Release Of Arterial Occlusion Research Articles

Post-occlusive reactive hyperemia and skeletal muscle capillary hemodynamics.

In female Sprague-Dawley rats (n=6), the spinotrapezius muscle was exteriorized for evaluation of capillary hemodynamics pre-occlusion, 5min of feed artery occlusion (Occ), and 5min of reperfusion (Post-Occ). There were no differences in mean arterial pressure (MAP) or capillary diameter (Dc) between pre-occlusion and post-occlusion (P>0.05). During 30s of PORH, capillary fRBC was increased (pre: 59±4 vs. 30s-post: 77±2 cells/s; P<0.05) and VRBC was not changed (pre: 300±24 vs. 30s post: 322±25μm/s; P>0.05). Capillary hematocrit (Hctcap) was unchanged across the pre- to post-occlusion conditions (P>0.05). Following occlusion, there was a 20-30% decrease in the number of capillaries supporting RBC flow at 30s and 300s-post occlusion (pre: 92±2%; 30s-post: 66±3%; 300s-post: 72±6%; both P<0.05). Short-term feed artery occlusion (i.e. 5min) resulted in a more heterogeneous capillary flow profile with the presence of capillary no-reflow, decreasing the percentage of capillaries supporting RBC flow. A complex interaction between myogenic and metabolic mechanisms at the arteriolar level may play a role in the capillary no-reflow with PORH. Measurements at the level of the conduit artery mask significant alterations in blood flow distribution in the microcirculation.

Forearm vasodilator responses to environmental stress and reactive hyperaemia are impaired in young South Asian men

PurposePrevalence of cardiovascular disease (CVD) is greater in South Asians (SAs) than White Europeans (WEs). Endothelial dysfunction and blunted forearm vasodilatation to environmental stressors have been implicated in CVD. We investigated whether these features are present in young SA men.MethodsIn 15 SA and 16 WE men (19–23 years), we compared changes in forearm blood flow, arterial blood pressure (ABP), forearm vascular conductance (FVC), heart rate, and electrodermal resistance (EDR; sweating) following release of arterial occlusion (reactive hyperaemia endothelium-dependent) and 5 single sounds at 5–10 min intervals (stressors).ResultsAll were normotensive. Peak reactive hyperaemia was smaller in SAs than WEs (FVC increase: 0.36 ± 0.038 vs 0.44 ± 0.038 units; P < 0.05). Furthermore, in WEs, mean FVC increased at 5, 15, and 20 s of each sound (vasodilatation), but increased at 5 s only in SAs, decreasing by 20 s (vasoconstriction). This reflected a smaller proportion of SAs showing forearm vasodilatation at 15 s (5/15 SAs vs 11/16 WEs: P < 0.01), the remainder showing vasoconstriction. Concomitantly, WEs showed greater bradycardia and EDR changes. Intra-class correlation analyses showed that all responses were highly reproducible over five sounds in both WEs and SAs. Moreover, sound-evoked changes in ABP and FVC were negatively correlated in each ethnicity (P < 0.01). However, WEs showed preponderance of forearm vasodilatation and depressor responses; SAs showed preponderance of vasoconstriction and pressor responses.ConclusionsEndothelium-dependent vasodilatation is blunted in young SA men. This could explain their impaired forearm vasodilatation and greater pressor responses to repeated environmental stressors, so predisposing SAs to hypertension and CVD.

Effects of modest hyperoxia and oral vitamin C on exercise hyperaemia and reactive hyperaemia in healthy young men.

We have argued that breathing 40 % O2 attenuates exercise hyperaemia by decreasing production of O2-dependent vasodilators. However, breathing 100 % O2 attenuated endothelium-dependent vasodilatation evoked by acetylcholine and this effect was prevented by vitamin C, implicating reactive oxygen species (ROS). We have therefore used vitamin C to test the hypothesis that 40 % O2 modulates exercise hyperaemia and reactive hyperaemia independently of ROS. In a cross-over study on 10 male subjects (21.1 ± 0.84 years), we measured forearm blood flow (venous occlusion plethysmography) and calculated forearm vascular conductance (FVC) at rest and following static handgrip at 60 % maximum voluntary contraction for 2 min and following arterial occlusion for 2 min, after placebo or oral vitamin C (2000 mg), and when breathing air or 40 % O2. During air breathing, vitamin C augmented the peak increase in FVC following static contraction, or release of arterial occlusion, by ~50 or 60 %, respectively (P < 0.05). Breathing 40 % O2 in the presence of placebo attenuated post-contraction hyperaemia by ~25 % (P < 0.05), but had no effect on reactive hyperaemia. By contrast, in the presence of vitamin C, 40 % O2 attenuated the peak increase in FVC following static contraction, or release of arterial occlusion by ~25 and 50 %, respectively (P < 0.05). These results indicate that in young men, exercise hyperaemia following strenuous muscle contraction and reactive hyperaemia are blunted by ROS. However, they are also consistent with the view that modest hyperoxia induced by breathing 40 % O2 acts independently of ROS to attenuate not only post-contraction hyperaemia, but also reactive hyperaemia, by decreasing release of O2-dependent vasodilators.

Dynamic Contrast-Enhanced Ultrasound for Assessment of Skeletal Muscle Microcirculation in Peripheral Arterial Disease

: This feasibility study was performed to assess whether dynamic contrast-enhanced ultrasound (CEUS) and transient arterial occlusion are able to detect alterations in the microvascular perfusion and arterial perfusion reserve in patients suffering from peripheral arterial disease (PAD) in comparison with healthy volunteers. : Twenty patients with PAD, Rutherford classification grade I, category III (mean age, 64 years; mean height, 173 cm; mean weight, 81.8 kg), and 20 volunteers (mean age, 50 years; mean height, 174 cm; mean weight, 77.8 kg) participated in the study. Low-mechanical index CEUS (7 MHz; MI, 0.28) was performed to the dominant lower leg after start of a continuous automatic intravenous injection of 4.8 mL suspension with microbubbles containing sulfur hexafluoride (SonoVue) within 5 minutes. Perfusion of the calf muscle was monitored by CEUS before, during, and after release of arterial occlusion at the thigh level lasting for 60 seconds. Several parameters, especially the time to maximum enhancement after release of occlusion (tmax), the maximum enhancement after release of occlusion (maxenh), the total vascular response after release of occlusion (AUCpost), and the resulting slope (m2) to maximum enhancement were calculated. : After release of the occlusion, a significantly delayed increase of the CEUS signal to maxenh was observed in the patients with PAD (32 ± 17 seconds) compared with volunteers (17 ± 8 seconds, P = 0.0009). maxenh was 66.5 ± 36.6 (∼mL) in PAD versus 135.6 ± 75.1 (∼mL) in volunteers (P = 0.0016). AUCpost was 3016.5 ± 1825.8 (∼mL·s) in PAD versus 5906.4 ± 3173.1 (∼mL·s) in volunteers (P = 0.0013), and m2 was significantly lower in PAD (3.8 ± 5.2 vs. 14.8 ± 9.7 [∼mL/s], P = 0.0001). : Microvascular perfusion deficits and reduced arterial perfusion reserve in patients with PAD are clearly detectable with dynamic CEUS after transient arterial occlusion.

Comparison of Hyperemic Changes in Carotid-Radial Pulse Wave Velocity by Upper and Lower Arm Cuff Occlusion

Carotid-radial pulse wave velocity (PWV) normally decreases following release of upper arm cuff occlusion (hyperemia). Lower arm (LA) elicits less brachial artery dilation than upper arm (UA) occlusion but more closely reflects endothelial function. Using applanation tonometry, we compared changes (Δ) in PWV induced by UA and LA hyperemia in 65 healthy participants. Pulse wave velocity was measured serially. Both techniques decreased PWV maximally at 1 minute with gradual return to baseline by 9 minutes. ΔPWV(1min) was greater for UA than LA occlusion (-11.5% vs -6.8%, P = .02). Multivariate analysis showed arm location independently related to ΔPWV (P = .036). In participants with variable cardiovascular risk, PWV decline lessened with increasing Framingham risk for both techniques. UA and LA occlusion decrease PWV maximally at 1 minute after release of arterial occlusion. PWV(1min) decline are more marked after UA than LA occlusion and progressively lessens with increasing Framingham risk.

Role of nitric oxide in reactive hyperemia in human forearm vessels.

The role of nitric oxide (NO) in reactive hyperemia (RH) is not well known. We investigated whether NO plays a role in RH in human forearm vessels by examining the effects of NG-monomethyl-L-arginine (L-NMMA), a blocker of NO synthesis, on reactive hyperemic flow. Forearm blood flow (FBF) was measured by strain-gauge plethysmography with a venous occlusion technique. The left brachial artery was cannulated for drug infusion and direct measurement of arterial pressure. To produce RH, blood flow to the forearm was prevented by inflation of a cuff on the upper arm to suprasystolic pressure for intervals of 3 and 10 minutes. After the release of arterial occlusion (AO), FBF was measured every 15 seconds for 3 minutes. Resting FBF was 4.3 +/- 0.3 mL.min-1.100 mL-1 before 3 minutes of AO and 4.1 +/- 0.6 mL.min-1.100 mL-1 before 10 minutes of AO. FBF increased to 32.3 +/- 1.9 and 38.2 +/- 3.1 mL.min-1.100 mL-1 immediately after 3 and 10 minutes of AO, respectively, and gradually decayed (n = 13). Intra-arterial infusion of L-NMMA (4 mumol/min for 5 minutes) decreased baseline FBF (P < .01) without changes in arterial pressure. L-NMMA did not affect the peak reactive hyperemic FBF after 3 and 10 minutes of AO. L-NMMA significantly decreased total reactive hyperemic flow (flow debt repayment) by 20% to 30% after 3 and 10 minutes of AO. Simultaneous infusion of L-arginine (a precursor of NO) with L-NMMA reversed the effects of L-NMMA. Our results suggest that NO plays a minimal role in vasodilation at peak RH but plays a modest yet significant role in maintaining vasodilation after peak vasodilation. Our results also suggest that reactive hyperemia in human forearms is caused largely by mechanisms other than NO.

Renal corticomedullary metabolite gradients during graded arterial occlusion

In order to investigate the role of the outer medulla in acute ischemic renal failure (Epstein FH, Balaban RS, Ross BD: Redox state of cytochrome aa3 in isolated perfused rat kidney. Am J Physiol 1982;243: F356-F363), the distribution of ATP in the in vivo porcine kidney and its relationship to Na transport and to ischemia was examined by using localized 31P magnetic resonance spectroscopy. Renal cortex (ATP) was higher than medulla. Reduction in Na transport produced by partial renal arterial occlusion ("hypofiltration"), resulted in a 13% increase in the ATP/Pi ratio of the whole kidney (from 2.61 +/- 0.26 to 2.96 +/- 0.27; P less than 0.03). This increase was accounted for by a statistically significant increase in (ATP) in the cortex, with medulla contributing to an insignificant extent. Further occlusion of the renal artery to reduce GFR to zero ("hypoperfusion") resulted in a 70% fall in ATP/Pi ratio. (ATP) was reduced most in the cortex, but pH fell equally in cortex and medulla. After release of arterial occlusion, cortical ATP recovered less completely than medulla ATP. Intracellular pH and Pi were restored in both cortex and medulla. It was concluded that cortex and medulla contribute equally to the pattern of disordered energy metabolism in acute renal failure. Sparing of ATP during hypofiltration may reflect the reduced energy requirements of active Na transport.

Characteristics of flow-mediated brachial artery vasodilation in human subjects.

In an effort to determine whether arterial conductance vessels dilate in response to increased blood flow stimuli, brachial artery area (cm2) and diameter (cm) were derived by simultaneous measurement of forearm blood flow (ml/min.100 ml) and brachial artery blood flow velocity (cm/sec) following the release of arterial occlusion. Measurements were made at rest and at the time of maximal flow after the release of graded periods of forearm arterial occlusion (20 seconds to 10 minutes). These studies showed a graded large vessel dilation following occlusions of up to 1 minute (baseline diameter, 0.33 +/- 0.01; after 1 minute occlusion, 0.45 +/- 0.02 cm; p less than 0.05) after which time diameter plateaued (after 10 minutes of occlusion, 0.48 +/- 0.02 cm). In addition, the time course of diameter and flow changes after 3 minutes of arterial occlusion were examined. Flow was maximal at 5 seconds but diameter was maximal at 15-30 seconds after release. Furthermore, the half time for the return of diameter to baseline was longer than that for blood flow. We also measured the diameter after forearm heating (42 degrees C) and noted a substantial increase in diameter (before heating, 0.32 +/- 0.01; after heating, 0.39 +/- 0.02 cm; p less than 0.05). Finally, we applied pressure to the venous side of arteriovenous fistulae in five hemodialysis patients. This maneuver was associated with large reductions in forearm blood flow (baseline flow, 63.3 +/- 10.6; venous compression flow, 36.0 +/- 4.4 ml/min.100 ml; p less than 0.05) and a decrease in brachial artery size (baseline diameter, 0.63 +/- 0.07; venous compression diameter, 0.58 +/- 0.06 cm; p less than 0.05). We conclude that 1) the human brachial artery size changes in response to changes in blood flow, and 2) the maximal dilation occurs after maximal flow is noted. Although alternate explanations are possible for each of our observations, our results are most consistent with a flow-mediated, localized vasodilating process.

Experimental Model for Repetitive Ischemic Attacks in the Gerbil: The Cumulative Effect of Repeated Ischemic Insults

An experimental model for repeated ischemic attacks, which allows easy induction of cerebral ischemia of any desired duration and frequency, has been developed in the gerbil. With this procedure, a pronounced cumulative effect on development of edema and tissue injury was observed using 3 separate, 5-min bilateral occlusions of the common carotid arteries spaced at various time intervals. This effect was most evident when the occlusions were carried out at 1-h intervals, i.e., during the period of marked postischemic hypoperfusion. Such animals, killed after 24 h of recirculation, showed significantly more severe edema and brain tissue injury in the areas exposed to ischemia than was observed in animals killed 24 h after single 5- or 15-min occlusions. The changes of regional CBF, assayed with a [3H]nicotine method, indicated a relatively rapid onset of hypoperfusion of similar degree after each release of arterial occlusion. The hypoperfusion recovered significantly within 6 h of recirculation following either single or multiple occlusions, and no residual hypoperfusion was observed in animals which, when killed at 24 h, showed severe edema and brain tissue injury. This model should prove useful in elucidating the pathophysiological mechanisms operative in repetitive cerebral ischemia.

Enhanced maximal metabolic vasodilatation in the dominant forearms of tennis players.

In an effort to evaluate potential peripheral adaptations to training, maximal metabolic vasodilation was studied in the dominant and nondominant forearms of six tennis players and six control subjects. Maximal metabolic vasodilation was defined as the peak forearm blood flow measured after release of arterial occlusion, the reactive hyperemic blood flow (RHBF). Two ischemic stimuli were employed in each subject: 5 min of arterial occlusion (RHBF5) and 5 min of arterial occlusion coupled with 1 min of ischemic exercise (RHBF5ex). RHBF and resting forearm blood flows were measured using venous occlusion strain-gauge plethysmography (ml X min-1 X 100 ml-1). Resting forearm blood flows were similar in both arms of both groups. RHBF5ex was similar in both arms of our control group (dominant, 40.8 +/- 1.2 vs. nondominant, 40.9 +/- 2.1). However, RHBF5ex was 42% higher in the dominant than in the nondominant forearms of our tennis player population (dominant, 48.7 +/- 4.0 vs. nondominant, 34.4 +/- 3.4; P less than 0.05). This intraindividual difference in peak forearm blood flows was not secondary to improved systemic conditioning since the maximal O2 consumptions in the two study groups were similar (controls, 45.4 +/- 3.9 vs. tennis players, 46.1 +/- 1.7). These findings suggest a primary peripheral cardiovascular adaptation to exercise training in the dominant forearms of the tennis players resulting in a greater maximal vasodilatation.

Effect of cigarette smoking on reactive hyperaemia in the human finger

The effect elicited by cigarette smoking on the reactive hyperaemia that develops following release of arterial occlusion in human skin was investigated, and compared to the corresponding effects elicited by oral administration of indomethacin (an inhibitor of the prostaglandin-forming enzyme cyclo-oxygenase) or nicotine, or by smoking of nicotine-free cigarettes. Finger blood flow was determined in human volunteers, using venous occlusion plethysmography, in the basal state and after 5 min of arterial occlusion. All subjects were studied before and after they had smoked two tobacco cigarettes, two herbal (nicotine-free) cigarettes, or chewed a nicotine chewing gum. The determinations before and after tobacco smoking were repeated after administration of indomethacin. In separate series, the effects of smoking on heart rate and systemic blood pressure were recorded. The basal finger blood flow was significantly (P less than 0.05) diminished following cigarette smoking, by about 35%, and so was the reactive hyperaemia (P less than 0.05), by about 55%. The reactive hyperaemia after administration of indomethacin in combination with cigarette smoking did not differ from that obtained after cigarette smoking alone. The reactive hyperaemia was not affected by oral administration of nicotine, or by smoking of two herbal cigarettes. Cigarette smoking elicited increases in heart rate and systemic blood pressure that were of similar magnitude before and after indomethacin. From these data, we conclude that cigarette smoking elicits an inhibitory effect on the reactive hyperaemia in the human finger. This effect is probably not caused by nicotine, and seems to act via blockade of the vascular relaxation normally medicated by locally formed cyclo-oxygenase products.

Evaluation of response time of a transcutaneous oxygen tension electrode.

Response characteristics of a transcutaneous PO2 electrode to step changes in PaO2 were determined. In vitro lag time and 95% response time of a transcutaneous PO2 monitor were compared to in vivo response. Release of arterial occlusion was used to produce rapid local PaO2 changes in human infants and adults. In vitro lag time and 95% response time varied according to whether an increment or decrement in PO2 was produced. In vivo 95% response time of this electrode was two to six times slower than previous estimates, and it varied significantly with the magnitude of the step change, subject age, anatomic location, and local hemodynamic factors. Also, we found that in vivo lag time is two to three times faster than previously reported.

Mechanisms of increased tissue oxygen delivery following release of arterial occlusion in canine skeletal muscle and skin.

Tissue oxygen delivery is dependent on the local blood flow and the extent of oxygen extraction. Concerning the intrinsic microvascular control of tissue O2 delivery, a recent system analysis (1) and experimental data (2) suggest that adequate tissue oxygenation is maintained over a wide range of metabolic stresses, the relative contribution of blood flow and O2 extraction to the regulation of tissue O2 delivery being determined by the prevailing venous oxygen level. The previous study (2) has shown that in skeletal muscle perfused with constant pressure, both reactive hyperemia and elevated arteriovenous (A-V) O2 difference contribute to the O2 debt repayment following arterial occlusion when the initial A-V O2 difference is in the normal range. However, at low prevailing A-V O2 difference, increased O2 extraction is the major mechanism by which the tissue repays its O2 debt and the contribution of blood flow is minimal. As the prevailing venous O2 reserve is lowered, the contribution of O2 extraction diminishes and reactive hyperemia becomes more important for the compensation. Thus, the immediate post-occlusion O2 extraction is only slightly elevated or even transiently depressed.KeywordsArterial OcclusionReactive HyperemiaLocal Blood FlowAnterior Tibial ArteryDebt RepaymentThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Renal contribution to thoracic duct lymph in dogs.

1. The renal contribution to thoracic duct lymph was measured in seventeen anaesthetized fasting dogs by measurement of thoracic duct flow before and after renal arterial occlusion.2. In eight experiments it was shown that thoracic duct flow and glomerular filtration rate were not significantly affected by the operation to expose the renal artery.3. In three experiments occlusion of the renal vein, after release of arterial occlusion, resulted in a sudden increase in thoracic duct flow.4. In animals infused with isotonic saline or dextrose (approximately 1 ml./min) the average values obtained for control thoracic duct flow, left renal flow and right renal flow were approximately 2.0, 0.7 and 0.3 ml./hr/kg body wt.: in non-infused animals these values were 1.4, 0.4 and 0.35 ml./hr/kg body wt. respectively.5. Possible reasons for the apparently smaller lymph flow from the right than the left kidney, and the relationship between the renal contribution to thoracic duct flow and actual renal lymph flow are discussed.6. Close correlation was found between control thoracic duct flow and body weight and between renal lymph flow and control thoracic duct flow.

Blood-borne vasodilating agent from ischemic tissues.

Plethysmographic measurements of forearm blood flow show a drop to minimal values immediately after release of arterial occlusion of a leg; this is soon followed by a somewhat greater and more sustained increase to values above the control. Prepacking the leg with blood before arterial occlusion, or exercise before occlusion, or a combination of these procedures does not significantly alter the response. Calculated peripheral resistance in the forearm follows the pattern implied by the blood flow changes. It is suggested that the initial vasoconstriction is a reflex whereas the later vasodilatation is due to a stable, circulating agent from the previously ischemic leg. Submitted on April 29, 1960

ポーラログラフ法による末梢循環に関する研究

The polarographic method for the measurement of the oxygen tension in tissue is a beneficial addition to the group of the methods available for the study of the peripheral circulation.In this paper, the author analysed 1) the blood flow change in the muscle and the skin, 2) role of the arteriovenous anstomosis (AVA), in combination with the skin temperature measurement by thermocouple, the finger volume plethysmograph and N24 clearance.The summary and conclusion of the experiment were as follows.1) The apparatus used is simular to what was described by Davies and Brink. The reliability, and the influence of the physico-chemical factors were retested, and it was concluded that this method could be available for the study of the peripheral circulation.2) By arterial occlusion, the skin PG and muscle PG descended and by oxygen inhalation they ascended. In this respect some consideration was made about the oxygen consumption of tissue, the oxygen diffusion and the blood circulation time.3) It was found that the skin PG showed the spontaneous fluctuation and moreover, every simultaneous record at two points of the body showed high correlation. It seemed the fluctuation might be in close relationship with the blood flow change caused by the nervous control probably in the vicinity of the arterioles.4) When the skin PG and temperature were recorded simultaneously, both curves often showed close simularity. It was suggested that the skin temperature change might in some occasion indicate the skin capillary blood flow change. Contrally, in the cases of poor correlation between them the explanation may be possible by increased blood flow through the AVA, where it is supposed that the oxygen can scarecely pass through the wall and that fluctuation differs from that of the arteriole.5) Simultaneous record of the skin PG and finger volume plethysmograph were carried out and in some occasion they showed correlation. This is a interesting finding to evaluate each method.6) The reactive hyperemia after release of arterial occlusion and caloric vestibular stimulation were studied and no definite tendency was seen polarographically.7) The spontaneous fluctuation was seen in the muscle PG which as in the case of the skin PG showed close simularity when recorded at every two points. And, the muscle PG had no close correlation to the skin PG.8) The reaction to cold, "Hunting" phomenon by Lewis, was studied with simultaneous record of skin PG and skin temperature during finger cooling. Both curves showed the huntung in much simular way. And, at various points of the hunting shown by temperature curve, oxygen inhalation lets the PG elevate variously. The interpretation is that the hunting depends not mainly upon the increase of blood flow of AVA, but upon the change of capillary blood flow.9) The changes of the muscle PG and the skin PG in indirect thermal application were compared with the reports based upon the conventional methods. By polargraphic method it may be possible to analyse the blood flow changes in the skin and the muscle separately.Also, the blood flow change of muscle and skin in Adrenaline administration were studied.

Polarographic oxygen, the epicardial electrocardiogram and muscle contraction in experimental acute regional ischemia of the left ventricle.

This study is the first attempt to correlate myocardial oxygen availability by the polaro-graphic method with direct electrocardiographic leads and cinematographic records of muscle contraction during experimental acute coronary branch occlusion and narrowing. The comparative insensitivity and slowness of the epicardial electrocardiogram as an index of acute regional ischemia is demonstrated. Special attention is given to the rates of myocardial oxygen change immediately following attainment of a significant degree of coronary obstruction, the effects of pure oxygen inhalation on the experimental situations, and alterations in coronary vein color following release of arterial occlusion.

Contour of the toe pulse, reactive hyperemia, and pulse transmission velocity: Group and repeat variability, effect of age, exercise, and disease

1. 1. In 170 normal young men, 270 normal middle-aged men, 57 patients with arterial hypertension, and 36 patients with peripheral vascular disease, the toe pulse was photoelectrically recorded before and for vive minutes after arterial occlusion (reactive hyperemia). The following items were measured: absolute and relative crest time (per cent of cycle length); relative amplitude (per cent of peak amplitude) at one-fourth and one-half of the diastolic phase; amplitude changes during reactive hyperemia (in per cent of amplitude before arterial occlusion). 2. 2. There was an initial drop of the amplitude ten seconds after release of arterial occlusion in the normal groups and in the patients with peripheral vascular disease, but not in the hypertensive patients. 3. 3. The reactive hyperemia was not significantly different in the normal younger and older age groups but was much weaker and delayed in patients with peripheral vascular disease; in the more advanced cases it was entirely absent. The maximum increase of the amplitude during reactive hyperemia was moderately decreased also in the hypertensive patients. 4. 4. There was a statistically highly significant increase of the absolute and relative crest time, and slowing of the decline in the diastolic phase with age. 5. 5. The hypertensive patients showed no significant differences in the crest time, but a significantly slower diastolic decline as compared to normals. 6. 6. The rise as well as the decline of the pulse was significantly slower in patients with peripheral vascular disease. 7. 7. The separation of the patients with peripheral vascular disease from normals, investigated by distribution analysis, was excellent for all items of the contours analysis, particularly for the relative crest time and relative amplitude at one-fourth of the diastolic phase, and superior to the separation by means of reactive hyperemia. 8. 8. In about 10 per cent of hyperentsive patients the crest time and the diastolic decline were significantly delayed, even in the absence of clinical peripheral arteriosclerosis. 9. 9. The deviation of pulse contour and reactive hyperemia in patients with peripheral vascular disease depends on the degree of impairment rather than on the type of disease. 10. 10. The highly significant separation between the groups with all items of contour analysis is contrasted by a relatively poor consistency in repeat experiments in twenty-six normal young men. 11. 11. The pulse transmission velocity was determined in meters per second from the interval first heart sound to footpoint of the pulse, a correction for the isometric phase of contraction, and the distance from heart to toe. The values are in general agreement with earlier observations. The increase of the pulse transmission velocity with age and in hypertension, and the decrease in perpheral vascular disease were statistically highly significant. 12. 12. There was no interindividual correlation between blood pressure and pulse transmission time in the normal groups, but there was a significant correlation between intraindividual variations of blood pressure and pulse wave transmission time. In hypertensive patients, there was a significant inter-individual correlation. 13. 13. The effect of exercise on pulse transmission velocity, contour of the toe pulse, and reactive hyperemia was studied in seven normal young men. 14. 14. The results substantiate the diagnostic value of analysis of the digital pulse for early recognition of vascular degeneration with age or in disease, and normal limits for separation of normal and abnormal are suggested.

Simplified determination of arterial insufficiency; plethysmographic observation of reactive hyperemia following fifteen minute arterial occlusion at the ankle.

Reactive hyperemia following 15 minute arterial occlusion at the ankle was studied in plethysmographic tracings using the venous occlusion technic. The resulting curves present an essentially different pattern in normal subjects and patients with various types of peripheral arterial disease. Several characteristic features can be distinguished, notably the level of highest blood flow after release of arterial occlusion, the time required until the highest blood flow is reached, and the degree of secondary vasoconstriction. Evaluation of these factors permits an estimate of the therapeutic value of lumbar sympathectomy.

Failure of Antihistaminic Drugs to Reduce Reactive Hyperemia in Man.

Summary and Conclusions1. In 6 subjects reactive hyperemia was produced in the legs by release of arterial occlusion maintained for from one-half to 10 minutes. Blood flow in the foot and distal portion of the leg was measured with a venous occlusion plethysmograph. The initial inflow rate immediately following release of arterial occlusion is taken as representative of the degree of vasodilatation resulting from the occlusion.2. After administration of effective amounts of antihistaminic drugs the reactive hyperemia was not diminished.3. The mechanism of reactive hyperemia has not been shown to be due to release of histamine or “H-substance.” It is as yet unexplained.