evaluated at 24-hour trough (hour 0) and at hour 1 after dosing. Each subject was crossed over between periods after a 1-week washout interval. RESULTS: Twenty-eight subjects (mean age 26 +/- 9 years) completed this study. Several comparisons were noted to be significant between groups by slit-lamp biomicroscopy: first, at hour 0 latanoprost had significantly less hyperemia than bimatoprost; second, at hour 0 latanoprost showed significantly less change than bimatoprost compared with the study baseline (visit 2); third, at hour 1 latanoprost had significantly less hyperemia than travoprost; fourth, at hour 1 latanoprost demonstrated significantly less change from baseline in hyperemia than travoprost (visit 2); fifth, at hour 1 latanoprost had less change in hyperemia than bimatoprost or travoprost between the study and the nonstudy eye (P = .03); and last, at hour 1 latanoprost showed significantly less change than bimatoprost and travoprost compared with hour 0 (P = .04). Additionally, similar grades were observed by photographs with latanoprost demonstrating the lowest levels of hyperemia. Subjects complained less about other people noticing their red eye with latanoprost than bimatoprost or travoprost (P = .048). No serious adverse events were noted. CONCLUSIONS: This study suggests that latanoprost may cause significantly less short-term conjunctival hyperemia on average than bimatoprost or travoprost in healthy subjects.

Adult↗
PubMed1992

Role of adenosine for reactive hyperemia in normal and stunned porcine myocardium.

The role of adenosine for reactive hyperemia in normal and stunned myocardium was examined in 16 open-chest barbiturate-anesthetized pigs. Interstitial adenosine concentration was reduced or enhanced by intracoronary infusion of adenosine deaminase or the nucleoside transport inhibitor R 75231, respectively. In normal myocardium, adenosine deaminase reduced volume of hyperemia (Doppler flowmetry) after a 30-s left anterior descending coronary artery (LAD) occlusion by 20% (6-34%; P < 0.05), whereas R 75231 increased volume of hyperemia by 15% (2-24%; P < 0.05). Adenosine deaminase reduced volume of hyperemia after a 2-min LAD occlusion by 27% (13-37%; P < 0.001), whereas R 75231 increased volume of hyperemia by 66% (53-159%; P < 0.001). Adenosine deaminase and R 75231 did not affect maximal hyperemia. Volume of hyperemia after a 2-min LAD occlusion was reduced in stunned myocardium (%systolic segment length shortening reduced by approximately 45%, ultrasonic technique) but not further altered by either adenosine deaminase or R 75231. These findings show that adenosine contributes to reactive hyperemia after 30-120 s of ischemia in normal myocardium and indicate that the reduced reactive hyperemia in stunned myocardium is due to reduced accumulation of adenosine during ischemia.

Adenosine↗
PubMed2005

Local hyperemia to heating is impaired in secondary Raynaud's phenomenon.

Accurate and sensitive measurement techniques are a key issue in the quantification of the microvascular and endothelial dysfunction in systemic sclerosis (SSc). Thermal hyperemia comprises two separate mechanisms: an initial peak that is axon reflex mediated; and a sustained plateau phase that is nitric oxide dependent. The main objective of our study was to test whether thermal hyperemia in patients with SSc differed from that in patients with primary Raynaud's phenomenon (RP) and healthy controls. In a first study, we enrolled 20 patients suffering from SSc, 20 patients with primary RP and 20 healthy volunteers. All subjects were in a fasting state. Post-occlusive hyperemia, 0.4 mg sublingual nitroglycerin challenge and thermal hyperemia were performed using laser Doppler flowmetry on the distal pad of the third left finger. In a second study, thermal hyperemia was performed in 10 patients with rheumatoid arthritis and 10 patients with primary RP. The thermal hyperemia was dramatically altered in terms of amplitude and kinetics in patients with SSc. Whereas 19 healthy volunteers and 18 patients with primary RP exhibited the classic response, including an initial peak within the first 10 minutes followed by a nadir and a second peak, this occurred only in four of the SSc patients (p < 0.0001). The 10 minutes thermal peak was 43.4 (23.2 to 63), 42.6 (31 to 80.7) and 27 (14.7 to 51.4) mV/mm Hg in the healthy volunteers, primary RP and SSc groups, respectively (p = 0.01), while the 44 degrees C thermal peak was 43.1 (21.3 to 62.1), 42.6 (31.6 to 74.3) and 25.4 (15 to 52.4) mV/mm Hg, respectively (p = 0.01). Thermal hyperemia was more sensitive and specific than post-occlusive hyperhemia for differentiating SSc from primary RP. In patients with rheumatoid arthritis, thermal hyperemia was also altered in terms of amplitude. Thermal hyperemia is dramatically altered in patients with secondary RP in comparison with subjects with primary RP. Further studies are required to determine the mechanisms of this altered response, and whether it may provide additional information in a clinical setting.

Adult↗
PubMed2006

Short duration of reactive hyperemia in the forearm of subjects with multiple cardiovascular risk factors.

BACKGROUND: Peripheral vascular endothelial dysfunction is an independent predictor of cardiovascular events, and can be assessed noninvasively by measuring reactive hyperemia, either by vascular ultrasound measurement of flow-mediated vasodilatation or, less commonly, by measurement of blood flow using plethysmography. In the present study reactive hyperemia was measured using plethysmography in healthy subjects with multiple cardiovascular risk factors. METHODS AND RESULTS: Reactive hyperemia was measured following 5-min occlusion of the upper arm in 449 healthy subjects (302 men, 147 women, age range 20-70 years) with (n=352) and without (n=97) risk factors such as smoking, hypertension, diabetes mellitus, hypercholesterolemia, obesity, family history of cardiovascular disease, and menopause. Maximum blood flow and minimum vascular resistance in reactive hyperemia did not differ between subjects with and without risk factors regardless of gender. Duration of reactive hyperemia, however, was significantly shorter in subjects with risk factors. Age-adjusted mean value of duration of reactive hyperemia was significantly smaller in men with a smoking habit, diabetes mellitus, hypercholesterolemia or obesity, and in women with smoking habit, hypertension, diabetes mellitus or obesity. The number of risk factors significantly correlated with the duration of reactive hyperemia in both men (r=-0.56, p<0.001) and women (r=-0.62, p<0.001), suggesting that endothelial dysfunction increases with the number of risk conditions clustering in a single individual. CONCLUSIONS: Duration of reactive hyperemia reflects cardiovascular risk factors and decreases with the number of risk conditions. These findings suggest that the duration of reactive hyperemia measured with plethysmography is potentially useful for assessing endothelial dysfunction.

Adult↗
PubMed1995

Focal cerebral hyperemia after focal head injury in humans: a benign phenomenon?

To assess the relationship between posttraumatic cerebral hyperemia and focal cerebral damage, the authors performed cerebral blood flow mapping studies by single-photon emission computerized tomography (SPECT) in 53 patients within 3 weeks of brain injury. Focal zones of hyperemia were present in 38% of patients. Hyperemia was correlated with clinical features and early computerized tomography (CT) and magnetic resonance (MR) imaging performed within 48 hours of the SPECT study and late CT and MR studies at 3 months. The hyperemia was observed primarily in structurally normal brain tissue (both gray and white matter), as revealed by CT and MR imaging, immediately adjacent to intraparenchymal or extracerebral focal lesions; it persisted for up to 10 days, but was never seen within the edematous pericontusional zones. The percentage of patients in the hyperemic group having brief (< 30 minutes) or no loss of consciousness was significantly higher than in the nonhyperemic group (twice as high, p < 0.05). Other clinical parameters were not significantly more common in the hyperemic group. The mortality of patients with focal hyperemia was lower than that of individuals without it, and the outcome of survivors with hyperemia was slightly better than patients without hyperemia. These results differ from the literature, which suggests that global post-traumatic hyperemia is primarily an acute, malignant phenomenon associated with increased intracranial pressure, profound unconsciousness, and poor outcome. The current results agree with more recent studies which show that posttraumatic hyperemia may occur across a wide spectrum of head injury severity and may be associated with favorable outcome.

Brain Concussion↗
PubMed1995

Relative participation of adenosine and endothelium derived mediators in coronary reactive hyperemia in the dog.

The metabolites that mediate coronary reactive hyperemia have not been definitely identified. Although adenosine and endothelium derived substances seem to be involved, their relative contributions have not been defined yet. In the canine coronary circulation, we studied the relative participation of adenosine, nitric oxide and prostacyclin in reactive hyperemia, by measuring the changes produced by interfering with the synthesis or action of these metabolites. The dose-response curve for flow changes vs intracoronary administration of adenosine was displaced to the right after the inhibition of nitric oxide synthesis with N-omega-nitro-L-arginine, revealing that nitric oxide release partly mediates the vasodilator action of adenosine. The inhibition of PGI-2 synthesis with indomethacin did not modify reactive hyperemia. Interference with adenosine action, by administration of adenosine deaminase plus theophylline, decreased reactive hyperemia by 31.0 +/- 4.0% (p < 0.001). Inhibition of nitric oxide synthesis decreased reactive hyperemia by a larger (p < 0.005) magnitude, 41.0 +/- 3.9% (p < 0.001), revealing the existence of other stimuli for nitric oxide release in reactive hyperemia besides adenosine. Simultaneous inhibition of nitric oxide and PGI-2 syntheses and of adenosine action reduced reactive hyperemia, but the effect was not additive, reaching 49.5 +/- 4.5% of control. Since nitric oxide and adenosine are the most important mediators in reactive hyperemia so far described, our results suggest that other metabolites, acting directly or through mediators other than adenosine or nitric oxide, are responsible for about 50% of coronary reactive hyperemia.

Adenosine↗
PubMed2004

Hyperemia following aneurysmal subarachnoid hemorrhage: incidence, diagnosis, clinical features, and outcome.

OBJECTIVE: Hyperemia is a known phenomenon after aneurysmal subarachnoid hemorrhage, but only a few reports describe and analyze hyperemia in these patients. This could be the result of diagnostic difficulties in order to identify elevated cerebral blood flow; thus, it seems that hyperemia could be an underdiagnosed clinical state. The aim of the study was to evaluate this phenomenon in comparison with clinical outcome and imaging data in order to describe the frequency of hyperemia after subarachnoid hemorrhage and maybe improve clinical diagnosis. DESIGN: Retrospective analysis of our cerebral blood flow and transcranial Doppler sonography data bank. SETTING: . Neurosurgical/Anesthesiological intensive care unit University of Regensburg, Regensburg, Germany. PATIENTS AND PARTICIPANTS: A total of 37 patients were included (24 women and 13 men). All patients suffered from aneurysmal subarachnoid hemorrhage. MEASUREMENTS AND RESULTS: Standard transcranial Doppler ultrasonography, as well as the Xenon(133) clearance technique for cerebral blood flow measurements, was employed. We observed 37 increases of flow velocities in 37 patients according to Doppler ultrasonography. In order to distinguish between ischemia and hyperemia a Xenon(133) regional cerebral blood flow examination was performed. Global hyperemia was detected in 5 patients (14%). Hyperemia correlated only to favorable outcome ( p=0.01) and fewer ischemic lesions in the computed tomography ( p<0.05). CONCLUSION: The results indicate that while global hyperemia is a frequent phenomenon that cannot be detected by standard Doppler ultrasonography or clinical examination, hyperemic cerebral blood flow values following aneurysmatic subarachnoid hemorrhage are correlated to favorable outcome.

Adult↗
PubMed2004

Post pressure hyperemia in the rat.

In prior studies in man, we have demonstrated that pressure-induced hyperemia lasts for prolonged periods as compared to the short-term hyperemia created by proximal arterial occlusion. We have analyzed this phenomenon in our well-studied rat model of skin blood flow. Skin blood flow was measured using laser Doppler techniques in Wistar Kyoto rats at the back, a nutritively perfused site, and at the plantar surface of the paw, where arteriovenous anastomotic perfusion dominates. A customized pressure feedback control device was used to vary applied pressures. At the back, pressures in excess of 80 mmHg resulted in occlusion, whereas at the paw 150 mmHg was required. The peak hyperemic flow after release of pressure was comparable to that elicited by proximal arterial occlusion with a blood pressure cuff. However, the post pressure hyperemia peak descended to a plateau value, which was 50-100% greater than baseline and continued for up to 20 min while the peak following proximal arterial occlusion returned to baseline within 4 min. At the back, post pressure hyperemia reached a maximum after application of 100 mmHg pressure. The application of higher pressures than required for occlusion produced no greater hyperemic response. At the paw, maximum post pressure hyperemia occurred at 100 mmHg, although this pressure level was not totally occlusive. Higher pressures resulted in no greater hyperemia. At the back, 10 min of occlusion produced a maximal peak value whereas 1 min was sufficient at the paw. The application of pressure to a heated probe with subsequent release, produced a hyperemic response. Normalized to baseline blood flow, there was no difference between the hyperemic responses at basal skin temperature and at 44 degrees C. There is a prolonged hyperemic response following local pressure occlusion compared to a much shorter period following proximal ischemic occlusion. One can presume two different mechanisms, one related to ischemia and the other a separate pressure related phenomenon. The thermal vasodilatory response is additive, not synergistic with the post pressure hyperemia we have demonstrated. This finding suggests that different mechanisms are involved in thermal vasodilation and post pressure hyperemia.

Animals↗
PubMed2002

Absence of a diastolic velocity notch does not indicate hyperemia in traumatic brain injured patients without elevated cerebral blood flow velocity.

Elevated blood flow velocity (BFV), measured by transcranial Doppler (TCD), has been associated with hyperemia and cerebral vasospasm. This study examined whether the lack of a diastolic notch within the TCD waveform was associated with relative hyperemia within 5 days after injury in 35 traumatic brain injured (TBI) patients. Hyperemia (avD(O2) of < 4 ml/dL) was present in 16 patients and absent in 19 patients. Two clinicians independently coded TCD waveforms based on the presence of a diastolic notch (88% agreement). There was no significant difference in the presence of a diastolic notch by group; a diastolic notch was present in 57% (11/19) of patients without hyperemia and 81% (13/16) of patients with hyperemia. Sensitivity and specificity of detecting hyperemia using the diastolic notch was 18.7% and 57.9% respectively. The results showed that relative hyperemia was present without an elevation in blood flow velocities, and that the lack of a diastolic notch did not detect the presence of hyperemia in the TBI patient.

APACHE↗
PubMed2001

Parameters of postocclusive reactive hyperemia measured by near infrared spectroscopy in patients with peripheral vascular disease and in healthy volunteers.

The main purpose of our study was to determine the parameters of the postocclusive reactive hyperemia test that could help and provide the clinician with information about the tissue oxygenation, the severity of the disease, and the results of the applied therapies. Near infrared spectroscopy (NIRS) proved to be a valid noninvasive trend monitor useful for investigating the physiology of oxygen transport to tissue. Important advantages of NIRS over transcutaneous oximetry (TcpO2) are: (a) a more dynamic nature of the NIRS signals which reflects more closely the actual response of the peripheral vasculature to the occlusive provocation; (b) larger sampling volume; and (c) the ability of assessing tissue oxygenation at deeper tissue levels. We demonstrated that the time parameters of reactive hyperemia, the rate of reactive hyperemia, and the maximal change during reactive hyperemia, all calculated from the oxyhemoglobin (HbO2) signal of the NIRS, clearly distinguish between healthy volunteers and patients with vascular disorder. The time parameters of reactive hyperemia were significantly longer (p<0.01), and the rate of reactive hyperemia (p=0.01) as well as the maximal change during reactive hyperemia (p=0.02) were significantly lower in patient group compared to healthy volunteers. These parameters were also in good correlation with the values of ankle brachial index (ABI) and the resting values of oxygen partial pressure (TcpO2). Values of the chosen parameters obtained from the HbO2 signal were further compared between groups of diabetic and nondiabetic patients with peripheral vascular disease. Although longer time parameters of reactive hyperemia and lower rates of hyperemic response were detected, the difference between both groups was not statistically significant.

Aged↗
PubMed1992

Microvascular sites and mechanisms responsible for reactive hyperemia in the coronary circulation of the beating canine heart.

Our aim was to elucidate the site and mechanism responsible for reactive hyperemia in coronary circulation. In in vivo beating canine hearts, microvessels of the left anterior descending coronary artery (LAD) were observed through a microscope equipped with a floating objective. Flow velocity of the LAD was measured with a suction-type Doppler probe. The LAD was occluded for 20 or 30 seconds and then released, and reactive hyperemia was observed before and after 8-phenyltheophylline (7.5 mg/kg i.v.) or glibenclamide (200 micrograms/kg into the LAD) infusion. During the occlusion, only arterial microvessels smaller than 100 microns in diameter dilated. Dilation of those vessels was partially attenuated by 8-phenyltheophylline and completely abolished with glibenclamide. In the early phase of reactive hyperemia, all arterial microvessels dilated, and the magnitude of peak dilation was greater in vessels smaller than 100 microns compared with those larger than 100 microns. Vasodilation during reactive hyperemia ceased within 60 seconds in vessels smaller than 100 microns but was sustained for more than 120 seconds in those larger than 100 microns. 8-Phenyltheophylline did not change peak dilation of arterial microvessels but reduced dilation after the peak. Glibenclamide remarkably attenuated dilation of all arterial microvessels in the whole phase of reactive hyperemia. These results indicate that all arterial microvessels are responsible for reactive hyperemia after coronary artery occlusions of 20-30 seconds, but there is greater participation of vessels smaller than 100 microns in the early phase of reactive hyperemia. Dilation of vessels larger than 100 microns assumes an important role in the later phase. ATP-sensitive K+ channels mediate dilation of arterial microvessels both in brief ischemia and reactive hyperemia.

Adenosine↗
PubMed2001

Influence of nitric oxide synthase and adrenergic inhibition on adenosine-induced myocardial hyperemia.

BACKGROUND: Myocardial perfusion during adenosine-induced hyperemia is used both in clinical diagnosis of coronary heart disease and for scientific investigations of the myocardial microcirculation. The objective of this study was to clarify whether adenosine-induced hyperemia is dependent on endothelial NO production or is influenced by adrenergic mechanisms. METHODS AND RESULTS: In 12 healthy men, myocardial perfusion was measured with PET in 2 protocols performed in random order, each including 3 perfusion measurements. First, perfusion was measured at rest. Second, either saline or the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 4 mg/kg) was infused, and perfusion during adenosine-induced hyperemia was determined. Last, in both protocols, the alpha-receptor blocker phentolamine was infused, and perfusion during adenosine-induced hyperemia was determined again. Resting perfusion was similar in the 2 protocols (0.69+/-0.14 and 0.66+/-0.18 mL. min(-1). g(-1)). L-NAME increased mean arterial blood pressure by 12+/-7 mm Hg (P<0.01) and reduced heart rate by 16+/-7 bpm (P<0.01). Adenosine-induced hyperemia (1.90+/-0.33 mL. min(-1). g(-1)) was attenuated by L-NAME (1.50+/-0.55 mL. min(-1). g(-1), P<0.01). The addition of phentolamine had no effect on the adenosine-induced hyperemia (2.10+/-0.34 mL. min(-1). g(-1), P=NS). In the presence of L-NAME, however, when the adenosine response was attenuated, phentolamine was able to increase hyperemic perfusion (2.05+/-0.44 mL. min(-1). g(-1), P<0.05). CONCLUSIONS: Inhibition of endogenous NO synthesis attenuates myocardial perfusion during adenosine-induced hyperemia, indicating that coronary vasodilation by adenosine is partly endothelium dependent. alpha-Adrenergic blockade has no effect on adenosine-induced hyperemia unless NO synthesis is inhibited.

Adenosine↗