Vasomotor Changes Research Articles

REFLEX SYMPATHETIC DYSTROPHY OF THE HEAD

The case of a patient who was involved in a car crash is presented. On the right side her wrist and zygomatic arch were fractured. At both localizations she developed a painful syndrome. The diagnosis of reflex sympathetic dystrophy of her arm was made within 3 weeks after the injury and therapy instituted. The pain in her face and skull were accompanied by vasomotor changes which increased after exercise and by hypesthesia, hyperpathia, paresis, and hyperhidrosis. Disorders of the cranial nerves were excluded by physical examination and electromyography and structural disorders by CT scanning. The diagnosis reflex sympathetic dystrophy of the head was made one year after the injury. The problems in diagnosis are discussed.

Effect of sympathetic nervous system activation on the tonic vibration reflex in rabbit jaw closing muscles.

1. In precollicular decerebrate rabbits we investigated the effect of sympathetic stimulation, at frequencies within the physiological range, on the tonic vibration reflex (TVR) elicited in jaw closing muscles by small amplitude vibrations applied to the mandible (15-50 microns, 150-180 Hz). The EMG activity was recorded bilaterally from masseter muscle and the force developed by the reflex was measured through an isometric transducer connected with the mandibular symphysis. 2. Unilateral stimulation of the peripheral stump of the cervical sympathetic by the TVR, and a marked decrease or disappearance of the ipsilateral EMG activity. No significant changes were detected in the EMG contralateral to the stimulated nerve. Bilateral CSN stimulation reduced by 60-90% the force reflexly produced by the jaw closing muscles and strongly decreased or suppressed EMG activity on both sides. This effect was often preceded by a transient TVR enhancement, very variable in amplitude and duration, which was concomitant with the modest increase in pulmonary ventilation induced by the sympathetic stimulation. 3. During bilateral CSN stimulation, an increase in the vibration amplitude by a factor of 1.5-2.5 was sufficient to restore the TVR reduced by sympathetic stimulation. 4. The depressant action exerted by sympathetic activation on the TVR is mediated by alpha-adrenergic receptors, since it was almost completely abolished by the I.V. administration of either phentolamine or prazosin, this last drug being a selective antagonist of alpha 1-adrenoceptors. The sympathetically induced decrease in the TVR was not mimicked by manoeuvres producing a large and sudden reduction or abolition of the blood flow to jaw muscles, such as unilateral or bilateral occlusion of the common carotid artery. 5. The effect of sympathetic stimulation was not significantly modified after denervation of the inferior dental arch and/or anaesthesia of the temporomandibular joint, i.e. after having reduced the afferent input from those receptors, potentially affected by CSN stimulation, which can elicit either a jaw opening reflex or a decrease in the activity of the jaw elevator muscle motoneurons. 6. These data suggest that, when the sympathetic nervous system is activated under physiological conditions, there is a marked depression of the stretch reflex which is independent of vasomotor changes and is probably due to a decrease in sensitivity of muscle spindle afferents.

Modulatory effect of the renin-angiotensin system on the plasma levels of calcitonin gene-related peptide in normal man.

Calcitonin gene-related peptide (CGRP) has positive chronotropic and inotropic effects in animals and humans, and produces the most potent vasodilation known for an endogenous peptide. Yet, a physiological role for CGRP in the regulation of vascular tone and blood pressure has not been demonstrated. We studied the effects of 1) assumption of the upright position and 2) iv infusion of angiotensin-II (sequential doses of 8, 16, and 32 ng/kg.min, each dose for 20 min) in eight normal subjects (four men). Serial venous blood samples were taken to determine the plasma CGRP, epinephrine, norepinephrine, and aldosterone levels and PRA. Blood pressure and heart rate were continuously monitored at the finger with a Finapres 2300 instrument. After assumption of the upright posture, a quick rise in plasma CGRP levels was observed together with the expected increases in plasma norepinephrine and aldosterone and PRA. A transient increment was also observed for diastolic blood pressure and heart rate. Angiotensin-II infusion caused dose-dependent increases in plasma CGRP and aldosterone concentrations, already significant at the lowest infusion rate and parallel with the blood pressure rise. Plasma catecholamines significantly increased only at higher infusion rates. Our data demonstrate that modifications of plasma CGRP concentrations are part of the normal response to postural and vasomotor changes. These findings suggest a physiological role for CGRP in regulation of the peripheral vascular tone and possibly blood pressure in man.

The Effects of Preinduction Warming on Temperature and Blood Pressure during Propofol/Nitrous Oxide Anesthesia

Core temperature decreases rapidly after induction of anesthesia, largely because heat is redistributed to peripheral tissues. The hypothesis that warming peripheral tissues before induction of general anesthesia (prewarming) minimizes hypothermia was tested. Because circulating blood volume may be greater during exposure to heat compared to cold, the hypothesis that prewarming decreases the amount of hypotension associated with induction of anesthesia was tested also. Finally, the hypothesis that the difference between direct radial arterial blood pressure and blood pressure measured oscillometrically at the brachial artery depends on thermoregulatory and anesthetic conditions was tested. Each of six volunteers underwent general anesthesia (propofol and nitrous oxide) twice on the same day. Each anesthetic lasted 1 h and was preceded by either 2 h of active warming with forced air or 2 h of passive cooling by exposure to a typical operating room environment. After induction of each anesthetic, volunteers were fully exposed to the ambient environment. Volunteers recovered for 2 h before starting the second preinduction treatment. Initial tympanic membrane temperatures were similar before each preinduction treatment: 36.7 +/- 0.4 degrees C when volunteers were not warmed and 36.7 +/- 0.6 degrees C when volunteers were warmed. Tympanic membrane temperature did not change during the preinduction period without warming but increased slightly (delta T = 0.4 +/- 0.2 degree C) during warming. After induction of anesthesia, core temperatures decreased to 36.1 +/- 0.4 degree C over 1 h when volunteers were prewarmed but decreased to 34.9 +/- 0.4 degrees C when they were not. Radial arterial systolic, diastolic, and mean blood pressures were lower before induction of anesthesia when volunteers were warmed compared to when no warming was given. Oscillometric diastolic and mean pressures also were lower during prewarming; however, oscillometric systolic pressure did not differ significantly. Prewarming did not result in less hypotension after induction. Without warming, the difference (radial arterial minus oscillometric) in systolic blood pressure measurements was approximately 17 mmHg. Warming was associated with a reversal of the systolic pressure difference to approximately -6 mmHg. After induction of anesthesia, the differences in systolic and mean pressure measurements became more negative with respect to the preinduction values regardless of preinduction warming treatment. These data confirm our hypothesis that redistribution hypothermia can be minimized by preinduction warming of peripheral tissues. Prewarming decreases blood pressure but does not prevent subsequent hypotension after induction. The difference between radical arterial blood pressure and oscillometric blood pressure depends on thermoregulatory vasomotor changes but also may be influenced by vasodilation associated with administration of propofol and nitrous oxide.

Modulation of the jaw jerk reflex by the sympathetic nervous system.

The effect of sympathetic stimulation on the jaw jerk reflex has been studied in precollicular decerebrate rabbits. This reflex was elicited by a downward mandibular movement applied to the lower jaw through a servo controlled puller. Unilateral stimulation of the cervical sympathetic nerve at 10/s consistently induced a decrease in the JJR, i.e. a marked reduction of the EMG activity in the ipsilateral masseter muscle, accompanied by a 30-40% decrease in the reflexly developed force. In these trials EMG of the contralateral muscle, recorded as control, was not significantly affected. Bilateral stimulation of cervical sympathetic nerve strongly reduced or suppressed the EMG activity in both sides and produced a parallel decrease in the developed force which reached values ranging from 12.5% to 37.0% of controls (with an average of 28.9% +/- 8.9, S.D.). The effect of sympathetic stimulation was also tested on the contraction of the masseter muscle elicited by direct electrical stimulation. Sympathetic activation induced a modest increase in both amplitude and duration of muscle twitch, thus showing that the reduction in the reflex response can not be attributed to an action exerted by the adrenergic mediator on the muscular contraction. All these effects were almost completely abolished by the blockade of alpha-adrenergic receptors. They were proved not to be secondary to the sympathetically-induced vasomotor changes. Therefore the marked JJR reduction produced by activation of the sympathetic nervous system is suggested to be due to the sympathetically-induced decrease in neuromuscular spindle sensitivity to muscle length changes, previously reported.

Electroencephalogram and cardiovascular responses to noise during daytime sleep in shiftworkers.

Intermittent noise occurring during sleep has been found to induce heart rate, peripheral vasomotor and electroencephalogram (EEG) changes. This study analysed these responses during the daytime and night-time sleep of shiftworkers doing a three shift system, to determine the influence of the inversion of the sleep-wake cycle on the sensitivity to noise. A group of 14 shiftworkers [aged 37 (SD 5) years] underwent an habituation daytime sleep, two experimental daytime sleeps and a night-time sleep. Traffic noises were presented during sleep [truck, 71 dB(A); motorbike, 67 dB(A); and car, 64 dB(A)] at a rate of nine each hour. The EEG measurements of sleep, electrocardiogram and finger pulse amplitude were recorded continuously. The results were expressed by computing the percentage of observed cardiac response (%HRR) and vasoconstrictive response (%FPR), magnitude of heart rate variation (heart rate response; HRR), percentage of reduction of the digital blood flow (finger pulse response, FPR), cardiac cost (CC = % HRR x HRR) and vasomotor cost (VC = % FPR x FPR). The results showed that, compared to night-time sleep, there was change in the structure of daytime sleep, that is an increase in slow wave sleep (SWS), especially stage 4 sleep decrease of stage 2 and rapid eye movement (REM) sleep latencies, and an earlier SWS and REM sleep barycentric point. During daytime sleep the % FPR was significantly smaller in SWS than in stage 2 or REM sleep. Large differences were observed in % HRR, HRR and CC between daytime sleep stages (SWS less than stage 2 less than REM sleep).(ABSTRACT TRUNCATED AT 250 WORDS)

The causalgia-dystonia syndrome.

We report 18 patients (16 women and two men) with causalgia and dystonia, triggered by peripheral injuries in 15 cases and occurring spontaneously in three. The injury was often trivial, and did not cause overt peripheral nerve lesions. The mean age at presentation was 28.5 years. None had a family history of dystonia. The leg was affected initially in 12 patients, the arm in the remaining six cases. All had burning pain, allodynia and hyperpathia, along with vasomotor, sudomotor and trophic changes. All developed dystonic muscle spasms in the affected part. Dystonia always appeared at the same time or after the causalgia. The spasms were typically sustained, producing a 'fixed' dystonic posture, in contrast to the mobile spasms characteristics of idiopathic torsion dystonia. There was spread of the causalgia and of the dystonia from its initial site both in the affected limb and to other extremities, the latter in hemiplegic, transverse and triplegic distribution. All investigations were normal. All modes of conventional treatment failed to relieve either the pain or the dystonia, but two patients recovered spontaneously. At present it is impossible to decide whether this distressing syndrome is a true functional disorder of the central nervous system, or is of psychogenic origin.

Somatic sympathetic vasomotor changes documented by medical thermographic imaging during acupuncture analgesia.

Acupuncture is widely used for pain relief in many musculoskeletal disorders, and evidence suggests that modulation of the sympathetic nervous system responses which play an integral part in somatic pain, is an important mechanism of acupuncture action. This prospective study of 20 patients with neck and arm pain measured finger temperature, controlled by somatic sympathetic vasomotor activity before and after needle acupuncture. Responses were correlated with visual analogue scale (VAS) of pain severity. An association was found between pain relief and reduced sympathetic vasomotor activity. In 10 patients with significant reduction in visual analogue scale (VAS) pain (p less than .05), the mean change in temperature (delta t degrees C) was 0.55 (SD +/- 0.86) with significant difference in pre to post treatment temperatures (p less than .01). In 10 patients without significant pain relief on VAS scoring (p greater than .05), the mean t degrees C was 0.20 (SD +0.72) without significant difference in pre to post treatment temperatures (p greater than .05). The relevance of somatic sympathetic influences on musculoskeletal pain and modulation of sympathetic activity by acupuncture will be discussed.

Abnormal vasomotor changes early after coronary angioplasty. A quantitative arteriographic study of their time course.

To study the impact of percutaneous transluminal coronary angioplasty (PTCA) on coronary vasomotion, we prospectively analyzed spontaneous changes in coronary diameter and the response to the cold pressor test and intracoronary nitroglycerin in 11 patients subjected to successful single-vessel PTCA. All antianginal medications were stopped 48 hours before each study. The minimum diameter of the PTCA segment and the diameter of a distal segment in the angioplastied vessel and of a segment in a control vessel not manipulated by the balloon catheter or guide wire were measured by computerized edge detection immediately before PTCA and 5 minutes after, 4 hours after, and 8 days after PTCA. At 4 hours, PTCA and distal segments were constricted by 38 +/- 9% and 16 +/- 5%, respectively, compared with the values at 5 minutes (p less than 0.01). Before angioplasty, the cold pressor test caused vasoconstriction of PTCA and distal segments by 23 +/- 6% (p less than 0.0001) and 15 +/- 4% (p less than 0.008), respectively, but no constrictor response was elicited at 5 minutes or 4 hours after angioplasty. Eight days after PTCA, the basal coronary diameters were similar to those observed 5 minutes after PTCA and the response to the cold pressor test was similar to that observed before PTCA. All segments dilated significantly with nitroglycerin at all times, and no vasoconstriction changes were found in the control segments. Four hours after PTCA, transient spontaneous vasoconstriction of the PTCA and distal segments occurs, which is so intense that the cold pressor test does not cause any further constriction. These abnormalities resolve within 8 days of PTCA.

Loss of integrative control of peripheral circulation during desynchronized sleep

Regional blood flow (BF) changes during sleep were measured in rabbits at low, neutral, and high ambient temperatures (Ta) with radioactive microspheres. At both low and high Ta, peripheral vasomotor changes at the onset of desynchronized sleep (DS) were incompatible with thermoregulatory homeostasis. At low Ta, BF decreased in muscle (with the disappearance of shivering), whereas it increased in the arteriovenous anastomoses (AVA) and in the splanchnic bed. At high Ta, BF decreased in muscle (with the disappearance of panting) and in the AVA, whereas it increased in the splanchnic bed. An impaired central nervous regulation underlies the disruption of peripheral circulation patterns in this sleep stage. The lack of adaptive vasomotor adjustments in DS, which has little consequence in normal conditions, may become relevant in cardiovascular pathophysiology when BF redistribution through increased neurogenic vasomotor activity becomes a major compensating mechanism.

Reflex sympathetic dystrophy syndrome of the lower limbs in renal transplant patients treated with cyclosporin A

In a 36-month period, 240 patients at our institution received kidney transplants from cadaver donors. Cyclosporin A (CsA) was used as the initial immunosuppressive therapy. Seven patients (5 men and 2 women) developed severe pain, periarticular soft tissue swelling with no effusion, and vasomotor changes in affected areas. Although articular mobility was conserved, most of the patients had great difficulty in walking. A patchy osteoporotic pattern was seen radiographically and increased uptake of 99mtechnetium with a periarticular distribution in the clinically affected areas were found. All of these symptoms and radiographic and scintigraphic signs are compatible with definite reflex sympathetic dystrophy syndrome (RSDS). Articular symptoms began within 3 months after kidney transplantation in all patients; all but 1 patient had plasma CsA levels greater than 200 ng/ml at that time. When the dosage of CsA was reduced, there was concomitant improvement in the RSDS, which appeared when the plasma CsA levels declined to less than 200 ng/ml. The mean duration of the clinical symptoms of RSDS was 8 months. We believe RSDS should be added to the list of complications that may appear in kidney transplant patients who receive CsA treatment.

Posttraumatic reflex sympathetic dystrophy: Mechanisms and medical management

Reflex sympathetic dystrophy (RSD) refers to a symptom complex of posttraumatic pain associated with a wide and varying spectrum of vasomotor and neurologic changes. The diagnosis of reflex sympathetic dystrophy is made almost entirely on clinical grounds, and is often confirmed by observation of the results of diagnostic local anesthetic nerve blocks. Laboratory and radiographic investigations are useful adjuncts to diagnosis. The key to successful management is early recognition, as delays in treatment are associated with worse outcome. A multimodal approach to treatment is recommended that may include nerve blocks, rehabilitation, and pharmacologic and behavioral pain management. The role of other modalities including surgery and electrical stimulation remains controversial.

On the reliability of the Penaz cuff during systemic and local fingertip vasodilatation at rest and in exercise

To compare the readings of blood pressure by the Riva-Rocci (RR) method with those of peripheral arterial pressure (PAP) as recorded by the Finapres (FP) device, exercise was performed by six male subjects on a cycle ergometer at a constant exercise intensity of 140 W. In addition, forearm volume was determined by impedance plethysmography. At rest, systolic FP values exceeded RR values by greater than or equal to 10 mmHg. During 60-min exercise both values at first increased almost in parallel with each other. While RR reached a plateau after 3 min, FP then started to decrease continuously up to the 10th min and finally stabilized at 20-30 mmHg below RR. The impedance values showed a similar declining slope, indicating vasodilatation. To separate the effects of sympathetic drive from heat elicited vasodilatation, a second experimental series was performed with ischaemic static calf exercise (5 min, 90 N), since this increases the sympathetic tone but prevents systemic heat distribution. In contrast to findings reported from intra-arterial measurements, no exercise effect on the pulse pressure amplification was obtained. However, the heating of one fingertip distal to the FP-cuff led to a significant decrease in PAP compared to the control recording made simultaneously from the other hand. It was concluded that heat induced vasodilatation may make FP unrepresentative of systemic blood pressure, in particular during exercise. Moreover, the FP-cuff seemed to induce substantial vasoconstriction due to venous occlusion. The FP method would therefore be useful for monitoring continuously systemic blood pressure if no (dilative) vasomotor changes occurred or their ranges and time courses were known sufficiently well.

Differential sensitivity in the sites of fever production by prostaglandin E1 within the hypothalamus of the rat.

1. The febrile sensitivity of male Sprague-Dawley rats to microinjections of prostaglandin E1 (PGE) was investigated at three different locations in the rostromedial hypothalamic region. These were the preoptic anterior hypothalamic area (PO-AH), the organum vasculosum laminae terminalis (OVLT) and the rostral third ventricle (3V). 2. Stainless-steel cannula guide tubes were implanted in the OVLT region of one group of animals, within the PO-AH area of a second group and into the third ventricle of a third group of rats. After their recovery, the febrile response of each group was tested to a variety of doses of PGE, each administered in a volume of 1 microliter sterile 0.9% saline, via a sterile cannula inserted into the implanted guide tubes. Metabolic, vasomotor and rectal temperature changes were monitored continuously for the duration of the fevers. 3. Surprisingly, not only did the introduction of PGE into the OVLT region produce fevers, but the sensitivity of this region to PGE in the production of fever greatly exceeded that of the PO-AH area and the third ventricle. Fevers produced by microinjection of PGE into the PO-AH and 3V were identical. 4. Doses of PGE as low as 0.5 ng injected into the OVLT produced fevers of 0.5 degrees C. The fever dose threshold for the OVLT region was one-fifth those of the PO-AH area and the 3V, and the slope of the OVLT dose-response curve was twice those of the PO-AH and the 3V dose-response curves. 5. This study demonstrates that there is an anatomically distinct, regional sensitivity in the febrile responsiveness to PGE within the hypothalamus. These results are interpreted as evidence that the site of action of PGE in the production of fever is located within or immediately adjacent to the OVLT region, rather than within the medial PO-AH neuropil as has been believed previously.

Heparinase treatment suggests a role for the endothelial cell glycocalyx in regulation of capillary hematocrit

Physiological stimuli induce rapid and unexplained increases in the number of red blood cells within capillaries of skeletal muscle. We hypothesized that such alterations in intracapillary red cell numbers might be due to an undefined interaction between one or more components of blood and the luminal surface of the capillary. This proposition was tested by in situ microperfusion of capillaries with enzymes directed against macromolecules likely to be expressed on the surface of endothelial cells. The instantaneous fractional volume of red blood cells within a capillary (tube hematocrit) was used as an index of a capillary's response to enzyme microperfusion. Five to 8 min of perfusion with enzyme vehicle (0.25% albumin-Ringer solution) produced no significant alteration in capillary tube hematocrit. Perfusion with solutions containing heparinase raised the tube hematocrit at least twofold (P less than 0.05) without a significant change in red cell velocity. Heat-denatured heparinase and other enzymes such as neuraminidase, hyaluronidase, papain, pronase E, and clostripain had no detectable effect on the tube hematocrit (P greater than 0.05). After enzyme treatment, application of adenosine (10(-4) M) or oxygen caused brisk vasomotor responses in arterioles feeding perfused capillary units, but the usual changes in the tube hematocrit were not observed. Thus heparinase treatment results in a sustained elevation in the capillary tube hematocrit and a dissociation of the typical relationship between vasomotor changes and red cell distribution in capillaries. These findings suggest that physiological stimuli which alter the number of red blood cells within capillaries may operate by modifying interactions between plasma and one or more components on the luminal surface of capillaries.

The movement disorder of reflex sympathetic dystrophy

We present 43 patients with reflex sympathetic dystrophy (RSD) who manifested abnormalities of movement. The patients have focal dystonia, weakness, spasms, tremor, difficulty initiating movement, and increased tone and reflexes. These motor signs and symptoms may precede other manifestations of the illness by weeks or months. They most frequently, but not invariably, occur concomitantly with sudomotor or vasomotor changes and pain. Lioresal is effective in reducing spasms. Early in the course of RSD, the motor manifestation may be alleviated by intense sympathetic blockade or sympathectomy. In many patients, the movement disorder becomes independent of sympathetic innervation.

High and low doses of luteinizing hormone induce different changes in testicular microcirculation.

To study the effects of LH on total testicular blood flow and microcirculation, rats were treated with 2.5 or 25 micrograms LH sc and measurements were made on control rats and on LH-treated rats 1, 2, 3, 4, 6 and 12 h, after treatment. After treatment with 25 micrograms LH, total testicular blood flow, as measured with the radioactive microsphere method, was decreased at 6 h and increased at 12 h. Testicular microcirculatory blood flow was recorded with laser Doppler flowmetry and regular oscillations in blood flow, vasomotion, was observed in control rats. Vasomotion was not present 4 and 6 h after treatment with 25 micrograms LH, but returned at 12 h. Prior to and concomitantly with these changes in vasomotion, polymorphonuclear leukocytes accumulated in testicular microvessels and migrated into the interstitial tissue. These changes were followed, 6 h after treatment, by an increased vascular permeability, measured as increased testicular interstitial fluid volume. The lower dose of LH (2.5 micrograms), doubled plasma testosterone concentration and initially decreased interstitial fluid volume, and later induced a slight increase in blood vessel leukocytes. At the times studied, no changes could be observed in the other vascular parameters. In conclusion, it is suggested that LH, probably via some Leydig cell product, promotes regulatory effects on testicular microcirculation, but different magnitudes of LH stimulation induce different responses.

Comparison of finger and intra-arterial blood pressure monitoring at rest and during laboratory testing.

The accuracy of blood pressure values obtained by continuous noninvasive finger blood pressure recording via the FINAPRES device was evaluated by comparison with simultaneous intraarterial monitoring both at rest and during performance of tests known to induce fast and often marked changes in blood pressure. The comparison was performed in 24 normotensive or essential hypertensive subjects. The average discrepancy between finger and intra-arterial blood pressure recorded over a 30-minute rest period was 6.5 +/- 2.6 mm Hg and 5.4 +/- 2.9 mm Hg for systolic and diastolic blood pressure, respectively; a close between-method correspondence was also demonstrated by linear regression analysis. The beat-to-beat changes in finger systolic and diastolic blood pressure were on average similar to those measured intra-arterially during tests that induced a pressor or depressor response (hand-grip, cold pressor test, diving test, Valsalva maneuver, intravenous injections of phenylephrine and trinitroglycerine) as well as during tests that caused vasomotor changes without major variations in blood pressure (application of lower body negative pressure, passive leg raising). The average between-method discrepancy in the evaluation of blood pressure changes was never greater than 4.3 and 2.0 mm Hg for systolic and diastolic blood pressure, respectively; the corresponding standard deviations ranged between 4.6 and 1.6 mm Hg. Beat-to-beat computer analysis of blood pressure variability over the 30-minute rest period provided standard deviations almost identical when calculated by separate consideration of intra-arterial and finger blood pressure tracings (3.7 and 3.8 mm Hg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Cancer pain. Anatomy, physiology, and pharmacology.

Cancer pain can be divided into three classes: somatic, visceral, and deafferentation. Somatic and visceral pain result from activation of nociceptors by tumor infiltration of tissues and from secondary inflammatory changes with release of algesic chemicals that act to sensitize nociceptors. Pain may be experienced locally (somatic and visceral) or referred to remote cutaneous sites (visceral). Deafferentation pain results from injury to the nervous system due to tumor infiltration or cancer therapy and may persist even after the cause of the injury has been removed. Somatic, visceral, and deafferentation pain may be complicated by sympathetically maintained pain, in which efferent sympathetic activity promotes persistent pain, hyperpathia, and vasomotor and sudomotor changes after tissue injury from cancer or its therapy. The neurobiology of cancer pain is complex and incompletely understood. This article summarizes current knowledge in this area and briefly discusses approaches to cancer pain management that are based on this knowledge.

Chapter 16 Integration of cardiorespiratory responses in the ventrolateral medulla

Interventions confined to the region adjacent to the VMS can produce both respiratory and circulatory effects. Although it has been suggested that both breathing and vasomotor changes arise from the same neural elements near the VMS, our own investigations indicate that the neurons involved are closely linked but not identical. This belief is supported by recent studies which show that AII and angiotensin antagonists microinjected into the rostral portion of the VMS can significantly modify blood pressure and respiration but can produce effects of different sign. These observations, coupled with previous studies of the VMS, indicate the possibility that regions near the VMS may contribute to integration of circulatory and respiratory responses.