The effect of clonidine on adrenal sympathetic nerve responses to mechanical, noxious and innocuous stimulation of the skin in rats

The effect of clonidine on the reflex responses of the adrenal sympathetic nerve to mechanical stimulation of the lower chest skin was studied in anesthetized CNS intact and spinalized rats. Clonidine (3-120 micrograms/kg i.v.) administration resulted in a dose-related decrease in spontaneous adrenal efferent nerve activity in both CNS intact and spinalized rats. In CNS intact rats, noxious pinching caused a reflex increase in adrenal nerve activity while innocuous brushing caused a reflex decrease. In both cases, clonidine reduced the reflex response in a dose-dependent manner. In spinalized rats, both noxious and innocuous stimulation caused reflex increases in adrenal nerve activity, and clonidine produced a similar dose-dependent decrease in these responses as seen in CNS intact animals. The similar dose-response relationships for adrenal nerve tone or reflex response in CNS intact and spinalized animals suggest, although not conclusively, that at least some of clonidine's effect in CNS intact animals may be mediated at the spinal level.     

Responses of adrenal sympathetic nerve activity and catecholamine secretion to cutaneous stimulation in anesthetized rats

Reflex effects of cutaneous mechanical stimulation on adrenal sympathetic efferent nerve activity and secretion rates of the adrenal medullary hormones (epinephrine and norepinephrine) were studied in anesthetized rats. Noxious pinching stimulation of the lower chest or hindpaw skin for 3 min produced proportional reflex increases in both the nerve activity and secretion rates of epinephrine and norepinephrine from the adrenal medulla in animals with an intact central nervous system. However, lower chest stimulation elicited a longer lasting response than hindpaw stimulation, 7-17 min vs 1 min after cessation of the stimulation, respectively. After spinal transection at the C1-2 level, only lower chest stimulation was capable of producing a reflex response, lasting 1 min after cessation of the stimulation. Contrary to the responses elicited by pinching, non-noxious brushing stimulation of the lower chest or hindlimb skin for 3 min in animals with an intact central nervous system produced proportional reflex decreases in nerve activity and epinephrine and norepinephrine secretion rates during the stimulation period only. Some slight increases in both nerve activity and secretion rates, lasting several minutes, followed cessation of the stimulation. However, in spinalized animals, non-noxious lower chest or hindlimb stimulation produced opposite effects, increasing both the nerve activity and secretion rates of epinephrine and norepinephrine. In spinalized animals lower chest brushing stimulation elicited a much stronger response than hindlimb brushing stimulation. It was concluded that; (1) the secretion of adrenal medullary hormones can be controlled reflexly by mechanical cutaneous stimulation through the central nervous system via adrenal sympathetic efferent nerves; (2) the excitatory effect of the cutaneo-adrenal medullary reflexes was independent of noxious or non-noxious stimulation at the spinal level, whereas in rats with an intact central nervous system the effect was either excitatory or inhibitory in response to noxious or non-noxious stimulation, respectively; (3) there is a marked segmental organization of this reflex at the spinal level which is modified into a generalized response through supraspinal central structures.     

Responses of blood pressure and renal sympathetic nerve activity to colorectal distension in anesthetized rats

We investigated the effects of visceral stimulation by colorectal distension (CRD) on mean arterial blood pressure (MAP) and renal sympathetic nerve activity (RSNA), the latter being an index of vasoconstrictor activity, in anesthetized central nervous system (CNS)-intact and C2 spinalized rats. The CRD stimulation was induced by the distention of a balloon inserted into the colorectum. In CNS-intact rats, there were significant reductions in MAP and RSNA in response to intraballoon pressures of 60 and 80 mmHg, but not to 20 and 40 mmHg. However, spinalized rats demonstrated significant increases in MAP in response to intraballoon pressures of 60 and 80 mmHg and increases in RSNA in response to intraballoon pressures of 40, 60, and 80 mmHg. These results suggest that noxious visceral stimulation at lower spinal levels reduces MAP by inhibiting sympathetic output in CNS-intact anesthetized rats. On the other hand, noxious visceral stimulation results in an increase in sympathetic-induced MAP in spinalized anesthetized rats.     

Reflex responses evoked in the adrenal sympathetic nerve to electrical stimulation of somatic afferent nerves in the rat

The present study was initiated to determine the role of somatic A (myelinated) and C (unmyelinated) afferent fibers in both responses of increases and decreases in adrenal sympathetic nerve activities during repetitive mechanical pinching and brushing stimulations of the skin in anesthetized rats with central nervous system (CNS) intact. Accordingly, changes in adrenal sympathetic nerve activity resulting from repetitive and single shock electrical stimulation of various spinal afferent nerves, especially the 13th thoracic (Th13) spinal nerve and the sural nerve, were examined in urethane/chloralose-anesthetized rats. Repetitive electrical stimulation of A afferent fibers in Th13 spinal or sural nerve decreased the adrenal nerve activity similarly as brushing stimulation of skin of the lower chest or hindlimb did, while repetitive stimulation of A plus C afferent fibers of those nerves increased the adrenal nerve activity as pinching stimulation of those skins did. Single shock stimulation of spinal afferent nerves evoked various reflex components in the adrenal nerve: an initial depression of spontaneous activity (the early depression); the following reflex discharge due to activation of A afferent fibers (the A-reflex); a subsequent reflex discharge due to activation of C afferent fibers (the C-reflex); and following post-excitatory depressions. These reflexes seem to be mediated mainly via supraspinal pathways since they were abolished by spinal transection at the C1-2 level. Although the supraspinal A- and C-reflexes could be elicited from stimulation of a wide variety of spinal segmental afferent levels, the early depression was more prominent when afferents at spinal segments closer to the level of adrenal nerve outflow were excited. It is suggested that the decreased responses of the adrenal nerve during repetitive electrical stimulation of A afferent nerve fibers are attributable to summation of both the early depression and post-excitatory depression evoked by single shock stimulation, while the increased responses during repetitive stimulation of A plus C afferent fibers are attributable to summation of the C-reflex after single shock stimulation. In spinalized rats, repetitive stimulation of Th13 always increased the adrenal nerve activities regardless of whether A fibers alone or A plus C fibers were stimulated, just as brushing and pinching of the lower chest skin always increased them. The increased responses in spinal animals seem to be related to the fact that single electrical stimuli of Th13 produced A- and C-reflexes of spinal origin without clear depressions.     

The articulo-cardiac sympathetic reflex in spinalized, anesthetized rats

Somatic afferent regulation of heart rate by noxious knee joint stimulation has been proven in anesthetized cats to be a reflex response whose reflex center is in the brain and whose efferent arc is a cardiac sympathetic nerve. In the present study we examined whether articular stimulation could influence heart rate by this efferent sympathetic pathway in spinalized rats. In central nervous system (CNS)-intact rats, noxious articular movement of either the knee or elbow joint resulted in an increase in cardiac sympathetic nerve activity and heart rate. However, although in acutely spinalized rats a noxious movement of the elbow joint resulted in a significant increase in cardiac sympathetic nerve activity and heart rate, a noxious movement of the knee joint had no such effect and resulted in only a marginal increase in heart rate. Because this marginal increase was abolished by adrenalectomy suggests that it was due to the release of adrenal catecholamines. In conclusion, the spinal cord appears to be capable of mediating, by way of cardiac sympathetic nerves, the propriospinally induced reflex increase in heart rate that follows noxious stimulation of the elbow joint, but not the knee joint.     

Functional role of lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex of the cat

The role of the lumbar sympathetic nerves and supraspinal mechanism in the defecation reflex was investigated in 30 adult cats and 6 kittens. One or two propulsive contractions, whose mean pressure evoked was more than about 90 cmH2O (adult cats) and 50 cmH2O (kittens), were induced in the rectum of all animals by rectal distension. These propulsive contractions could be generated at the descending and the transverse colons. The removal of the supraspinal influence by spinal transection at T13 or removal of pelvic afferents to the supraspinal center by spinal transection at L abolished the propulsive contractions. Successive lumbar sympathectomy restored the contractions. Lumbar sympathectomy and the successive removal of the supraspinal influence did not affect the propulsive contractions. In both cases, the final exclusion of the sacral segments by pithing of the spinal cord abolished the propulsive contractions. These results suggest that the sacral excitatory reflex mediated via pelvic nerves and the lumbar inhibitory reflex mediated via lumbar sympathetic nerves can function during rectal distension in spinal cats and that the lumbar inhibitory reflex is suppressed by the supraspinal sympathetic inhibitory reflex activated by pelvic afferents in intact cats, as in guinea pigs, resulting in propulsive contractions.     

Neural Mechanisms Involved in the Noxious Physical Stress-Induced Inhibition of Ovarian Estradiol Secretion

Stress is known to change the secretion of ovarian steroid hormones via the hypothalamic–pituitary–ovarian (HPO) axis. Noxious physical stress can cause reflex responses in visceral function via autonomic nerves. This article reviews our recent animal studies on neural mechanisms involved in ovarian estradiol secretion induced by noxious physical stress stimulation. In anesthetized rats, noxious physical stress (pinching the hindpaw or electrical stimulation of the tibial nerve) decreased ovarian estradiol secretion. These noxious stress-induced ovarian hormonal responses were observed after decerebration but were abolished after spinal transection. Electrical stimulation of the ovarian sympathetic nerves (superior ovarian nerves: SON) decreased ovarian estradiol secretion. The reduced secretion of ovarian estradiol induced by hindpaw pinching was abolished by bilateral severance of the SON. Efferent activity of the SON was increased following hindpaw pinching. Thus, the inhibition of ovarian estradiol secretion during noxious physical stress was mainly integrated in the brainstem, and this inhibitory response was due to reflex activation of sympathetic nerves to the ovary. In rats, the sympathetic inhibitory regulation of ovarian estradiol secretion was pronounced when the HPO axis was inhibited by chronic estradiol treatment. Considering the female life cycle, extensive physical stress may inhibit ovarian function, especially before puberty and during old ages when the HPO axis is inactive. Anat Rec, 302:904–911, 2019. © 2019 Wiley Periodicals, Inc.     

Reflex changes in heart rate after mechanical and thermal stimulation of the skin at various segmental levels in cats

Heart rate can be changed by cutaneous stimulation. In anesthetized cats with the central nervous system intact, a reflex increase in heart rate was elicited after natural stimuli such as pinching (noxious mechanical stimulation), rubbing (non-noxious mechanical stimulation), warming and cooling (thermal stimuli) were applied to the skin of the neck, chest, abdomen or perineum. It was shown that this cutaneo-cardiac acceleration reflex was produced mainly by a reflex increase in the discharges of the cardiac sympathetic efferent nerves and partially by a reflex decrease in the discharges of the cardiac vagal efferent nerves. On the other hand, in spinal cats, only stimulation of the chest and abdominal skin produced a reflex increase in heart rate. A possible explanation of this difference between central nervous system intact and spinal cats is that a spinal, segmentally organized component of the cutaneo-cardiac acceleration reflex is dominated by a supraspinal, diffusely distributed component in central nervous system intact cats.     

Enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with heart failure induced by adriamycin

Our previous studies have shown that the cardiac sympathetic afferent reflex is enhanced in rats with chronic heart failure(CHF) induced by coronary artery ligation and contributes to the over-excitation of sympathetic activity.We sought to determine whether sympathetic activity and cardiac sympathetic afferent reflex were enhanced in adriamycin-induced CHF and whether angiotensin II(Ang II) in the paraventricular nucleus(PVN) was involved in enhancing sympathetic activity and cardiac sympathetic afferent reflex.Heart failure was induced by intraperitoneal injection of adriamycin for six times during 2 weeks(15 mg/kg).Six weeks after the first injection,the rats underwent anesthesia with urethane and α-chloralose.After vagotomy and baroreceptor denervation,cardiac sympathetic afferent reflex was evaluated by renal sympathetic nerve activity and mean arterial pressure(MAP) response to epicardial application of capsaicin(1.0 nmol).The response of MAP to ganglionic blockade with hexamethonium in conscious rats was performed to evaluate sympathetic activity.The renal sympathetic nerve activity and cardiac sympathetic afferent reflex were enhanced in adriamycin rats and the maximum depressor response of MAP induced by hexamethonium was significantly greater in adriamycin rats than that in control rats.Bilateral PVN microinjection of angiotensin II(Ang II) caused larger responses of the cardiac sympathetic afferent reflex,baseline renal sympathetic nerve activity and MAP in adriamycin rats than control rats.These results indicated that both sympathetic activity and cardiac sympathetic afferent reflex were enhanced and Ang II in the PVN was involved in the enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with adriamycin-induced heart failure.     

Memory traces in primate spinal cord produced by operant conditioning of H-reflex

1. Study of memory traces in higher animals requires experimental models possessing well-localized and technically accessible memory traces--plasticity responsible for behavioral change, not dependent on control from elsewhere, and open to detailed investigation. Our purpose has been to develop such a model based on the wholly spinal, largely monosynaptic path of the spinal stretch reflex. Previous studies described operant conditioning of this reflex and of its electrical analog, the H-reflex. In this study, we sought to determine whether conditioning causes changes in the spinal cord that affect the reflex and are not dependent on continued supraspinal influence, and thus qualify as memory traces. 2. Sixteen monkeys underwent chronic conditioning of the triceps surae H-reflex. Eight were rewarded for increasing H-reflex amplitude (HR increases mode), and eight were rewarded for decreasing it (HR decreases mode). In each animal, the other leg was an internal control. Over several months of conditioning, H-reflex amplitude in the conditioned leg rose in HR increases animals and fell in HR decreases animals. H-reflex amplitude in the control leg changed little. 3. After HR increases or HR decreases conditioning, each animal was deeply anesthetized and surgically prepared. The reflex response to supramaximal dorsal root stimulation was measured from the triceps surae nerve as percent of response to supramaximal ventral root stimulation, which was the maximum possible response. Data from both legs were collected before and for up to 3 days after thoracic (T9-10) cord transection. The animal remained deeply anesthetized throughout and was killed by overdose. 4. The reflex asymmetries produced by conditioning were still present several days after transection removed supraspinal influence: reflexes of HR increases animals were significantly larger in HR increases legs than in control legs and reflexes of HR decreases animals were significantly smaller in HR decreases legs than in control legs. 5. Reflex amplitude was much greater in the control legs of anesthetized HR decreases animals than in the control legs of anesthetized HR increases animals. 6. Chronic conditioning had at least two effects on the spinal cord. The first effect, task-appropriate reflex asymmetry, was evident both in the awake behaving animal and in the anesthetized transected animal. The second effect, larger control leg reflexes in HR decreases than in HR increases animals, was evident only in the anesthetized animal. By removing supraspinal control, anesthesia and transection revealed a previously hidden effect of conditioning.(ABSTRACT TRUNCATED AT 400 WORDS)     

Interaction between the hypothalamic defence reaction and cardiac ventricular receptor reflexes.

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.     

Role and localization of a region in the pons which has a descending inhibitory influence on sympathetically mediated inhibition of the recto-rectal reflex of guinea pigs

The present study revealed the site of origin and the possible function of a supraspinal descending-inhibitory influence over the lumbar sympathetic component of the recto-rectal reflex of guinea pigs. The recto-rectal reflex contraction was not changed by suprapontine transection. It completely disappeared after subpontine transection, but returned immediately after additional section of the colonic nerves, which contain the sympathetic inhibitory outflow to the rectum, i.e., subpontine transection with the lumbar colonic nerves transected did not suppress the recto-rectal reflex. These results indicate that a descending pathway which can inhibit the lumbar sympathetic component of the reflex may originate in the pons. On stimulation at sites within the pons of animals which had been spinalized at L4 we were able to evoke an increase of rectal motility and an inhibition of the lumbar colonic efferent discharges, thus producing a response which is comparable to the reflex response produced by afferent stimulation of the rectum. The sites from which this effect could be evoked were mainly located in a band running rostrocaudally through the lateral reticular formation of the rostral part of the pons, medial to the sensory nucleus of the trigeminal nerve.     

Spinal and supraspinal components of the reflex discharges into lumbar and thoracic white rami

1. In chloralose anaesthetized cats reflex discharges in thoracic and lumbar white rami were elicited by single shock stimulation of intercostal, spinal and hind limb nerves.2. In animals with an intact neuraxis single stimuli of sufficient strength usually elicited a white rami mass discharge having two distinct components. Following spinal transection only the late reflex component disappeared.3. The early (spinal) reflex component had its largest amplitude if the afferent volley entered the spinal cord at the same or an adjacent segment of the white ramus under observation, whereas the size of the late (supraspinal) component was rather independent of the segmental level of the afferent input.4. It was concluded that somatic afferent volleys have a twofold action on the sympathetic nervous system: a more generalized action via the supraspinal sympathetic reflex centres and a more circumscribed action on the preganglionic neurones at the segmental level.     

Comparison of the effects on spinal reflexes of acetylsalicylate and metamizol in spinalized and normal rats

The effects of nonsteroidal antiinflammatory drugs, acetylsalicylate and metamizol, on spinal monosynaptic reflexes were investigated in spinalized and normal rats. Adult rats (n=36) weighing 150-200 g were anesthetized with ketamine and artificially ventilated. Half of rats were spinalized at C1 level. A laminectomy was performed in the lumbosacral region. Following electrical stimulation of the sciatic nerve by single pulses, reflex potentials were recorded from the ipsilateral L5 ventral root. Acetylsalicylate was administered orally (100 mg/kg for both spinalized and normal rats). Metamizol was administered intramuscularly (15 mg/kg for both spinalized and normal rats). These drug administrations significantly decreased the amplitude of reflex response in all groups (p < 0.05). These data verify that observed inhibition by acetylsalicylicate and metamizol may be at the level of spinal cord. Also we suggested that the cyclooxygenase products of arachidonic acid may play an important role in regulating the reflex potential.     

Differentiation of sympathetic activity at the spinal level in Response to central cold stimulation

Summary Thermally induced adjustments of skin blood flow in chronically spinalized dogs may occur without alterations of arterial pressure and heart rate. In lightly anesthetized rabbits with chronic spinal transection at the level of C₆/C₇, the question was investigated, whether the isolated spinal cord can produce differentiated changes of regional sympathetic activity as a response to central cold stimulation.Selective cooling of the thoraco-lumbar spinal cord in chronically spinalized rabbits induced an increase in vasoconstrictor tone of the ear skin vessels as indicated by a drop of ear skin temperature at constant core and ambient air temperatures. Simultaneously, a decrease of activity in a splanchnic nerve branch was observed. Arterial pressure and heart rate remained unaffected on the average. 24 h after spinal transection, this response seemed to be less pronounced than 3 or more days after the operation. The presented results show that the pattern of regional vasomotor responses induced by central cold stimulation is, on principle, identical in intact and chronically spinalized rabbits. Therefore, the vasomotor pattern described in spinalized animals seems to represent a thermoregulatory response mediated by a vicarious spinal control system.     

Mediation of reflex tachycardia becomes exclusively beta-adrenergic in old Fischer 344 rats

To study how baroreflex regulation changes with age we compared reflex heart rate responses elicited in awake Fischer 344 rats of different ages during intravenous infusions of phenylephrine or sodium nitroprusside. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Basal heart rates always tended to be lower in old than in young rats, but the differences became statistically significant only after beta-adrenergic or combined cholinergic and beta-adrenergic blockade. Most reflex heart rate responses (i.e. except reflex tachycardia in males during depressor responses to sodium nitroprusside) were initially weaker in old than in younger rats. Reflex bradycardia and tachycardia were reduced equally in both age groups after cholinergic blockade, but were reduced more in old than in young rats after beta-adrenergic blockade. beta-adrenergic blockade alone reduced reflex tachycardia as much as did combined blockade thereby suggesting that the predominant neural mechanism was beta-adrenergic. Taken altogether these results are compatible with the interpretation that efferent pathways for mediating heart rate reflexes in Fischer 344 rats are altered with age such that as parasympathetic mediation diminishes, residual mediation particularly of reflex tachycardia, becomes almost exclusively beta-adrenergic or sympathetic.     

Interaction between the Hypothalamic Defence Reaction and Cardiac Ventricular Receptor Reflexes

The interference with regard to the cardiovascular and gastric motility responses which follows stimulation of the hypothalamic defence area (D.A.) and a simultaneous afferent input from cardiac ventricular receptors was analysed in chloralose-anesthetized cats. In spinalized animals with only the vagal efferent innervation of autonomic effectors from supraspinal structures intact, a D.A. stimulation increased the heart rate to the same level irrespective whether the cardiac receptor afferents were stimulated or not. This suggests that the vagal component of the reflex bradycardia of cardiac receptor origin was completely suppressed by the D.A. stimulation. The reflex gastric relaxation to cardiac receptor activation, mediated via vagal efferent non-adrenergic fibres, was similarly completely blocked by D.A. stimulation. In contrast, the reflex inhibition of the sympathetic outflow to the heart and vessels from cardiac receptors was still effective during a D.A. stimulation, a phenomenon which seems compatible with a simple summation of excitatory D.A. and inhibitory cardiac receptor influences on the sympathetic neurons. The modifying influence from ventricular receptors on D.A. responses closely resembles that exerted by the arterial baroreceptors. The two reflex mechanisms thus work in concert and synergistically with the hypothalamic influences to produce maximal cardiac output and skeletal muscle perfusion without undue increases of pressure load on the pump during a defence reaction.     

Long term observation of micturition by spinal cord transected rabbits

Neurogenic bladder was observed in chronic spinalized animals. Since these animals are difficult to maintain for long periods, there are few reports of systemic study of these preparations. We have recently observed micturition by spinalized rabbits over a period of 4 weeks. In thoracic or lumbar spinalized rabbits, urinary bladder contraction and external urethral sphincter activity were initially recorded from 1-2 days postoperative. Contraction coincided with appearance of hind-limb spasticity. This micturition was the so-called detrusor-external urethral sphincter dyssynergy with residual urine. In sacral spinalized rabbits, no micturition reflex, external urethral sphincter activity, or hind-limb spasticity were observed and the flaccid state continued for 4 weeks. It is suggested that a segmental micturition reflex pathway exists initially in the rabbit sacral cord, because reappearance of the micturition reflex was extremely quick (1-2 days) compared to that of cats (2-3 weeks). Animal hypnosis enabled immobilization during measurement without anesthetic or decerebration. Chronic spinalized rabbits, which are very intolerant to spinal damage, can be maintained alive by intensive care at and post operation and are useful for systemic study of spinal cord injury.     

Enhanced sympathetic mediation of chronotropic baroreflexes in old Sprague-Dawley rats

We compared reflex heart rate responses elicited during intravenous infusions of phenylephrine or sodium nitroprusside in conscious 4- and 24-month-old male Sprague-Dawley rats to determine whether baroreflex regulation changes with age. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Basal blood pressures always tended to be higher, while corresponding heart rates were lower, in old than in young rats. Reflex bradycardia (but not tachycardia) was initially weaker in 24-month-old rats as were reductions in both reflex bradycardia and tachycardia after cholinergic blockade. On the other hand, the reduction in reflex tachycardia following beta-adrenergic blockade in old rats was more pronounced and almost equal to that produced by combined cholinergic and beta-adrenergic blockade. From these results we conclude that with old age in male Sprague-Dawley rats, just as has been shown previously in Fischer 344 rats, predominant efferent pathways for regulating heart rate reflexes are also altered to become almost exclusively beta-adrenergic or sympathetic.     

Cutaneous Mechanical Stimulation Regulates Ovarian Blood Flow via Activation of Spinal and Supraspinal Reflex Pathways in Anesthetized Rats

The reflex effects of noxious mechanical stimulation of a hindpaw or abdominal skin on ovarian blood flow, and the reflex pathways involved in those responses were examined in anesthetized rats. Blood flow in the left ovary was measured using a laser Doppler flowmeter, and the activity of the left ovarian sympathetic nerve and mean arterial pressure (MAP) of the common carotid artery were recorded. Stimulation of the left or right hindpaw for 30 s produced marked increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the left ovarian sympathetic nerves were severed, the same stimulus produced a remarkable monophasic increase in ovarian blood flow that was explained by passive vasodilation due to a marked increase in MAP. After spinal transection at the third thoracic (T3) level, the responses of MAP, ovarian sympathetic nerve activity, and ovarian blood flow to hindpaw stimulation were nearly abolished. Stimulation of the abdomen at the right or left side for 30 s produced slight increases in ovarian sympathetic nerve activity and MAP. Ovarian blood flow slightly decreased during the stimulation and then slightly increased after the stimulation. After the ovarian sympathetic nerves were severed, the response of the ovarian blood flow changed to a monophasic increase due to an increase in MAP. After spinal transection, stimulation of the left abdomen produced a moderate increase in MAP, a remarkable increase in ovarian sympathetic nerve activity and a slight decrease in ovarian blood flow during the stimulation. In contrast, stimulation of the right abdomen produced a smaller response in ovarian sympathetic nerve activity during the stimulation while it increased the MAP to a similar degree. Ovarian blood flow slightly increased after the end of stimulation, which was explained as passive vasodilation due to the increase in MAP. In conclusion, stimulation of somatic afferents affects ovarian blood flow by inducing changes in ovarian sympathetic nerve activities and blood pressure. When stimulation was applied to a hindpaw whose segment of afferent input is far from the segment of the ovarian sympathetic nerves, it took a supraspinal reflex pathway. However, when stimulation was applied to the abdomen whose spinal segment of the afferent is close to the segment of the ovarian sympathetic nerve output, there are spinal segmental reflex pathways. The present results demonstrate that spinal reflexes depend on the laterality of the stimulus, while supraspinal reflexes do not depend on the laterality of the stimulus.