Biomedical subjects

Robert D Foreman

Publications and source records attributed to Robert D Foreman.

At least 37 records · Page 2Linked to original sources

PubMed2003

Responses and afferent pathways of C1-C2 spinal neurons to cervical and thoracic esophageal stimulation in rats.

Because vagal and sympathetic inputs activate upper cervical spinal neurons, we hypothesized that stimulation of the esophagus would activate C(1)-C(2) neurons. This study examined responses of C(1)-C(2) spinal neurons to cervical and thoracic esophageal distension (CED, TED) and afferent pathways for CED and TED inputs to C(1)-C(2) spinal neurons. Extracellular potentials of single C(1)-C(2) spinal neurons were recorded in pentobarbital-anesthetized male rats. Graded CED or TED was produced by water inflation (0.1-0.5 ml) of a latex balloon. CED changed activity of 48/219 (22%) neurons; 34 were excited (E), 12 were inhibited (I), and 2 were E-I. CED elicited responses for 18/18 neurons tested after ipsilateral cervical vagotomy, for 12/14 neurons tested after bilateral vagotomy and for 9/11 neurons tested after bilateral vagotomy and C(6)-C(7) spinal cord transection. TED changed activity of 31/190 (16%) neurons (28E, 3 I). Ipsilateral cervical vagotomy abolished TED-evoked responses of 5/12 neurons. Bilateral vagotomy eliminated responses of 2/4 neurons tested, and C(6)-C(7) spinal transection plus bilateral vagotomy eliminated responses of 2/2 neurons. Thus inputs from CED to C(1)-C(2) neurons most likely entered upper cervical dorsal roots, whereas inputs from TED were dependent on vagal pathways and/or sympathetic afferent pathways that entered the thoracic dorsal roots. These results supported a concept that C(1)-C(2) spinal neurons play a role in integrating visceral information from cervical and thoracic esophagus.

Afferent Pathways↗

PubMed2003

Afferent pathways and responses of T3-T4 spinal neurons to cervical and thoracic esophageal distensions in rats.

The purposes of this study were to (1) compare responses of T(3)-T(4) spinal neurons to thoracic and cervical esophageal distension (TED, CED) and (2) determine afferent pathways for esophageal input to these neurons. Extracellular potentials of single superficial and deeper T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Graded TED or CED was produced by water inflation (0.1-0.5 ml) of a latex balloon. TED changed activity of 121/432 (28%) neurons (114 were excited); CED activated 69/269 (26%) neurons (56 were excited). Of 151 neurons that were tested for responses to both TED and CED, 40 (26%) neurons responded to both TED and CED. Mean duration of excitatory responses in convergent neurons to TED was significantly longer than the duration of responses to CED (31.4+/-2.8 vs. 25.4+/-1.0 s, n=34, P<0.05). A total of 105 out of 121 (87%) and 66 out of 69 (96%) neurons responsive to TED and CED had somatic fields. Spinal transection at rostral C(1) and at C(7)-C(8) indicated that excitatory responses to TED resulted from activation of afferent input that entered thoracic spinal segments; whereas, excitatory responses to CED resulted from afferent inputs entering cervical or thoracic spinal segments. These data showed that the upper thoracic spinal cord received sensory information from the esophagus through cervical and/or thoracic spinal visceral afferent pathways.

Afferent Pathways↗

PubMed2003

Spinal neuronal responses to urinary bladder stimulation in rats with corticosterone or aldosterone onto the amygdala.

Elevating glucocorticoids in the amygdala produces colorectal hypersensitivity through activation of lumbosacral spinal neurons. The aim of this study was to determine if descending modulation from the amygdala affects spinal processing of input from urinary bladder afferents. Fischer-344 rats received cholesterol (inactive control)-, corticosterone-, or aldosterone-containing micropellets placed stereotaxically on the dorsal margin of the left and right amygdala (n = 10 for each group). Seven days after amygdaloid implantation, extracellular potentials of single L6-S1 spinal neurons were examined for the responses to graded (0.5-2.0 ml, 20 s) urinary bladder distension (UBD). Spontaneous activity of neurons with excitatory responses to UBD in aldosterone-implanted rats [11.0 +/- 1.7 (SE) imp/s], but not in corticosterone-implanted rats, was higher than in the cholesterol-implanted group (6.6 +/- 1.1 imp/s, P < 0.05). Noxious UBD (1.5 ml) produced a greater excitatory response (21.6 +/- 2.6 imp/s) in aldosterone-implanted rats compared with cholesterol- or corticosterone-implanted rats (15.1 +/- 1.5 and 13.6 +/- 1.4 imp/s; P < 0.05). In contrast, the duration of excitatory responses to UBD in corticosterone-implanted rats (38.5 +/- 3.4 imp/s) was significantly longer than those in the aldosterone or control groups (26.8 +/- 1.8 and 24.7 +/- 1.5 imp/s). Neurons with low thresholds for excitatory responses to UBD were seen more frequently in aldosterone-implanted rats than in corticosterone or cholesterol treated rats (74 vs. 44% and 39%, P < 0.05). No difference in somatic field properties of spinal neurons responsive or nonresponsive to UBD was found among the three groups. These findings suggest that both mineralocorticoid- and glucocorticoid-mediated mechanisms in the amygdala are involved in descending modulation to lumbosacral spinal neurons receiving inputs from the urinary bladder; and this mechanism may play a role in the activation and maintenance of primary central sensitization to noxious visceral stimuli.

Action Potentials↗

PubMed2003

Effects of urinary bladder distension on activity of T3-T4 spinal neurons receiving cardiac and somatic noxious inputs in rats.

The aims of this study were to examine effects of urinary bladder distension (UBD) on T(3)-T(4) spinal neurons receiving cardiac and somatic noxious inputs and to determine the pathway involved in transmitting urinary bladder inputs to thoracic spinal segments. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized male rats. Either bradykinin solution (10(-5) M) or an allogenic mixture (adenosine 10(-3) M, bradykinin, histamine, serotonin, prostaglandin E2 10(-5) M each) was administered intrapericardially. UBD was produced by saline inflation (0.5-2.0 ml, 20 s). Of 487 neurons tested for responses to UBD, 70 were inhibited and 37 were excited. Seventy-six out of 336 neurons received convergent input from UBD and heart; 69/76 viscerovisceral convergent neurons had somatic fields. Spinal transection at rostral C(1) abolished UBD inhibition in 5/9 neurons; whereas transections at L(1)-L(2) abolished UBD inhibition in 3/3 cells tested. Results showed that T(3)-T(4) spinal neurons processing cardiac and somatic nociceptive information were primarily inhibited by input from the urinary bladder through either supraspinal structures or direct intraspinal pathways.

Action Potentials↗

PubMed2003

Cardiopulmonary sympathetic and vagal afferents excite C1-C2 propriospinal cells in rats.

The purpose of this study in anesthetized rats was to determine the effects of stimulating cardiopulmonary sympathetic afferents (CPSA) and vagal afferents on C1-C2 descending propriospinal neurons. We hypothesized that inhibition of spinal sensory neurons produced by CPSA or vagus activation might relay in C1-C2 spinal segments. Extracellular action potentials were recorded from 73 C1-C2 neurons whose axons were antidromically activated in lumbar segments. CPSA input excited 22 cells, inhibited two cells and excited/inhibited one cell, whereas vagal input excited eight cells and inhibited two cells. Results are consistent with the hypothesis that CPSA input can be processed in C1-C2 segments to produce neural modulation in distant spinal segments.

Action Potentials↗

PubMed2003

Responses and afferent pathways of C(1)-C(2) spinal neurons to gastric distension in rats.

Some evidence shows that the upper cervical spinal cord might play an important role in propriospinal processing as a sensory filter and modulator for visceral afferents. The aims of this study were to determine (1). the responses of C(1)-C(2) spinal neurons to gastric distension and (2). the relative contribution of vagal and spinal visceral afferent pathways for transmission of gastric input to the upper cervical spinal cord. Extracellular potentials of single C(1)-C(2) spinal neurons were recorded in pentobarbital anesthetized male rats. Graded gastric distension (20-80 mm Hg) was produced by air inflation of a latex balloon surgically placed in the stomach. Sixteen percent of the neurons (32/198) responded to gastric distension; 17 neurons were excited and 15 neurons were inhibited by gastric distension. Spontaneous activity of neurons with inhibitory responses was higher than those neurons with excitatory responses (18.1+/-2.7 vs. 3.8+/-1.7 impulses s(-1), p<0.001). Twenty-eight of thirty-two (87.5%) neurons responded to mechanical stimulation of somatic fields on head, neck, ears or shoulder. Most lesion sites of neurons with excitatory responses were found in laminae V, VII; however, neurons with inhibitory responses were in laminae III, IV. Bilateral cervical vagotomy abolished responses of 4/8 neurons tested. Spinal transection at C(6)-C(7) abolished responses of the other four neurons that still responded to gastric distension after bilateral vagotomy. Results of these data supported the concept that a group of C(1)-C(2) spinal neurons might play a role in processing sensory information from the stomach that travels in vagal and spinal visceral afferent fibers.

Afferent Pathways↗

PubMed2003

Local cooling alters neural mechanisms producing changes in peripheral blood flow by spinal cord stimulation.

This study was performed to investigate the respective role of sensory afferent and sympathetic fibers in peripheral vasodilatation induced by spinal cord stimulation at different hindpaw skin temperatures. Cooling the skin was used as a strategy to enhance sympathetic activity [Am. J. Physiol.: Heart Circ. Physiol. 263 (1992) H1197]. Cutaneous blood flow in the footpad of anesthetized rats was recorded using laser Doppler flowmetry. Local cooling (<25 degrees C) or moderate local cooling (25-28 degrees C) of the hindpaw was produced with a cooling copper coil. Spinal cord stimulation delivered at clinically relevant parameters and with 30%, 60%, and 90% of motor threshold induced the early phase of vasodilatation in the cooled and the moderately cooled hindpaw. In addition, spinal cord stimulation at 90% of motor threshold produced the late phase of vasodilatation only in the cooled hindpaw, which was possible to block by the autonomic ganglion-blocking agent, hexamethonium. The early responses to spinal cord stimulation in the moderately cooled hindpaw were not affected by hexamethonium. In contrast, both the early and the late phase responses were eliminated by CGRP (8-37), an antagonist of the calcitonin gene-related peptide receptor. After dorsal rhizotomy, spinal cord stimulation at 90% of motor threshold elicited hexamethonium-sensitive vasodilatation in the cooled hindpaw (late phase). These results suggest that spinal cord stimulation-induced vasodilatation in the cooled hindpaw (<25 degrees C) is mediated via both the sensory afferent (early phase of vasodilatation) and via suppression of the sympathetic efferent activity (late phase) although the threshold for vasodilatation via the sympathetic efferent fibers is higher than that via sensory nerves. In contrast, vasodilatation via sensory afferent fibers may predominate with moderate temperatures (25-28 degrees C). Thus, two complementary mechanisms for spinal cord stimulation-induced vasodilatation may exist depending on the basal sympathetic tone.

Animals↗

PubMed2003

Visceromotor and spinal neuronal responses to colorectal distension in rats with aldosterone onto the amygdala.

Stereotaxic delivery of corticosterone onto the amygdala produces colorectal hypersensitivity through activation of lumbosacral spinal neurons. Since corticosterone activates both the mineralocorticoid (MR) and glucocorticoid (GR) receptors, the aim of this study was to determine the importance of MRs in the regulation of colorectal hypersensitivity through the use of aldosterone that preferentially binds to MRs. Fischer-344 rats received either aldosterone (n = 18)- or cholesterol (control, n = 18)-containing micropellets bilaterally placed stereotaxically on the dorsal margin of the amygdala. After 1 wk, colorectal sensitivity to distension (30 mmHg) was measured in a subgroup of rats (n = 8/group). In other rats (n = 10/group), extracellular potentials of single L6-S1 spinal neurons in response to colorectal distension (CRD; 10-80 mmHg) were recorded. In aldosterone-implanted rats, CRD produced a greater visceromotor behavioral response compared with cholesterol controls (19 +/- 0.5 vs. 11.5 +/- 2.7; P < 0.01). A total of 68/182 (37%) and 56/167 (34%) of spinal neurons responded to noxious CRD in aldosterone-implanted and control groups, respectively. A total of 36/42 (86%) neurons excited by CRD had spontaneous activity in aldosterone-implanted groups compared with control (19/33, 58%, P < 0.01). Neurons with low thresholds for excitatory responses to CRD were seen more frequently in aldosterone-implanted rats than those in the control group (35/39 vs. 18/31, P < 0.05). Maximal excitatory responses of neurons to CRD in aldosterone-implanted rats were significantly greater (23.9 +/- 2.2 vs. 16.4 +/- 2.0 imp/s, P < 0.05), and the durations were longer (34.3 +/- 2.7 vs. 24.9 +/- 1.4 s, P < 0.05) than those in control group. Finally, a greater number of neurons had wide dynamic range responses to somatic stimulation in aldosterone-treated rats compared with cholesterol controls. Our findings suggest that, in the amygdala, MR receptor-mediated mechanisms are likely involved in descending pathways onto lumbosacral spinal neurons that induce colorectal hypersensitivity to luminal distension.

Aldosterone↗

PubMed2003

Attenuation by spinal cord stimulation of a nociceptive reflex generated by colorectal distention in a rat model.

The mechanisms underlying the cause and treatment of visceral pain of gastrointestinal origin are poorly understood. Previous clinical studies have shown that spinal cord stimulation (SCS) attenuates neuropathic and ischemic pain, and animal experiments have provided knowledge about probable physiological mechanisms. The goal of the present study was to investigate whether SCS influences colonic sensitivity in a conscious rat. A visceromotor behavioral response (VMR), induced by colorectal distention, was used to quantify the level of colonic sensitivity. Under anesthesia, an electrode (cathode) was placed on the dorsal surface of the spinal cord at L1. One week after implantation of the SCS electrode, the effects of stimulation delivered with different intensities (50 Hz, 0.2 ms for 30 min) on colonic sensitivity were determined. Nociceptive levels of colorectal distention (60 mm Hg for 10 min) induced an enhanced VMR quantified as an increased number of abdominal muscle contractions compared to controls in which the balloon catheter was inserted into the colorectal region but not distended. Colonic sensitization with acetic acid increased the VMR to innocuous levels of colorectal distention (30 mm Hg for 10 min). We found that SCS induced a significant depression of the VMR produced by colorectal distention in both normal rats and those with sensitized colons. The suppressive effect of SCS on colonic sensitivity suggests that SCS may have therapeutic potential for the treatment of visceral pain of gastrointestinal origin associated with abdominal cramping and painful abdominal spasms.

Animals↗

PubMed2003

Role of primary afferents in spinal cord stimulation-induced vasodilation: characterization of fiber types.

Selected patients with peripheral vascular disease can be treated with spinal cord stimulation (SCS) to improve blood flow in the limbs. However, the mechanisms producing these effects remain unclear. The present study was designed to investigate if SCS produces cutaneous vasodilation via antidromic activation of the unmyelinated C-fibers and/or the small myelinated fibers. SCS was applied to anesthetized rats with a ball electrode at the L2-L3 spinal level. In Protocol 1, effects of capsaicin were examined. Blood flow changes in the hindpaw induced by SCS were measured in the footpad with laser Doppler flowmeters. Topical application of capsaicin (1%) on the tibial nerve did not affect SCS-induced vasodilation at 30 and 60% of motor threshold (MT). However, the duration of vasodilation induced by SCS at 90% MT and at 10 times MT was significantly reduced after capsaicin application on the tibial nerve. In Protocol 2, antidromic compound action potentials (CAPs) of the tibial nerve were recorded in response to SCS. CAPs of the large and the small myelinated afferent fibers were observed in response to SCS at all intensities. However, even with SCS at ten times MT, CAPs of C-fibers could not be detected in the tibial nerve. In Protocol 3, antidromic CAPs of the dorsal root were measured in response to SCS. Antidromic CAPs of C-fibers in dorsal roots were evoked by SCS at >or=90% of MT. It is concluded that SCS-induced vasodilation at or=90% of MT may also involve antidromic activation of some unmyelinated C-fibers.

Action Potentials↗

PubMed2003

Chemical activation of cardiac receptors affects activity of superficial and deeper T3-T4 spinal neurons in rats.

The purposes of this study were to examine responses of superficial (depth <300 microm) and deeper thoracic spinal neurons to chemical stimulation of cardiac afferents and effects of descending influences on these neurons. Extracellular potentials of single T(3)-T(4) neurons were recorded in pentobarbital anesthetized, paralyzed and ventilated male rats. A catheter was placed in the pericardial sac to administer 0.2 ml of a mixture of algogenic chemicals that contained adenosine (10(-3) M), bradykinin, histamine, serotonin, prostaglandin E(2) (10(-5) M). Fifteen of 55 (27%) superficial neurons responsive to intrapericardial chemicals were compared to 80/169 (47%) deeper neurons. All 15 superficial neurons that responded to cardiac afferents were excited (E), whereas 66 deeper neurons were excited, ten were inhibited and four showed excitation-inhibition. Spontaneous activity of superficial neurons with short-lasting excitatory responses was significantly lower than that of deeper neurons (P<0.05). Somatic receptive fields on chest, axilla, arm and upper back areas were found for 77/95 (81%) neurons that responded to intrapericardial chemicals. The proportion of somatic field properties and their sizes in superficial neurons were similar to deeper neurons. After cervical spinal transection, both spontaneous activity and responses to chemical stimulation of cardiac afferents significantly increased in six out of six neurons excited by intrapericardial injections. Results showed that chemical stimulation of cardiac afferents excited superficial T(3)-T(4) spinal neurons, whereas deeper neurons exhibited multiple patterns of responses. Some characteristics of subgroups of superficial neurons were quantitatively different from deeper neurons. Thoracic spinal neurons processing cardiac nociceptive information were under tonic descending inhibition.

Afferent Pathways↗

PubMed2003

Combined sodium and calcium channel blockade in prevention of lethal arrhythmias.

Anti-arrhythmic compounds with multiple actions reduce arrhythmic death risk in post-myocardial infarction (MI) patients. Sudden death prevention, however, may rely more on implantable defibrillators than anti-arrhythmic drugs due to ineffective pharmacologic intervention. Widespread use of implantable defibrillators should not obscure the need for development of new anti-arrhythmic drugs. This study tested the hypothesis that combined blockade of I(Na) and I(Ca(L)) prevents ischemia-dependent ventricular fibrillation (VF) in conscious dogs after MI. I(Na) and I(Ca(L)) blockade was accomplished with levosemotiadil in 11 dogs known to be at high risk for VF during 2 min of coronary occlusion during submaximal treadmill exercise 30 days after MI. Negative chronotropic effect of levosemotiadil was examined using the heart rate response to isoproterenol and comparing it with response to propranolol. Levosemotiadil prevented VF in 64% (7 of 11) of the high-risk animals. Heart rate responses to myocardial ischemia and to graded doses of isoproterenol were blunted by the high dose of levosemotiadil. Propranolol prevented VF in 73% (8 of 11) of the dogs. Levosemotiadil had approximately one half the beta-blocking activity of propranolol. The combination of I(Na) and I(Ca(L)) channel blockade coupled with partial beta-adrenergic blockade was equally effective in preventing VF as propranolol.

Adrenergic beta-Antagonists↗

PubMed2003

Autonomic modulation during acute myocardial ischemia by low-dose pirenzepine in conscious dogs with a healed myocardial infarction: a comparison with beta-adrenergic blockade.

Experimental and clinical evidence documents the beneficial effects of blocking sympathetic activity and modulating heart rate to reduce risk for lethal events in ischemic heart disease. Beside beta-adrenergic receptor blockade, vagal activation is a meaningful approach but not yet easily attainable. Promising results were shown with low-dose atropine and scopolamine, but no follow-up was done because of significant adverse side effects. Pirenzepine is an atropine analogue approved to treat peptic ulcer disease in Europe that is devoid of central actions, which are mostly responsible for anti-muscarinic agents side effects. The vagomimetic action of IV low-dose pirenzepine was studied at rest under control conditions, at rest during acute coronary artery occlusion, and during exercise in conscious dogs with a healed anterior myocardial infarction (MI). The effects of pirenzepine were then compared, by internal control analysis, with those of atenolol (1 mg/kg). Increasing doses of pirenzepine (from 0.01 to 1 mg/kg) were tested in 11 dogs at rest by measuring time and frequency domain heart rate variability (HRV). The most effective dose (0.1 mg/kg) was used in the study. At the most effective dose, pirenzepine increased all measures of time domain HRV by 40-50%. However, the vagomimetic action of pirenzepine was lost during exercise and brief ischemia and no anti-arrhythmic action was observed. Conversely, pirenzepine effectively modulated the heart rate increase during acute ischemia at rest with an effect comparable to that of atenolol. The vagomimetic action of pirenzepine in the acutely ischemic heart supports the possibility that this intervention may be helpful for chronic autonomic modulation in post-MI patients.

Acute Disease↗

PubMed2003

Corticosterone acts directly at the amygdala to alter spinal neuronal activity in response to colorectal distension.

Administration of glucocorticoids to the amygdaloid nucleus facilitates visceromotor responses to colorectal distension in rats. The aim of this study was to determine if colorectal hypersensitivity develops through central modulation of spinal neuronal activity. Stereotaxic delivery of corticosterone (n = 10) or cholesterol (control, n = 10) onto the dorsal margin of the amygdala was performed on male Fischer-344 rats. Seven days later, extracellular potentials of single L(6)-S(1) spinal neurons were examined for responses to colorectal distension (CRD, 20-80 mmHg, 20 s) in sodium pentobarbital anesthetized and paralyzed animals. The proportions of neurons that responded to noxious CRD in corticosterone-implanted (62/186, 33%) and cholesterol-implanted (55/163, 34%) animals were virtually identical. However, the mean excitatory response of spinal neurons to CRD in corticosterone-treated rats was significantly greater (26.7 +/- 2.2 vs. 16.4 +/- 1.8 imp/s, P < 0.01) and the duration was longer (37.0 +/- 3.9 vs. 25.8 +/- 1.5 s, P < 0.05) than in the control group. No significant differences were found in neural responses to nonnoxious and noxious mechanical stimulation of somatic fields between corticosterone-implanted and control groups. In conclusion, our data support the hypothesis that central stimulation of the amygdala by corticosterone sensitizes the lumbosacral spinal neurons that mediate visceromotor reflexes to CRD.

Amygdala↗

PubMed2002

Differential effects of urinary bladder distension on high cervical projection neurons in primates.

Projection neurons located in high cervical segments of primates are generally excited instead of inhibited by cardiopulmonary spinal inputs, which enter thoracic dorsal roots. Thus, high cervical neurons with axons that either ascend to the thalamus or descend to thoracolumbar spinal segments can process and transmit excitatory cardiac information. The purpose of this study was to determine whether the excitatory effects observed to cardiopulmonary afferent stimulation are a universal response in high cervical projection neurons to spinal visceral inputs. Urinary bladder distension (UBD) was used to stimulate visceral afferent inputs that enter lumbosacral dorsal roots. Effects were determined on extracellular activity of either spinothalamic tract (STT) neurons or descending propriospinal neurons that were recorded in high cervical segments of anesthetized monkeys. Results showed that 17/34 STT neurons were inhibited by UBD and 3/34 STT neurons were excited. Widespread visceral inputs, therefore, can excite high cervical STT neurons but the majority of responsive STT neurons were inhibited by UBD. Effects of UBD on high cervical descending propriospinal neurons were significantly different from responses in STT neurons. Extracellular activity of fewer propriospinal neurons was affected by UBD and responses were more variable; 3/26 neurons were inhibited, 5/26 neurons were excited and one neuron was excited/inhibited by UBD. These results showed that the generally excitatory responses of high cervical projection neurons to cardiopulmonary inputs were not duplicated by stimulation of sensory input from the urinary bladder. Furthermore, results of this study indicated that effects of sensory inputs on spinal neurons might vary depending on axonal projections of the neurons examined.

Animals↗

PubMed2002

Convergent pathways for cardiac- and esophageal-somatic motor reflexes in rats.

Chest pain of esophageal and cardiac origin is often difficult to distinguish due to similar sensations and localization. We have shown that spasm-like contractions of the spinotrapezius muscles evoked by noxious cardiac stimulation could potentially sensitize muscle afferent fibers and produce angina-like referred pain. In this study, we proposed that a similar type of spinotrapezius contraction evoked by esophageal stimulation could produce nociceptive responses with similar quality and localization as evoked by cardiac stimulation. An objective of this study was to show convergence of pathways to the spinotrapezius muscles by measuring electromyographic (EMG) activity between the cardiac- and esophageal-motor reflexes. We also investigated afferent pathways of esophageal-motor reflexes by disrupting or activating the left sympathetic chain and vagus nerves; these pathways form the afferent limbs of the cardiac-motor reflexes. Results showed that more than 95% of animals responding to noxious cardiac stimulation also responded to esophageal distension. Transection of the left sympathetic chain to reduce upper thoracic visceral afferent innervation significantly decreased cardiac-evoked EMG activity or total motor unit potentials (t-MUP). In contrast, however, the transection did not significantly decrease t-MUP evoked by esophageal distension. Bilateral vagotomy and vagal afferent stimulation increased and decreased the cardiac-evoked t-MUP, respectively. However, the same vagal manipulations did not influence t-MUP evoked by esophageal distension. This study demonstrated that the spinotrapezius muscle could be activated by noxious stimulation of two different visceral organs. The spinotrapezius muscle contractions evoked by esophageal distension are produced in part by activation of esophageal afferent fibers found in upper thoracic sympathetic nerves, but not by activation of the vagus nerves.

Animals↗

PubMed2002

Spinal inhibitory effects of cardiopulmonary afferent inputs in monkeys: neuronal processing in high cervical segments.

Noxious stimulation of spinal afferents inhibits primate spinothalamic tract (STT) neurons in segments distant from the region of afferent entry. Inhibitory effects of cardiopulmonary sympathetic afferent (CPSA) stimulation remain after C(1) transection but disappear with spinal transection between C(3) and C(7). We hypothesized that spinal inhibitory effects produced by CPSA stimulation are processed by neurons in C(1)-C(3) segments. One purpose of this study in anesthetized monkeys was to determine whether chemical activation of high cervical neurons reduced sacral STT cell responses to colorectal distension (CRD) and urinary bladder distension (UBD). First, effects and interactions of pelvic and cardiopulmonary visceral afferent inputs were determined in 10 monkeys on extracellular activity of sacral STT neurons recorded in deep dorsal horn. CRD and UBD increased activity in 95 and 91% of sacral STT neurons, respectively. CPSA and cardiopulmonary vagal stimulation decreased activity in 84 and 56% of STT neurons, respectively. CPSA stimulation decreased CRD-evoked activity in six of eight sacral STT neurons and decreased UBD-evoked activity in five of eight STT neurons tested. Excitatory amino acid application at C2 segment decreased CRD-evoked responses in 7 of 10 sacral STT neurons and decreased UBD-evoked responses in 9 of 12 STT neurons. The second purpose of this study was to examine responses of C(1)-C(3) descending propriospinal neurons to stimulation of cardiopulmonary afferent fibers. If C(1)-C(3) neurons process CPSA input to suppress STT transmission, then CPSA stimulation should excite C(1)-C(3) neurons with descending projections. Effects of thoracic vagus nerve stimulation also were examined. Vagal stimulation inhibits STT neurons in segments below C(3) but excites C(1)-C(3) STT neurons; we theorized that vagal inhibition of sensory transmission might relay in high cervical segments and, therefore, excite C(1)-C(3) descending propriospinal neurons. Extracellular discharge rate was recorded for C(1)-C(3) neurons antidromically activated from thoracic or lumbar spinal cord in 24 monkeys. CPSA stimulation increased activity of 16 of 45 neurons and inhibited one cell. Thoracic vagus stimulation increased activity of 20 of 43 neurons and inhibited one cell; stimulation of abdominal vagus fibers did not affect activity of six of six cells that were excited by thoracic vagal input. Mechanical stimulation of somatic fields excited 30 of 41 neurons tested. All neurons activated by visceral input received convergent somatic input from noxious pinch of somatic receptive fields that generally included the neck and upper body; 11 C(1)-C(3) propriospinal neurons did not respond to any afferent input examined. Results of these studies were consistent with the idea that modulation of spinal nociceptive transmission might involve neuronal connections in high cervical segments.

Animals↗

PubMed2002

Upper thoracic respiratory interneurons integrate noxious somatic and visceral information in rats.

The aim of this study was to determine if thoracic respiratory interneurons (TRINs) might receive peripheral noxious somatic and visceral inputs. Extracellular potentials of 78 respiration-related T(3) neurons, whose activity was driven by central respiratory output, were recorded from the intermediate zone in pentobarbital anesthetized, paralyzed, and ventilated male rats. These neurons were identified as interneurons by their locations and by the absence of antidromic activation from the cervical sympathetic trunk and cerebellum. Thoracic esophageal distension (ED) was produced by water inflation of a latex balloon (0.1-0.5 ml, 20 s). A catheter was placed in the pericardial sac to administer 0.2 ml bradykinin (10(-5) M) for noxious cardiac stimulation. Of 78 TRINs examined for ED, activity of 24 TRINs increased and activity of 8 TRINs decreased. Intrapericardial bradykinin increased activity in 26/65 TRINs tested and decreased activity in 5 TRINs. Seventy-four TRINs were tested for effects of brush, pressure, and pinch of the chest and upper back areas. No TRINs responded to brushing hair. Low-threshold responses to pressure were observed in 27 TRINs. Fourteen TRINs were wide dynamic range and 4 TRINs had high-threshold responses. Peripheral stimuli affected all types of TRINs, including inspiratory, expiratory, and biphasic neurons. Simultaneous phrenic recordings showed that effects of various somatic and visceral stimuli on TRINs were independent of central respiratory drive. Various somatovisceral and viscerovisceral patterns of input were observed in TRINs. The results suggested that TRINs participate in intraspinal processing and integration of nociceptive information from somatic fields and visceral organs.

Animals↗