Prostaglandin control of renal circulation in the unanesthetized dog and baboon.

Effects of indomethacin and meclofenamate, inhibitors of prostaglandin synthesis, were evaluated in the regulation of renal blood flow in conscious and anesthetized dogs and in tranquilized baboons, instrumented with arterial pressure catheters and renal blood flow probes. Indomethacin, 10 mg/kg, did not alter renal blood flow or resistance significantly in the conscious dog. In the anesthetized dog, however, indomethacin caused a reduction in renal blood flow (25 +/- 3% of control) and an elevation of renal vascular resistance (45 +/- 8% of control). Meclofenamate, 4 mg/kg, reduced renal flow (12 +/- 2%) and increased renal vascular resistance 15 +/- 4% in conscious dogs. In conscious dogs and tranquilized primates, indomethacin and meclofenamate reduced the reactive hyperemia in the renal bed after 15 s occlusion from a control of 36 +/- 5 ml to 6 +/- 2 ml, and after 45 s occlusion from a control of 98 +/- 9 ml to 17 +/- 5 ml. Methoxamine (10-50 mug/kg per min) and angiotensin II (0.03-0.12 mug/kg per min), infused in graded doses, induced significantly greater renal vasoconstriction in conscious dogs in the presence of indomethacin. Thus, in the conscious animal, prostaglandins appear to play only a minor role in the control of the renal circulation at rest, but are of greater importance in mediating the renal responses to reactive hyperemia and to vasoconstriction.     

Changes in the gastric motility by the chemical and mechanical stimulations in the dog

The effects of chemical and mechanical stimulations on gastric motility was studied in 19 anesthetized dogs by using electromyographical techniques. The animals were fasted for 18 hr or more before each experiment. Six or eight bipolar silver-wire electrodes were implanted on a gastric wall serially from the fundus to the terminal antrum. At the pre-stimulation stage, the periodic simple electrical activity, which is called electrical control activity (ECA), was regularly recorded from the corpus to the antrum of the stomach; the frequency of which was 4.5 +/- 0.5 cycles/min on the average. Mechanical stimulation (distention of the stomach) decreased the ECA frequency depending on the degree of distention. The ECA frequency was decreased to 2.9 +/- 0.4 cycles/min by the 400 ml distention. Chemical stimulations to the gastric antral mucosa also decreased the ECA frequency depending on the strength of acidity or alkalinity. The instillation of a solution of pH 1 or 12.5 into the stomach decreased the ECA frequency to 3.4 +/- 0.7, and 3.5 +/- 0.5 cycles/min, respectively. A stronger alkaline solution induced anti-peristaltic discharges in 4 of 6 cases. The results indicate that both mechanical and chemical stimulations decrease the ECA frequency depending on stimulus strength.     

Dissociation between changes in renal nerve activity and renal vascular resistance in conscious dogs

The effects of acute volume expansion and hemorrhage on renal nerve activity and renal vascular resistance were examined in chronically instrumented conscious dogs. In six conscious dogs, when the blood volume was expanded by 18 ml/kg, the mean arterial pressure increased by 14 +/- 3 mmHg, mean left atrial pressure increased by 5.3 +/- 0.7 mmHg, and renal nerve activity decreased by 87 +/- 3%, while the renal blood flow was not altered significantly and renal vasoconstriction occurred, i.e., the calculated renal vascular resistance increased by 12 +/- 4% from 0.49 +/- 0.05 mmHg/ml/min. Volume depletion, induced by 20 ml/kg hemorrhage, did not alter the mean arterial pressure (-4 +/- 6 mmHg), while it decreased the mean left atrial pressure by 4.0 +/- 0.7 mmHg and increased the renal nerve activity by 200 +/- 67%. However, the renal blood flow was well maintained at the pre-hemorrhagic control level and renal vasoconstriction did not occur. Thus, in conscious dogs, acute volume changes altered the renal nerve activity dramatically, but these changes in renal nerve activity did not exert any significant effects on renal vascular resistance.     

The relationships between glucose absorption and insulin secretion and the migrating myoelectric complex in the pig

Net glucose and free amino nitrogen absorption and insulin output in the pig hepatic portal vein were calculated from portal-arterial concentration differences and portal blood flow measured by thermodilution. Duodenal and jejunal motility were assessed by electromyography. In the fed pig, the migrating myoelectric complex (MMC) pattern of motility persisted; glucose and amino nitrogen absorption and insulin secretion all varied with the phase of the MMC, rising to maximum values 19.4 +/- 3.1 min before and falling to minimum values 16.7 +/- 4.4 min after phase III. The variations in glucose absorption with the MMC were caused primarily by changes in duodenal and jejunal motility rather than by changes in the rate of gastric emptying as glucose absorption and insulin secretion varied with the phase of the MMC during duodenal glucose infusions, with maximum values occurring 24.4 +/- 3.3 min before and minimum values 14.9 +/- 2.5 min after phase III activity. The mean glucose absorption time calculated by timing the appearance of glucose in the portal vein following an intraduodenal bolus injection was significantly longer when given in phase I showing that absorption was less rapid when the intestine was not contracting. A significant amount of glucose is metabolized by intestine, as during glucose infusion (500 mg min-1) the average portal glucose absorption (376 mg min-1) was less than the glucose infused.     

体外反搏对犬血流脉动性和血管阻力的影响

为了评价体外反搏是否具有扩张血管和增加血流脉动性的作用 ,制造了犬急性心肌梗塞模型 ,并使犬存活 6周。麻醉后 ,测定左侧颈总动脉血流量和右侧颈总动脉血压。计算反搏前和反搏中脉压差、血压脉动指数、血压的标准差、流量差、流量脉动指数、流量标准差和平均血管阻力。结果显示脉压差、血压脉动指数和血压标准差三个血压脉动性指标分别由反搏前的 30± 9mm Hg、1.2 6± 0 .0 5、8.7± 2 .5 mm Hg升高到反搏中的 4 3± 8mm Hg(P<0 .0 5 )、1.5 4± 0 .13、12 .4± 2 .0 mm Hg (P<0 .0 5 )。流量差、流量脉动指数和流量标准差三个血流脉动性指标分别由反搏前的 317± 4 8ml/ min、2 .85± 0 .2 1、96± 2 1ml/ min升高到反搏中的 4 4 7± 88m l/ min、4 .5 6± 0 .90、131±39m l/ m in,P值均于小 0 .0 5。平均血管阻力由反搏前的 5 78± 72 Wood单位降低到反搏中的 4 76± 85 Wood单位(P<0 .0 5 )。这表明体外反搏可使血管阻力下降 ,血压和血流脉动性增强。     

Carbon dioxide and liver blood flow.

This study was designed to determine blood flow to the liver during hypercapnia and combined hypercapnia-hypoxia with the portal vein and hepatic artery intact except for placement of an electromagnetic flow probe around these vessels. Twenty mongrel dogs weighing 30-45 kg were anesthetized with pentobarbital and flow probes and occluders were surgically implanted. Ten of these dogs were subjected to hypercapnia alone. During inspiration of 6% CO2 in room air, portal vein flow increased from 588 +/- 73 ml/min to 731 +/- 113 ml/min (p less than .05), while hepatic artery flow did not change significantly from its control mean of 221 +/- 38 ml/min. In the remaining dogs, inhalation of 6% O2 resulted in a reduction of portal blood flow within 30 min from 527 +/- 55 ml/min to 381 +/- 41 ml/min (p less than .01). Again, mean hepatic artery flow did not increase significantly above its control of 273 +/- 43 ml/min. Subsequent inhalation of 6% CO2 plus 6% O2 (combined hypercapniahypoxia) for 30 min in these same animals resulted in a significant increase of portal vein blood flow from 514 +/- 46 ml/min to 716 +/- 116 ml/min (p less than .05). Thus, hypercapnia alone increases total liver blood flow, primarily by an increase in portal vein flow. Hypoxia results in a decrease in portal vein flow. The superimposition of hypercapnia on hypoxia restores blood flow to a level close to that found with hypercapnia alone. Hypercapnia in the range of 63 +/- 4 mmHg PCO2 overwhelms the tendency toward a reduction of portal vein blood flow induced by an arterial PO2 of 42 +/- 5 mmHg in the presence of mild hypocapnia (PCO2 : 30.2 +/- 1 mmHg).     

Autoregulation of cerebral blood flow during early experimental renal hypertension in the conscious dog

Using the radioactive microsphere technique, cerebral blood flow (CBF) was measured in six conscious dogs before intervention and again on the 3rd-5th days after inducing hypertension by the one-kidney Goldblatt (1-KGH) procedure. Sham-operated controls were also studied. The normal temporal variability of CBF, as well as the precision of the microsphere technique in measuring CBF were also determined in other normal dogs. A left atrial catheter was used for the microsphere injections (15 micrometer diam spheres) and an aortic catheter was used for cardiac output and blood pressure measurements. On the 3rd-5th days after 1-KGH, mean aortic pressure increased from a control value of 94 +/- 7 mmHg to 135 +/- 20 mmHg (P less than 0.005). CBF did not change significantly from the control flow of 57.1 +/- 7.9 ml/100 g per min. Calculated cerebral vascular resistance increased by 47 percent (P less than 0.025) above the control value. Hence, the early phase of experimental renal hypertension is associated with adequate autoregulation of cerebral blood flow.     

Role of nitrergic input in mechanically and chemically induced gastric relaxation in conscious dogs.

Our aim was to study a role of nitrergic input in gastric relaxation in conscious dogs. Proximal gastric motor responses to mechanical distension and chemical stimulation (a lipid meal orally) were evaluated by electronic barostat. Effect of N(G)-monomethyl-L-arginine acetate (L-NMMA, 5 mg/kg) on these responses was studied. When mechanical stimulation was applied, we observed steep linear increases in intragastric pressure up to about 6 mmHg, then continued to increase gradually, and could be increased still further upon the addition of L-NMMA. Oral application of a lipid led to a prompt fall in intragastric pressure (gastric receptive relaxation; GRR). Lipid treatment also led to a considerable increase in gastric volume (means +/- S.D., 150.0 +/- 50.2 ml), this was followed by a plateau phase and a gradual return to baseline levels. Neither GRR nor the associated increase in gastric volume (167.6 +/- 53.0 ml) was sensitive to treatment with L-NMMA. Our conclusion is that nitrergic input is necessary for mechanically induced gastric relaxation, but not for either GRR or chemically-induced gastric relaxation in conscious dogs.     

Blood flows in the maxillocarotid anastomoses and internal carotid artery of conscious dogs

Although the external carotid artery is known to contribute to the cerebral blood flow in anesthetized dogs, quantitative information on the anastomoses and their role in conscious dogs is lacking. This study was carried out to determine blood flows in these anastomoses and the internal carotid artery, and also to examine the functional significance of the anastomoses in conscious dogs. Fifteen-micron radioactive microspheres were injected into common and external carotid arteries of four conscious dogs through chronically implanted catheters. Blood flows were determined by the reference sample method and by comparing microsphere distributions in the brain and the masseter muscle. Blood flows were estimated to be 140 +/- 32, 7.7 +/- 1.4, and 3.3 +/- 1.1 ml/minute (mean +/- SD) in the common carotid artery, internal carotid artery, and anastomoses on each side, respectively. Additional evidence indicated that the anastomotic flow so determined was primarily the flow in the anastomotic artery. Humoral responses to angiotensin II infusions were also studied in conscious dogs. External carotid angiotensin increased plasma 11-hydroxycorticosteroid concentration (used as an index of ACTH secretion) but did not increase plasma vasopressin concentration to the same extent as common carotid infusion. Therefore, the external carotid artery is functionally important in perfusing the brain in conscious dogs.     

Renal prostaglandin E2 secretion and excretion in conscious dogs.

Renal prostaglandin E2 (PGE2) secretion and excretion rates were determined in nine conscious dogs. Renal venous (RV) and urine PGE2 concentrations were measured by radioimmunoassay. In 21 controls tests RV PGE2 ranged from 37 to 215 pg/ml, with a mean concentration of 97 +/- 11 pg/ml. Basal left kidney PGE2 secretion was 317 +/- 42 pg.g-1.mm-1. Urine PGE2 concentration averaged 8,320 +/- 1,510 pg/ml with a PGE2 excretion rate of 3,260 +/- 480 pg/min from both kidneys. Indomethacin (2 mg/kg) reduced RV and urine PGE2 concentrations by 60 and 77%, respectively. Meclofenamate (2 mg/kg) decreased RV and urine PGE2 concentrations by 36 and 48%, respectively. PG inhibition had no significant influence on blood pressure or renal blood flow (RBF). PG inhibition reduced urine flow rate and increased urine osmolality. Indomethacin had no effect on urine sodium concentration or sodium excretion; meclofenamate increased urine sodium concentration and slightly diminished sodium excretion. These data demonstrate that PGE2 is released from the kidney in a conscious animal and that both indomethacin and meclofenamate significantly reduce the renal secretion and excretion of PGE2. In a normal, conscious animal prostaglandins do not control blood pressure or RBF but are involved in the excretion of water.     

Effect of pancreatic polypeptide on canine migrating motor complex and plasma motilin

A potential role of pancreatic polypeptide (PP) in the regulation of phase III of the migrating motor complex (MMC) was investigated in conscious dogs before and during bilateral vagal blockade. After a control fasting period, cyclical increments in plasma PP occurred with peak levels of 45 +/- 8 pmol/l coinciding with late phase II MMC motility. By contrast, after food a substantially higher (approximately five times peak fasting concentrations) and more prolonged elevation of PP was observed, in association with a postprandial pattern of activity. To approximate fasting plasma PP concentrations, porcine PP was infused at 100 pmol X kg-1 X h-1, which produced levels of plasma PP of 99 +/- 8 pmol/l. At this dose PP had no effect on phase III activity. However, at a dose of 400 pmol X kg-1 X h-1, which achieved plasma PP concentrations (283 +/- 33 pmol/l) similar to postprandial levels, there was a specific inhibition of phase III in the lower esophageal sphincter, stomach, duodenum, and upper jejunum. The phase III-associated increment of plasma motilin was also inhibited by this dose of PP. These inhibitory effects at the 400 pmol X kg-1 X h-1 dose of PP were also observed after bilateral blockade of the vagus nerves. Our results suggest that PP has no significant role in the modulation of phase III of the fasting MMC nor does it induce a typical feeding motor pattern. The selective inhibition of both phase III and the associated rise in plasma motilin by PP plasma levels similar to postprandial concentrations does, however, point to a possible role for pancreatic polypeptide in the postprandial inhibition of phase III of the MMC.     

Influence of the renin-angiotensin system on the autoregulation of renal blood flow and glomerular filtration rate in conscious dogs

Renal autoregulation of blood flow (RBF) and glomerular filtration rate (GFR) were examined in 10 conscious foxhounds under a normal sodium diet before and after a continuous intrarenal converting-enzyme inhibition (CEI) or during the application of the angiotensin II antagonist saralasin. In order to prevent alpha-adrenergic interference, phenoxybenzamine was infused into the renal artery. In contrast to studies performed in salt depleted dogs there was no impairment of RBF or GFR autoregulation after CEI or saralasin. Renal blood flow was autoregulated at a level of 3.81 +/- 0.18 ml min-1 g-1 in the control group, 3.98 +/- 0.16 ml min-1 g-1 after CEI and 3.97 +/- 0.41 ml min-1 g-1 after saralasin. The lowest point of autoregulation was very much the same between the individual groups (control: 65.0 +/- 1.4 mmHg; CEI: 66.5 +/- 4.6 mmHg; saralasin: 67.4 +/- 3.2 mm Hg). GFR acted in a similar manner (autoregulation level control: 0.50 +/- 0.03 ml min-1 g-1; CEI: 0.52 +/- 0.05 ml min-1 g-1; saralasin. 0.50 +/- 0.04 ml min-1 g-1). The lowest pressure of GFR autoregulation differed slightly more (control: 81.5 +/- 2.2 mmHg; CEI: 93.2 +/- 4.2 mmHg; saralasin: 85.9 +/- 2.1 mmHg). The results suggest that the renal autoregulation of GFR and RBF is independent of the renin-angiotensin system in conscious dogs during a normal sodium diet.     

Angiotensin II infusion increases vasopressin, ACTH, and 11-hydroxycorticosteroid secretion.

The effects of intravenous infusion of Asp1. Ile5-angiotensin II on blood pressure, plasma vasopressin, ACTH and 11-hydroxycorticosteroid levels and on plasma renin activity were studied in five trained, conscious dogs. The dogs were prepared with bilateral carotid loops. Infusion of angiotensin II at rates of 5, 10, and 20 ng/kg.min raised its plasma concentration from 23 +/- 7 to 48 +/- 8, 125 +/- 8, and 187 +/- 21 pg/ml, respectively. The lowest rate of infusion was mildly pressor, the two higher rates more so. All rates of infusion promptly increased vasopressin levels and depressed renin levels. The two higher rates also stimulated ACTH, although with a latency of 30-45 min. Since the rates of infusion of angiotensin II employed produced plasma levels within the physiological range, it is suggested that peripherally generated angiotensin II may play an important role in the regulation of vasopressin, and ACTH secretion.     

Role of arterial baroreceptors in mediating cardiovascular response to exercise.

The role played by the major arterial baroreceptor reflexes in the cardiovascular response to exercise was examined by comparing the responses of untethered conscious dogs instrumented for the measurement of aortic pressure and cardiac output with those of dogs with total arterial barorecptor denervation (TABD). Moderately severe levels of exercise (12 mph) in intact dogs increased cardiac output from 111 +/- 17 ml/kg per min, increased heart rate from 101 +/- 5 to 265 +/- 8 beats/min, and reduced total peripheral resistance from 0.039 +/- 0.003 to 0.015 +/- 0.002 mmHg/ml per min. Dogs with TABD responded in a very similar fashion; exercise increased cardiac output from 119 +/- 8 to 356 /+- 23 ml/kg per min, increased heart rate from 122 +/- 7 to 256 +/- 5 beats/min, and decreased total peripheral resistance from 0.042 +/- 0.005 to +/- 0.015 +/- 0.001 mmHg/ml per min. The reflex heart rate responses to intravenous bolus doses of methoxamine were also examined in intact animals, both at rest and during exercise. Methoxamine caused striking bradycardia at rest, but little bradycardia during exercise. These results suggest that the arterial baroreceptor reflex is normally turned off during severe exercise and thus does not modify significantly the cardiovascular response to exercise.     

Autonomic nervous contributions to the frequency of distension induced gastric motility in anesthetized dogs

Changes in gastric motility induced by distension of the stomach were studied electromyographically in anesthetized dogs. In vagotomized dogs, gastric distension decreased the electrical control activity (ECA) frequency. The magnitude of this decrease was correlated with the degree of gastric distension; its' frequency decreased from 4.7 to 3.5 Hz/min with 400 ml distension. In splanchnicectomized dogs, 400 ml gastric distension also evoked a decrease in ECA frequency from 3.9 to 2.9 Hz/min. In vagotomized and spinal transected dogs, 400 ml distension of the stomach evoked a decrease in ECA frequency from 4.3 to 3.4 Hz/min. In the vagotomized and splanchnicectomized dogs, ECA frequency decreased from 5.0 to 3.4 Hz/min with 400 ml distension. These values were similar to those of the intact stomach previously reported. The results of the present study suggest that the extrinsic autonomic nervous system does not contribute significantly to regulation of the ECA frequency following gastric distension in anesthetized dogs.     

Temporal dynamics of the partial pressure of brain tissue oxygen during functional forepaw stimulation in rats

The partial pressure of tissue oxygen (pO2) was measured in rat somatosensory cortex during periodic electrical forepaw stimulation of either 1 min or 4 s in duration, and correlated with simultaneous laser Doppler flowmetry. For both stimulus durations, a transient decrease in tissue pO2 preceded blood flow changes, followed by a peak in blood flow and an overshoot in tissue pO2. With protracted stimulation, tissue pO2 remained only slightly above pre-stimulus baseline, while blood flow was maintained at a reduced plateau phase. A sustained post-stimulus undershoot in tissue pO2 was observed only for the 1 min stimulus. These findings suggest a complex dynamic relationship between oxygen utilization and blood flow.     

Effect of pulseless perfusion on gastrointestinal blood flow and its distribution.

The effect of nonpulsatile (NP) arterial perfusion on gastrointestinal organ blood flow and intraorgan flow distribution was studied in 10 anesthetized (pentobarbital) dogs utilizing the radionuclide-labeled microsphere (15 micrometer) technique. Measurements of flow to the stomach, small intestine, and colon were made during a pulsatile perfusion control period and after 1- and 2-h periods of NP perfusion with a centrifugal left ventricular bypass pump (Medtronic). Total gastric blood flow (0.178 +/- 0.021 ml/min per g) as well as the partitioning of that flow between gastric subsegments such as antrum (17% of total gastric flow), body (83%), and mucosa (73%) was not significantly altered during the 2-h period of NP perfusion (P greater than 0.20). Similarly, flow to the intestine showed significant change during NP perfusion. Under conditions of equivalent hemodynamic states (mean perfusion pressure), nonpulsatile arterial perfusion results in no significant alteration in gastrointestinal blood flow or its intraorgan distribution.     

Cerebral blood flow and oxygen consumption in the newborn dog

Cerebral blood flow (CBF), CBF responses to changes in arterial CO2 tension, and cerebral metabolic rate for oxygen (CMRO2) were measured in newborn dogs, by means of a modification of the Kety and Schmidt technique employing 133Xe. Mongrel dogs of 1-7 days of age were paralyzed and passively ventilated with 70% N2O and 30% O2. CBF was derived by analysis of paired serial 20-microliter samples of arterial and of cerebral venous blood from the superior sagittal sinus. At an arterial PCO2 of 36.9 +/- 3.7 Torr and a mean arterial blood pressure of 62 +/- 10 Torr, CBF was 23 +/- 8 ml/min per 100 g. The arteriovenous oxygen content difference averaged 5.6 vol%, and CMRO2 was 1.13 +/- 0.30 ml O2/min per 100 g. CBF increased or decreased by 0.58 ml/min/100 g per Torr change in PCO2. Our results suggest that in the newborn, basal CBF and CBF responses to CO2 are considerably lower than in the adult and parallel the lower metabolic needs of the newborn brain.     

Epicardial propranolol administration for ventricular arrhythmias in dogs: matrix formulation and characterization.

The effect of propranolol on the prevention of ventricular tachycardia/fibrillation (VT/VF) due to acute coronary ischaemia was studied in dogs. A series of propranolol-polymer controlled release matrices in slab configuration using various polyurethanes and a polyurethane-silicone rubber copolymer were formulated and characterized. In general, drug release in vitro occurred with an initial burst phase followed by an exponentially declining delivery rate; the silicone rubber containing copolymer preparation had more sustained release properties than did pure polyurethane matrices. In the animal studies, dogs underwent 5-hourly 10 min complete occlusions of the left anterior descending coronary artery (LAD), followed by 50 min normal perfusion. During non-drug occlusions VT occurred at a frequency of 1.22 +/- 0.12 episodes/min. A propranolol-polyurethane matrix (30% w/w, 28-42 mg) was placed on the ischaemic zone of the left ventricular epicardium immediately after the fifth occlusion. After an hour of drug delivery a sixth occlusion took place. The number of arrhythmia episodes both before and after drug were quantified and compared. The time to ventricular fibrillation (when present) and the mean blood pressure were also assessed. The drug patch delivered propranolol at a dose of 140 +/- 45 micrograms/kg by the conclusion of the 1 h study period. Therapeutic drug levels were achieved in the peripheral blood samples (8.7-43.7 ng/ml) and were enhanced in coronary venous samples (360.9-556.2 ng/ml). Reduction of blood pressure and proarrhythmic events following epicardial controlled release propranolol administration were noted but were not statistically significant. Arrhythmia episodes before and after propranolol were not found to be significantly different (VT/min 1.02 +/- 0.31 and 1.22 +/- 0.12).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of dipyridamole and theophylline on reactive hyperaemia in subcutaneous adipose tissue in humans

The importance of adenosine for reactive hyperaemia in subcutaneous adipose tissue was studied in healthy volunteers, using the adenosine uptake inhibitor dipyridamole (bolus 0.1 mg/kg i.v. followed by infusion of 0.7 microgram/kg/min) and the adenosine receptor antagonist theophylline (4 or 6 mg/kg i.v.). Basal blood flow, total blood flow and hyperaemia (total minus basal flow) after a 20-min arterial occlusion were measured in the distal femoral region by the 133Xe washout technique with and without drug treatment. Basal blood flow (mean +/- SEM) was 2.4 +/- 0.3 ml/min/100 g, while total post-occlusive flow and total reactive hyperaemia were 97.3 +/- 8.4 and 61.8 +/- 6.5 ml/100 g, respectively, without drug treatment. Basal blood flow was unaffected by dipyridamole but the total flow and hyperaemia were enhanced by 49 +/- 24 and 60 +/- 31%, respectively (P less than 0.05 for both). This enhancement was due to increases in both amplitude and duration of the hyperaemia. Neither basal blood flow, total post-occlusive flow nor hyperaemia were significantly altered by theophylline. The amplitude of the enhanced hyperaemia during dipyridamole was not significantly counteracted by simultaneous theophylline treatment (6 mg/kg) but the duration of hyperaemia was reduced from 13 +/- 1 to 8 +/- 1 min (P less than 0.01). The results suggest that endogenous adenosine does not regulate basal blood flow or reactive hyperaemia of limited duration in human adipose tissue. However, reactive hyperaemia may be enhanced by pharmacological elevation of endogenous adenosine levels.