Heat-induced vasoconstriction in the fingers: a mechanism for reducing heat gain through the hand heated locally

This study examined the effect of local heating on the blood flow of the finger or forearm in male subjects in an environment of 35°C-40% (r.h.). One hand or forearm was immcrsed in a water bath the temperature of which (T _w) was raised by 1°C every 10th min from 35° to 43°C, while the other hand or forearm was kept at a constantT _w of 35°C. Blood-flow (BF) was measured by venous occlusion plethysmography, using temperature-compensated mercuryin-Silastic strain gauges. Finger BF in the heated hand was significantly lower than that in the control hand atT _ws of 37°–41°C, mostly for the first few minutes of each heating period. Thereafter, finger BF in the heated hand gradually returned toward the previous values. AtT _ws of 39°–40°C, liowever, finger BF in the heated hand remained lower than the control values for the entire period of heating. AtT _ws of 42°–43°C, finger BF in the heated hand greatly increased after an initial transitory fall. In the forearm skin, however, no such vasoconstriction in response to local heating was observed. All this suggests that a rise in skin temperature to above the core temperature produces paradoxical vasoconstriction in the finger, which may be a mechanism to reduce heat gain through the hand heated locally at higher temperatures.     

Effects of repeated carbon dioxide-rich water bathing on core temperature,cutaneous blood flow and thermal sensation

We examined the effects of repeated artificial CO₂ (1,000 ppm) bathing on tympanic temperature (T _ty), cutaneous blood flow, and thermal sensation in six healthy males. Each subject was immersed in CO₂-rich water at a temperature of 34°C up to the level of the diaphragm for 20 min. The CO₂-rich water was prepared using a multi-layered composite hollow-fiber membrane. The CO₂ bathing was performed consecutively for 5 days. As a control study, subjects bathed in fresh water at 34°C under the same conditions. T _ty was significantly lowered during CO₂ bathing (P<0.05). Cutaneous blood flow in the immersed skin (right forearm) was significantly increased during CO₂ bathing compared with that during fresh-water bathing (P<0.05), whereas cutaneous blood flow in the non-immersed skin (chest) was not different between CO₂ and fresh-water bathing. Subjects reported a "warm" sensation during the CO₂ bathing, whereas they reported a "neutral" sensation during the fresh-water bathing. The effects of the repeated CO₂ bathing were not obvious for core temperature and cutaneous blood flow, but the thermal sensation score during the CO₂ bathing was reduced sequentially by repeated CO₂ bathing (P<0.05). These thermal effects of CO₂ bathing could be ascribed largely to the direct action of CO₂ on vascular smooth muscles and to the activity of thermoreceptors in the skin. Serial CO₂ bathing may influence the activity of thermoreceptors in the skin. Electronic Publication     

Partitional measurement of capillary and arteriovenous anastomotic blood flow in the human finger by laser-Doppler-flowmeter

Summary This study was made to see whether changes in blood flow through the capillaries and arteriovenous anastomoses (AVA's) of the human finger can be measured by noninvasive flowmetry. Total finger blood flow (FBF) was measured by venous occlusion plethysmography; blood flow was measured by a laser-Doppler flowmeter (ADVANCE, ALF-2100, Tokyo, Japan) using probes with optic fiber separations of 0.3 mm (LDF-0.3) and 0.7 mm (LDF-0.7). The maximum sensitivities for LDF-0.3 and LDF-0.7 were at depths of 0.8 and 1.2 mm from the tissue surface respectively. Two series of experiments were performed on separate days. In the first series the test hand was immersed in a water bath whose temperature (T_w) was 25°C at an ambient temperature (T_a) of 25°C. T_w was raised to 35°C (local hand warming), which was then followed by an increase in T_a to 35°C (whole body warming). FBF, LDF-0.3, and LDF-0.7 increased during these thermal stimulations. However, the relationship of FBF to LDF-0.3 showed two different regression lines. In contrast, the relationship of FBF to LDF-0.7 showed a single regression line. In the second series, with T_a at 35°C, the test hand was immersed in a water bath at T_w 35°C. T_w was then raised every 10 min by 2°C steps from 35 to 41°C. At T_w 39–41°C, FBF and LDF-0.7 in the test hand were significantly decreased compared with those at T_w 35°C. In contrast, LDF-0.3 increased steadily as T_w rose from 35 to 41°C. These results suggest that laser-Doppler flowmetry, using flow probes with different optic fiber separations, can measure partitional blood flow through superficial vessels, predominantly capillaries, and deeper vessels, mainly AVA's, in the human finger.     

Effects of posture,hypotension and locally applied vasoconstriction on the middle ear microcirculation in anaesthetized humans

Studies by laser-Doppler flowmetry of middle ear microcirculation changes induced by physical and chemical stimuli in the animal have only recently been made. This prospective study, performed in humans, was designed to compare the effects of a postural manoeuvre (headup tilt 30°), hypotension and locally applied vasoconstriction on middle ear blood flow during anaesthesia. Circulatory changes provoked by a headup tilt of 30°, and successive intravenous boluses of potent vasodilators, were compared with circulatory changes provoked by locally applied adrenaline, in ten healthy patients in good physical states undergoing middle ear surgical repair. Heart rate and direct arterial pressure were continuously recorded via a radial artery cannula. Middle ear blood flow was continuously recorded via a laser-Doppler probe placed on the promontorium cavi tympani. Metabolic parameters (partial pressure of O₂ and CO₂ in arterial blood, pH, arterial lactate concentrations) and arterial concentrations of propofol were measured just before and just after the experiment. Headup tilt did not modify heart rate, mean arterial pressure or middle ear blood flow. Vasodilators (nicardipine, nitroprusside, nitroglycerin) provoked a fall in arterial pressure (P<0.0001,P<0.0001,P<0.019, respectively), but did not induce any significant variations in heart rate; variations occurred in middle ear blood flow (P>0.05, not significant) which were different according to patients and agents. Locally applied adrenaline provoked a fall in the middle ear blood flow (P<0.0012), with no effect on heart rate and arterial pressure. There were no significant changes in metabolic values, or propofol serum concentrations. The behaviour of the middle ear blood flow submitted to hypotension, posture, or to vasoconstriction could be related to counteracting regulatory responses and/or to direct vascular effects.     

Local cerebral blood flow in the rat during severe hypoglycemia,and in the recovery period following glucose injection

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N₂O, were injected with insulin to provide either an EEG pattern of slow-wave poly spikes, or cessation of spontaneous EEG activity for 5, 15, or 30 min (“coma”). In other animals, glucose was injected at the end of a 30 min period of “coma” and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with ¹⁴C-iodoantipyrine as the diffusible tracer. In the slow-wave poly spike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400–500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20–35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypotension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.     

Cardiovascular responses after brisk finger movement and their dependency on the “eigenfrequency” of the baroreflex loop

The baroreflex is mainly involved in short-term blood pressure regulation and strongly influenced by activations of medullary circulation centres in the brain stem and higher brain centres. One important feature of the baroreflex is its strong preference for oscillations around 0.1 Hz, which can be seen as resonance or “eigenfrequency” (EF) of the control loop (so-called Mayer waves). In the present study we investigated beat-to-beat heart rate intervals (RRI) and arterial blood pressure (BP) changes after brisk finger movement and their relationship to the “eigenfrequency” determined by cross spectral analysis between RRI and arterial blood pressure time series of 17 healthy subjects. The analyses revealed significant correlations between BP response magnitude (r = 0.63, p < 0.01) respectively RRI response magnitude (r = 0.59, p < 0.05) and EF. This can be interpreted in such a way that subjects with a “high” EF (>0.10 Hz) elicit larger BP responses as well as larger RRI responses when compared to subjects with a “low” EF (<0.10 Hz).     

Local cerebral blood flow in gently restrained rats: effects of propranolol and diazepam

Summary The cerebrovascular consequences of the gentle restraint commonly used for the measurement of local cerebral blood flow (LCBF) in conscious rats has been tested by using two drugs, propranolol and diazepam. Propranolol induced small LCBF decreases in 7 structures suggesting that the cerebral circulation was partially controlled by the activation of intra or extracerebral aminergic pathways in this protocol. Sedative doses of diazepam reduced LCBF in most of the structures but anxiolytic doses increased it in 4 structures. This effect may be due to a regionally differentiated modification of activity in the brain due to the selective inhibition of limbic structures by diazepam. Since propranolol and diazepam induced only small changes, the LCBF of gently restrained rats appeared to be minimally affected by the stressful situation imposed by the protocol.     

Interactive effects between isometric exercise and mental stress on the vascular responses in glabrous and nonglabrous skin

Cutaneous vascular responses to mental arithmetic (MA) and handgrip exercise (HG) were studied independently and combined at different local skin temperatures (T _loc). MA and HG induced (P < 0.05) vasoconstrictor responses in glabrous and nonglabrous skin at a higher level of T _loc, resulting in a nonadditive effect of these two stresses.     

Local cerebral glucose utilisation following acute and chronic bilateral carotid artery ligation in Wistar rats: relation to changes in local cerebral blood flow

The effects on local cerebral blood flow (LCBF) and glucose utilisation (LCGU) of permanent, bilateral carotid artery ligation (BCAL) were studied in conscious Wistar rats. LCBF and LCGU were measured using quantitative autoradiographic ¹⁴C-iodoantipyrine and the ¹⁴C-2-deoxyglucose (¹⁴C-DG) techniques in 24 anatomically discrete regions of the brain. LCBF in the cerebral hemispheres 2.5 h (acute) after BCAL significantly decreased to 25–87% of the sham control, with the exception of the mammillary body. After acute BCAL, there was a heterogeneous accumulation of ¹⁴C-DG in the caudate nucleus and cerebral cortices. Only in the lateral geniculate body did LCGU significantly decrease after BCAL. One week (chronic) later, LCBF was significantly decreased in 15 (containing the caudate nucleus and all the cerebral cortices) of 24 structures. LCGU in ten (containing the caudate nucleus and all the cerebral cortices) of 24 structures after chronic BCAL significantly decreased to 66–77% of the sham control, except for regions with neuronal damage in which there was a heterogeneous uptake of ¹⁴C-DG. The ratio of LCBF/ LCGU in chronic BCAL was unchanged in comparison with values in the corresponding sham-operated group. This model of acute and chronic cerebral ischaemia, with impairment in cerebral circulation and/or glucose metabolism, is expected to become a pertinent tool for the neurophysiologist.     

Spinal TRPA1 ion channels contribute to cutaneous neurogenic inflammation in the rat

In the spinal dorsal horn, TRPA1 ion channels on central terminals of peptidergic primary afferent nerve fibers regulate transmission to glutamatergic and GABAergic interneurons. Here we determine the cutaneous anti-inflammatory effect of a spinally administered TRPA1 channel antagonist to test the hypothesis that spinal TRPA1 channels contribute to cutaneous neurogenic inflammation induced by sustained noxious stimulation. According to the hypothesis, spinal TRPA1 channels facilitate transmission of injury discharge to GABAergic interneurons that induce a dorsal root reflex, which results in increased release of proinflammatory compounds in the skin. Intraplantar capsaicin, a TRPV1 channel agonist, was used to induce neurogenic inflammation in anesthetized rats that were pretreated intrathecally (i.t.), intraplantarly (i.pl.) or intraperitoneally (i.p.) with vehicle or Chembridge-5861526 (CHEM, a TRPA1 channel antagonist). For assessment of neurogenic inflammation, the capsaicin-induced increase of cutaneous blood flow was determined adjacent to the capsaicin-treated skin site with a laser Doppler flowmeter. Capsaicin-induced a marked increase in cutaneous blood flow. The capsaicin-induced blood flow increase was attenuated in a dose-related fashion by i.t. pretreatment with CHEM (3-10 μg). Pretreatment with CHEM at a dose of 3 mg/kg i.p. or 20 μg i.pl. failed to attenuate the capsaicin-induced increase of blood flow. The results indicate that spinal TRPA1 channels contribute to cutaneous neurogenic inflammation adjacent to the injury site, probably by facilitating a dorsal root reflex in peptidergic primary afferent nerve fibers.     

Regional differences in age-related decrements of the cutaneous vascular and sweating responses to passive heating

Ten older (aged 64–76 years) and ten younger (aged 20–24 years) healthy men were exposed to a standard heat stress [by placing the lower legs and feet in a water bath at 42°C while sitting in a controlled environment (ambient temperature 35°C and 45 % relative humidity) for 60 min]. During passive heating, the rectal temperature of the older men was significantly greater (P < 0.05) and mean skin temperature was lower (P < 0.001), compared to the younger men. Skin blood flow by laser Doppler flowmetry (LDF) was significantly lower on the chest and thigh for the older men (P < 0.001), but forehead LDF did not differ between the groups. The percentages of total LDF in the older men to total LDF in the younger men for the last 30 min were 99%, 58% and 50% on the forehead, chest and thigh, respectively. The age-related differences in LDF responses mirrored cutaneous vascular conductances (CVC), since no group and time effects were observed in mean arterial blood pressure during the test. During the last 30 min the local sweat rates (m_sw) on the back and thigh were significantly lower for the older men (P < 0.02), but not on forehead, chest and forearm, although the older men had lower m_sw during the first 30 min exposure regardless of site (P < 0.03). The percentages of total m_sw in the older men to total m_sw in the younger men during the last 30 min were 105%, 99%, 63%, 106% and 88% on the forehead, chest, thigh, forearm, and back, respectively. During the latter half of the exposure, the older men had similar LDF, CVC and m_sw on the forehead, lower LDF and CVC and a similar m_sw on the chest, and lower LDF, CVC and m_sw on the thigh, compared to the younger men. These results suggest firstly that regional differences exist in the age-related decrement of cutaneous vasodilatation as well as sweat gland function, secondly that the age-related decrement in cutaneous vascular function may precede a decrement in sweat gland function, and thirdly that the successive decrements may develop sequentially from the lower limbs to the upper body, and head.     

Inhibitory effect of pentobarbital anesthesia on venous stasis induced arteriolar vasoconstriction in the dog hindleg

The effect of close intrarterial administration of pentobarbital in the concentration of about 2times10^-4 mol/1 on the venous stasis induced arteriolar constriction in the dog hindleg was studied in 6 neurolept anesthetized dogs. It was found that the blood flows and vascular resistances in the legs before pentobarbital infusion were equal and the vasoconstrictor responses to venous stasis were the same. Pentobarbital infusion into the femoral artery in one of the legs increased the total leg blood flow compared to the control leg and abolished the increase in vascular resistance during venous stasis. In another experimental series the effect of general pentobarbital anesthesia on the vasoconstrictor activity in response to venous stasis locally in subcutaneous and muscle tissue in the hind limb was examined in 6 dogs. It was found that during the first 2–3 h of anesthesia the vasoconstrictor response was present in both tissues although the response in muscle tissue exhibited a great variation between the dogs during this period. However, after 4–5 h of anesthesia the response was abolished in both tissues. During neurolept anesthesia with fentanyl/N₂O the same vasoconstrictor response was demonstrated in the hindleg 1 h and 5 h after induction of the anesthesia. It is concluded that pentobarbital anesthesia abolishes the arteriolar constriction induced by venous stasis. The mechanism may be blockade of the local sympathetic vasoconstrictor fibres or interference with myogenic vasoconstrictor mechanism of the vascular smooth muscle cells or both. It is suggested that fentanyl/N₂O anesthesia is better suited for this kind of studies.     

Neuropeptide Y (NPY): a vasoconstrictor in the eye,brain and other tissues in the rabbit

The effect of neuropeptide Y (NPY) on uveal vascular resistance was studied in rabbits by direct determination of uveal blood flow from a cannulated vortex vein. Regional blood flows, in the eye, the brain and several other tissues, were measured, with radioactive microspheres, during neuropeptide Y-infusion in rabbits with and without α-adrenoceptor blockade. Intravenous infusion of increasing doses of neuropeptide Y caused a dose-dependent increase in the total uveal vascular resistance. Maximal effect, a 70% increase, was achieved with 120 pmol kg^-1 min^-1. In the microsphere experiments, this dose rate was given i.v. over 10 minutes and blood flow determinations were made before and at 2 and 10 minutes after the start of the infusion. After 2 minutes of neuropeptide Y, there were marked blood flow reductions in the spleen, kidneys, adrenal glands, gastro-intestinal tract, choroid plexus and pineal and pituitary gland. The effect in the eye was small at 2 minutes, but at 10 minutes local blood flows in the choroid and the ciliary body were decreased by 50% and the iridal blood flow by 30%. Retinal blood flow was not affected by neuropeptide Y. At 10 minutes there were also significant blood flow reductions in the brain, tongue, masseter muscle and several glandular tissues. The effects of neuropeptide Y on local blood flow in rabbits that had been subjected to α-adrenoceptor blockade were very similar to the effects in the animals without α-adrenoceptor blockade. The results show that, in the rabbit, neuropeptide Y has marked effects on local blood flows in several tissues, including the eye, and suggest that neuropeptide Y may significantly contribute to the uveal vasoconstriction during sympathetic nerve stimulation.     

Local blood flow in the thalamus and frontal cortex in alert and narcotized dogs

The magnitude of the local blood flow in the thalamus and cerebral cortex is studied on 22 sexually mature nonpedigree dogs. Mean values of local blood flow are obtained in alert animals, and the effect of narcosis (nitrous oxide) on the local cerebral blood flow is studied. The mean local blood flow in alert dogs is found to be 84.8±2.9 ml/100 g/min in the cerebral cortex and 68.7±1.6 ml/100 g/min in the thalamus. Insignificant fluctuations are found during a dynamic recording of the local blood flow during 7 days. Under narcosis (70% nitrous oxide) the local blood flow decreases 3–12%. According to the findings, nitrous oxide narcosis does not significantly affect the brain circulation, so that it is suitable for an experimental study of the latter.Translated from Fiziologicheskii Zhurnal SSSR imeni I. M. Sechenova, Vol. 73, No. 10, pp. 1321–1324, October, 1987.     

Intra- and extravascular volume changes in the human forearm after static hand grip exercise

Summary Studies have been conducted to evaluate intra- and extravascular volume changes and blood flow in the exercising human forearm by means of (1) combining plethysmographic and scintigraphic methods, (2) an indirect procedure using the relationship of blood flow and volume change from reactive hyperemia. A static hand grip exercise of 60% maximal voluntary contraction and 30 s duration increased the forearm volume by 3.03±0.65 ml/100 ml soft tissue, involving both the intra- and extravascular volume components. There is a quantitative and qualitative difference in the time course of change in these components, showing an extravascular part of about 50% for the 2-min postexercise value and a substantially slower rate of recovery. Experiments involving muscle work at intervals (50% maximal voluntary contraction, 30 s duration, 2-min intervals) caused a further increase in extravascular volume. Furthermore, the study suggests that the flow-volume relationship from reactive hyperemia may be considered to be available for the determination of local blood volume changes in exercise hyperemia. The results are discussed in connection with the influence of anaerobic muscle metabolism and conclusions referring to this are drawn about the use of plethysmographic methods.Supported by the Bundesinstitut für Sportwissenschaften, Köln     

Local blood flow in the dorsal hippocampus and cerebellar cortex in the offspring of iodine-deficient rats

Experimental studies demonstrated that hypothyroidism can lead to depressive behavior and that thyroid hormones can have antidepressant effects. Postnatal changes in local blood flow in the dorsal hippocampus and cerebellar cortex were studied in the offspring of rats kept in conditions of iodine deficiency at conception and throughout gestation. The data obtained from these studies showed that severe limitation of iodine intake before and during gestation leads to marked deficiency in the blood supply to both of these brain structures, though the decrease in local blood flow in the dorsal hippocampus was more marked. Addition of iodine to the diet of females prevented this deficit of blood flow in both structures. __________ Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 92, No. 3, pp. 292–298, March, 2006.     

Nicotine activation of neuronal nitric oxide synthase and guanylyl cyclase in the medulla increases blood flow of the common carotid artery in cats

Individual activation of nicotinic acetylcholine receptor (nAChR) or nitric oxide (NO) synthase in the dorsal facial area (DFA) increases blood flow of common carotid artery (CCA) supplying intra- and extra-cranial tissues. We investigated whether the activation of nAChR initiated the activation of NO synthase and guanylyl cyclase to increase CCA blood flow in anesthetized cats. Microinjections of nicotine (a non-selective nAChR agonist), or choline (a selective α7-nAChR agonist) in the DFA produced increases in CCA blood flow ipsilaterally. These increases were significantly reduced by pretreatment with NG-nitro-arginine methyl ester (l-NAME, a non-specific NO synthase inhibitor), 7-nitroindazole (7-NI, a relatively selective neuronal NO synthase inhibitor) or methylene blue (MB, a guanylyl cyclase inhibitor) but not by that with N5-(1-iminoethyl)-l-ornithine (l-NIO, a potent endothelial NO synthase inhibitor). Control microinjection with d-NAME (an isomer of l-NAME), artificial cerebrospinal fluid or DMSO (a solvent for 7-NI) did not affect resting CCA blood flow, nor did they affect nicotine- or choline-induced response. In conclusion, activation of nAChR, at least α7-nAChR, led to the activation of neuronal NO synthase and guanylyl cyclase in the DFA, which induced an increase in CCA blood flow.     

Regional cerebral blood flow in the frontal, parietal and occipital cortices increases independently of systemic arterial pressure during slow walking in conscious rats

Regional cerebral blood flow (rCBF) in the frontal, parietal and occipital cortices was measured using laser Doppler flowmetry during walking in conscious rats at moderate speed on a treadmill (4 cm/s) for a 30 s period. During walking rCBF increased in all these three cortices. The rCBF in the parietal cortex started to increase within a few seconds after the start of walking, and continued to increase 42 ± 16% (mean ± S.D.) until the end of walking. Within 90 s after walking had ceased, the increased rCBF returned to pre-walking basal levels. The rCBF responses in the frontal and occipital cortices were identical to that in the parietal cortex. Mean arterial pressure (MAP) in a caudal artery of the tail during walking was increased by about 10%. Injection of atropine (5 mg/kg, i.p.), a muscarinic cholinergic receptor antagonist that permeates the blood brain barrier (BBB), reduced the walking-induced increase in cortical rCBF, as determined by measurement of parietal rCBF, from 42 ± 12% to 28 ± 15%. However, injection of methylatropine (5 mg/kg, i.p.), a muscarinic cholinergic receptor antagonist that does not permeate the BBB, did not affect the response of rCBF. Neither drug affected the walking-induced response of MAP. Injection of mecamylamine (20 mg/kg, s.c.), a nicotinic cholinergic receptor antagonist that permeates the BBB, reduced the walking-induced increase in cortical rCBF from 47 ± 12% to 30 ± 12%. Injection of hexamethonium (20 mg/kg, s.c.), a nicotinic cholinergic receptor antagonist that does not permeate the BBB, did not affect the responses of rCBF. Both mecamylamine and hexamethonium decreased the resting basal MAP by about 50%, and abolished the walking-induced increase in MAP. It is suggested that the increase in cortical rCBF during walking, which is independent of MAP, is attributable to the walking-associated activation of cortical cholinergic nerves. Possible contribution of cholinergic neurons in the nucleus basalis of Meynert (NBM) to the walking-induced increase in cortical rCBF is discussed.     

The Effects of Fentanyl and Morphine on Local Blood Flow and Oxygen Tension in the Frontoparietal Cortex and Nucleus Accumbens of the Brain in White Rats

Studies on white rats showed that intraperitoneal administration of small doses of fentanyl (0.005 mg/kg) and morphine (1 mg/kg) decreased local blood flow and increased partial pressure of oxygen (pO2) in the frontoparietal area of the cerebral cortex but had the opposite effects in the nucleus accumbens--where there was a significant increase in local blood flow and just as significant a decrease in pO2. Analysis of the data led to the conclusion that these changes must result from significant changes in functional-metabolic activity in these structures, induced by intraperitoneal administration of fentanyl or morphine.