Biomedical subjects

R D Foreman

Publications and source records attributed to R D Foreman.

At least 37 records · Page 2Linked to original sources

PubMed1999

Correlation of ventricular mechanosensory neurite activity with myocardial sensory field deformation.

The mechanosensory activity generated by ventricular epicardial sensory neurites associated with afferent axons in thoracic sympathetic nerves was correlated with sensory field deformation (long axis, short axis, and transmural dimension changes), regional intramyocardial pressure, and ventricular chamber pressure in anesthetized dogs. Ventricular mechanosensory neurites generated activity that correlated best with strain developed along either the long or short axis of their epicardial sensory fields in most instances. Activity did not correlate normally to local wall thickness or to regional wall or chamber pressure development in most cases. During premature ventricular contractions, the activity generated by these sensory neurites correlated best with maximum strain developed along at least one sensory field epicardial vector. Identified sensory neurites were also activated by local application of the chemical bradykinin (10 microM) or by local ischemia. These data indicate that the activity generated by most ischemia-sensitive ventricular epicardial sensory neurites associated with afferent axons in sympathetic nerves is dependent on not only their local chemical milieu but on local mechanical deformation along at least one epicardial vector of their sensory fields.

Animals↗

PubMed1999

Chemical activation of cervical cell bodies: effects on responses to colorectal distension in lumbosacral spinal cord of rats.

We have shown that stimulation of cardiopulmonary sympathetic afferent fibers activates relays in upper cervical segments to suppress activity of lumbosacral spinal cells. The purpose of this study was to determine if chemical excitation (glutamate) of upper cervical cell bodies changes the spontaneous activity and evoked responses of lumbosacral spinal cells to colorectal distension (CRD). Extracellular potentials were recorded in pentobarbital-anesthetized male rats. CRD (80 mmHg) was produced by inflating a balloon inserted in the descending colon and rectum. A total of 135 cells in the lumbosacral segments (L(6)-S(2)) were activated by CRD. Seventy-five percent (95/126) of tested cells received convergent somatic input from the scrotum, perianal region, hindlimb, and tail; 99/135 (73%) cells were excited or excited/inhibited by CRD; and 36 (27%) cells were inhibited or inhibited/excited by CRD. A glutamate (1 M) pledget placed on the surface of C(1)-C(2) segments decreased spontaneous activity and excitatory CRD responses of 33/56 cells and increased spontaneous activity of 13/19 cells inhibited by CRD. Glutamate applied to C(6)-C(7) segments decreased activity of 10/18 cells excited by CRD, and 9 of these also were inhibited by glutamate at C(1)-C(2) segments. Glutamate at C(6)-C(7) increased activity of 4/6 cells inhibited by CRD and excited by glutamate at C(1)-C(2) segments. After transection at rostral C(1) segment, glutamate at C(1)-C(2) still reduced excitatory responses of 7/10 cells. Further, inhibitory effects of C(6)-C(7) glutamate on excitatory responses to CRD still occurred after rostral C(1) transection but were abolished after a rostral C(6) transection in 4/4 cells. These data showed that C(1)-C(2) cells activated with glutamate primarily produced inhibition of evoked responses to visceral stimulation of lumbosacral spinal cells. Inhibition resulting from activation of cells in C(6)-C(7) segments required connections in the upper cervical segments. These results provide evidence that upper cervical cells integrate information that modulates activity of distant spinal neurons responding to visceral input.

Action Potentials↗

PubMed1998

Propriospinal neurons in the C1-C2 spinal segments project to the L5-S1 segments of the rat spinal cord.

Physiological studies indicate that neurons in the upper cervical spinal cord have descending projections to the lumbosacral spinal cord and mediate inhibition of dorsal horn neurons activated from afferent input. In the present study, retrograde tracing techniques were used to examine the distribution of propriospinal neurons in C1-C2 spinal segments that project to lumbosacral spinal segments. Fluorogold or horseradish peroxidase were injected unilaterally or bilaterally into the L5-S1 spinal segments. After 2-4 days, rats were perfused with fixative and C1-C2 spinal segments were processed for retrograde labeling. Numerous neurons were found in the C1-C2 segments. In unilaterally and bilaterally injected rats, retrogradely labeled neurons were located on both the ipsilateral and contralateral sides. Retrogradely labeled neurons were located in the following locations: lateral cervical and spinal nuclei, nucleus proprius, ventral horn and the central gray region (area X). These studies demonstrate a descending projection from C1-C2 segments to the lower lumbar and sacral spinal cord. We hypothesize that many of these C1-C2 propriospinal neurons are important in modulating responses of spinal neurons at lower segmental levels to various peripheral stimuli.

Animals↗

PubMed1998

Phrenic nerve inputs to upper cervical (C1-C3) spinothalamic tract neurons in monkeys.

Afferent input from the phrenic nerve enters mid-cervical spinal segments, and previous results in monkeys show that mid-cervical spinothalamic (STT) neurons are activated by groups II and III phrenic afferent input arising from the diaphragm. In rats, dorsal horn neurons in C1-C2 segments receive phrenic input stimulated above the heart, but are not activated by phrenic input arising from diaphragm or abdomen. It is not known if this differential organization occurs in primate STT neurons. We hypothesized that high cervical STT neurons in monkeys also would be preferentially activated by phrenic inputs from thoracic structures, such as the pericardium. We examined extracellular discharge rate of C1-C3 STT neurons for responses to electrical stimulation of phrenic nerve fibers. Responses to stimulation of ipsilateral phrenic fibers above the heart were compared to effects of input stimulated below the heart and also to effects of contralateral phrenic input. We concluded that upper cervical STT neurons are most strongly excited by ipsilateral input from small diameter phrenic fibers arising from thoracic structures, but that group III and IV input from diaphragmatic fibers as well as input from contralateral phrenic fibers have a lesser effect on C1-C3 STT neurons and thus might be involved in nociceptive processing.

Afferent Pathways↗

PubMed1998

Antifibrillatory efficacy of ersentilide, a novel beta-adrenergic and Ikr blocker, in conscious dogs with a healed myocardial infarction.

OBJECTIVES: IKr blockade is ineffective in preventing ventricular fibrillation elicited by the interaction between acute myocardial ischemia and elevated sympathetic activity. This depends in part on the fact that adrenergic activation offsets more than 50% of the action potential prolonging effect of IKr blockade, and thus impairs its primary mechanism of action. This study examined the antifibrillatory effect of ersentilide (CK-3579), a novel antiarrhythmic agent which combines blockade of the rapid component of the delayed rectifier potassium channel (IKr) with relatively weak beta-adrenergic blockade, in a conscious canine model of lethal arrhythmias. METHODS: Ersentilide was tested in 19 dogs with a healed myocardial infarction (MI) undergoing two minutes of circumflex artery occlusion (CAO) during sub-maximal treadmill exercise. Epicardial monophasic action potential duration was measured before and after ersentilide in 8 anesthetized open chest dogs at baseline and during stimulation of the left stellate ganglion at constant paced heart rate. RESULTS: In the control tests 13 of the 19 dogs had ventricular fibrillation (VF) during the exercise and ischemia test, 6 did not. During a subsequent exercise test, ersentilide prevented VF in 85% (11 of 13) of the high risk animals and showed no proarrhythmic effects in the 6 dogs without arrhythmias in the initial test. Ersentilide lowered heart rate at all levels of exercise and during acute myocardial ischemia. The antifibrillatory effect was maintained in 3 of 4 dogs in which heart rate was kept at control levels by atrial pacing. Ersentilide prolonged left ventricular monophasic action potential duration by 30% (from 179 +/- 6 ms to 233 +/- 5 ms, p < 0.001) at a 360 ms cycle length and completely prevented its shortening during sympathetic stimulation. CONCLUSIONS: The combination of IKr and weak beta-adrenergic blockade, using ersentilide, represents a very effective and safe antiarrhythmic intervention able to overcome the limitations present in drugs devoid of any antiadrenergic effect. Such a combination may be very useful in the management of post-myocardial infarction patients at high arrhythmic risk.

Action Potentials↗

PubMed1998

Cardiopulmonary sympathetic input excites primate cuneothalamic neurons: comparison with spinothalamic tract neurons.

Stimulation of cardiopulmonary sympathetic afferent fibers excites thoracic and cervical spinothalamic tract (STT) cells that respond primarily to noxious somatic stimuli. Neurons in dorsal column nuclei respond primarily to innocuous somatic inputs, but noxious stimulation of pelvic viscera activates gracile neurons. The purpose of this study was to compare effects of thoracic visceral input on cuneothalamic and STT neurons. Stellate ganglia of 17 anesthetized monkeys (Macaca fascicularis) were stimulated electrically to activate cardiopulmonary sympathetic afferent fibers. Somatic receptive fields were manipulated with brush, tap, and pinch stimuli. Extracellular discharge rate was recorded for neurons antidromically activated from ventroposterolateral (VPL) thalamus. Stimulation of the ipsilateral stellate ganglion increased activity of 17 of 38 cuneothalamic neurons and of 1 gracilothalamic neuron with an upper body somatic field. Spinal cord transections showed that cardiopulmonary input to cuneothalamic neurons traveled in ipsilateral dorsal column and probably in dorsolateral funiculus. One of eight gracilothalamic neurons with lower body fields was inhibited by cardiopulmonary input, and none were excited. Stimulation of the ipsilateral stellate ganglion increased activity in 10 of 10 T3-T4 STT neurons. Evoked discharge rates, latencies to activation and durations of peristimulus histogram peaks were significantly less for cuneothalamic neurons compared with STT neurons. Furthermore, additional long latency peaks of activity developed in histograms for 6 of 10 STT neurons but never for cuneothalamic neurons. Contralateral cardiopulmonary sympathetic input did not excite cuneothalamic neurons but increased activity of 7 of 10 T3-T4 STT neurons. Most cuneothalamic neurons (24 of 31 cells tested) responded primarily to innocuous somatic stimuli, whereas STT neurons responded primarily or solely to noxious pinch of somatic fields. Neurons that responded to cardiopulmonary input most often had somatic fields located on proximal arm and chest. Results of this study showed that cardiopulmonary input was transmitted in dorsal pathways to cuneate nucleus and then to VPL thalamus and confirmed that STT neurons transmit nociceptive cardiopulmonary input to VPL thalamus. Differences in neuronal responses to noxious stimulation of cardiopulmonary sympathetic afferent fibers suggest that dorsal and ventrolateral pathways to VPL thalamus play different roles in the transmission and integration of nociceptive cardiac information.

Animals↗

PubMed1997

Cardiopulmonary sympathetic afferent input does not require dorsal column pathways to excite C1-C3 spinal cells in rats.

Effects of electrically stimulating the left stellate ganglion to activate cardiopulmonary sympathetic afferent (CPSA) fibers were determined on C1-C3 dorsal horn neurons in anaesthetized rats. Fifty-two of 53 dorsal horn neurons affected by CPSA stimulation were excited and one neuron was inhibited. In 6 experiments, dorsal columns and ventrolateral funiculi were sequentially lesioned to determine neuronal pathways involved in CPSA activation of C1-C3 neurons. In 6 additional experiments, spinal transection at rostral C1 was used to determine the contribution of supraspinal relays. We concluded that CPSA input to C1-C3 segments travelled bilaterally in ventrolateral pathways, and that supraspinal relays were not required for CPSA excitation of C1-C3 neurons. These results suggest that neurons in C1-C3 segments might play an important role in processing visceral spinal afferent information.

Afferent Pathways↗

PubMed1997

Classification of dorsal horn neurons based on somatic receptive fields in cats with intact and transected spinal cords: neural plasticity.

Classification of dorsal horn neurons based on cell activity responses to somatic receptive fields stimulation, was compared between anesthetized cats with transected or intact cords. Results showed a significant (P < or = 0.001) difference. In animals with transected cords, dorsal horn neurons responded with less specificity to noxious and innocuous stimulation. The results are consistent with the proposition that loss of supraspinal influences plays a significant role in determining response characteristics of dorsal horn neurons.

Animals↗

PubMed1997

Role of nitric oxide in cutaneous blood flow increases in the rat hindpaw during dorsal column stimulation.

OBJECTIVE: Dorsal column stimulation (DCS) increases blood flow to the extremities and may produce a limb-saving effect in addition to treatment of refractory chronic pain in patients with peripheral vascular disease. The purpose of this study was to examine the importance of nitric oxide in cutaneous vasodilation caused by DCS. METHODS: Male Sprague-Dawley rats were anesthetized with pentobarbital (60 mg/kg, intraperitoneally). A unipolar ball electrode was placed on the left-side of the exposed spinal cord at approximately L1-L2. Blood flow was concurrently recorded from both hindpaw foot pads with laser doppler flowmeters. Blood flow responses were assessed during 1 minute of DCS (0.6 mA at 50 Hz, 0.2-ms pulse) at 10-minute intervals. Nitric oxide synthase was inhibited with NG-nitro-L-arginine methyl ester (L-NAME). Four groups of animals were examined. The first and second groups involved examination of the effects of DCS after 2 and 10 mg/kg L-NAME, respectively. In the third group, the effect of another nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (10 mg/kg), was examined on the responses to DCS. The fourth group of animals entailed comparison of the effects of DCS under control conditions, after the nicotinic receptor antagonist, hexamethonium (10 mg/kg), and during the combined presence of hexamethonium and L-NAME (10 mg/kg). RESULTS: L-NAME markedly attenuated the cutaneous blood flow increases caused by DCS at doses of 2 or 10 mg/kg. Similarly, NG-monomethyl-L-arginine also attenuated the DCS response. Hexamethonium did not affect the cutaneous vasodilation caused by DCS. After hexamethonium, L-NAME no longer attenuated the DCS response. CONCLUSION: Our results demonstrated that nitric oxide played a significant role in producing the DCS-induced increase in rat cutaneous hindpaw blood flow. The involvement of nitric oxide does not require the presence of autonomic efferent function; however, ganglionic blockade may unmask a mechanism for vasodilation during DCS that is independent of nitric oxide release.

Animals↗

PubMed1997

Cutaneous vasodilation during dorsal column stimulation is mediated by dorsal roots and CGRP.

Dorsal column stimulation (DCS) is used clinically to provide pain relief from peripheral vascular disease and has the benefit of increasing cutaneous blood flow to the affected lower extremities. The purpose of this study was to examine the role of dorsal roots, calcitonin gene-related peptide (CGRP), and substance P in the cutaneous vasodilation induced by DCS. Male rats were anesthetized with pentobarbital sodium (60 mg/kg ip). A unipolar ball electrode was placed unilaterally on the spinal cord at the L1-L2 spinal segment. Blood flow was recorded in each hindpaw foot pad with laser Doppler flowmeters. Blood flow responses were assessed during 1 min of DCS (either 0.2 mA subdural or 0.6 mA epidural at 50 Hz, 0.2-ms pulse duration). Dorsal rhizotomy of L3-L5 (n = 5) abolished the cutaneous vasodilation to subdural DCS, whereas removal of T10-T12 (n = 5) and T13-L2 dorsal roots (n = 5) did not attenuate the DCS-induced vasodilation. The CGRP antagonist, CGRP-(8-37) (2.6 mg/kg iv, n = 7), eliminated the epidural DCS-induced vasodilation, whereas the substance P receptor antagonist, CP-96345 (1 mg/kg iv, n = 6), had no effect. In summary, L3-L5 dorsal roots and CGRP are essential for the DCS-induced vasodilation. We propose that DCS antidromically activates afferent fibers in the dorsal roots, thus causing peripheral release of CGRP, which produces cutaneous vasodilation.

Animals↗

PubMed1996

Effects of transcutaneous electrical nerve stimulation (TENS) on spontaneous and noxiously evoked dorsal horn cell activity in cats with transected spinal cords.

Effects of transcutaneous electrical nerve stimulation (TENS) on spontaneous and noxiously evoked dorsal horn neurons were studied in alpha-chloralose anesthetized cats after spinal cords had been transected at the T12 segment. Previous work in cats with intact cords showed that TENS applications to somatic receptive fields could significantly reduce and maintain decreased dorsal horn cell activity. The purpose of this study was to determine if supraspinal mechanisms were involved with the initial reduction of dorsal horn cell activity during TENS applications. Extracellular action potentials of dorsal horn neurons were recorded in the absence of supraspinal influences. The results demonstrated that spontaneously and noxiously evoked cell activities were reduced significantly during TENS and no significant difference was found between pre-TENS control activity and post-TENS application cell activity. This information implies that initial gating (reduction cell activity), which occurs during TENS applications, is due to a segmental effect.

Animals↗

PubMed1996

Cutaneous blood flow increases in the rat hindpaw during dorsal column stimulation.

The purpose of this study was to determine the optimal stimulation site and parameters that result in the greatest changes in cutaneous blood flow during dorsal column stimulation (DCS). Laser Doppler flowmetry was used to assess cutaneous blood flow changes in both rat hindpaws during DCS with a unipolar ball electrode. We found that stimulating the dorsal column at the L2 spinal segment at 0.6 mA at either 25 or 50 Hz with a pulse duration of 0.2 ms resulted in the largest cutaneous blood flow increases in the rat hindpaw. In addition, the DCS response appeared to be limited primarily to the hindpaw ipsilateral to the site of DCS.

Animals↗

PubMed1996

Thoracic visceral inputs use upper cervical segments to inhibit lumbar spinal neurons in rats.

We tested the hypothesis that cardiopulmonary sympathetic afferent (CPSA) input entering upper thoracic spinal segments relays in the cervical spinal cord to inhibit activity of lumbar spinothalamic tract (SST) cells and dorsal horn (DH) cells. Two sequential spinal transections in the same animal were made, one at rostral C1 and one at C4-C6 segments, to determine neuronal pathways involved in the inhibition. We concluded that inhibitory effects induced by CPSA and somatic stimulation might be mediated by propriospinal mechanisms located in upper cervical segments. Vagal inhibition required supraspinal pathways.

Afferent Pathways↗

PubMed1996

Vagal, sympathetic and somatic sensory inputs to upper cervical (C1-C3) spinothalamic tract neurons in monkeys.

1. Myocardial ischemia activates vagal and sympathetic cardiac afferent fibers. The purpose of this study was to determine a neuro physiological basis for cardiac pain referred to C1-C3 somatic dermatomes. We hypothesized that afferent fibers traveling in vagal or sympathetic nerves transmit nociceptive information to C1-C3 spinothalamic tract (STT) neurons. 2. Electrical stimulation of the left stellate ganglion to excite cardiopulmonary sympathetic afferent fibers increased extracellular activity of 44 of 77 C1-C3 STT neurons examined in 33 anesthetized male monkeys (Macaca fascicularis); responses increased as stimulus strength increased. Additionally, this stimulus inhibited 5 cells, increased/decreased activity of 2 cells, and did not affect 26 cells. 3. Electrical stimulation of the left (ipsilateral) thoracic vagus nerve excited 41 of 78 C1-C3 STT neurons, inhibited 4 neurons, increased/decreased activity of 2 neurons, and did not affect 31 neurons. Responses increased with increasing stimulus strength Contralateral vagal stimulation excited 7 of 39 cells tested, inhibited 4 cells and did not affect 28 cells. 4. Effects of stimulating one or more vagal branches were examined on 22 C1-C3 STT neurons excited by input from left thoracic vagus nerve. Stimulation of the cardiac branch excited 11 of 16 cells tested; stimulation of the recurrent laryngeal nerve excited 11 of 18 cells; stimulation of vagal fibers just rostral to the diaphragm excited 8 of 19 cells. 5. Excitatory somatic receptive fields ranged from small ipsilateral fields to large, sometimes bilateral or noncontinuous fields. Many fields included the ipsilateral neck and/or inferior jaw. Thirty-nine of 74 neurons examined were wide dynamic range (WDR), 21 were high threshold (HT), 6 were low threshold (LT), and 8 did not respond to brushing or noxious pinching of somatic tissues. Most (38 of 39) WDR cells responded to stimulation of the stellate ganglion or vagal fibers, as did 18 of 21 HT cells, 3 of 6 LT cells, and 2 of 8 cells unresponsive to brush or pinch stimuli. 6. Results of this study supported the concept that vagal and/ or sympathetic afferent activation of C1-C3 STT neurons might provide a neural mechanism for referred pain that originates in the heart or other visceral organs but is perceived in the neck and jaw region. Additionally, C1-C3 STT neurons processed sensory information from widespread regions of the body.

Adrenergic Fibers↗

PubMed1995

Role of intraaortic balloon pump counterpulsation in high risk coronary rotational atherectomy.

OBJECTIVES: This study sought to evaluate the role of intraaortic balloon pump counterpulsation in preventing hemodynamic instability and promoting a successful outcome during percutaneous transluminal coronary rotational atherectomy in high risk patients. BACKGROUND: The application of rotational atherectomy has widened to include patients with complex lesions and left ventricular dysfunction. Although intraaortic balloon pumping has been successfully used to provide hemodynamic support during balloon angioplasty, its role in high risk rotational atherectomy has not yet been defined. METHODS: In a retrospective review of 159 consecutive high risk patients who underwent rotational atherectomy, 28 had an intraaortic balloon pump placed electively before the procedure (Group 1) whereas 131 did not (Group 2). RESULTS: Group 1 was older and more likely to have multivessel disease and left ventricular dysfunction. Augmented diastolic pressure was maintained > 90 mm Hg in all Group 1 patients, and significant procedure-related hypotension was encountered in nine Group 2 patients, requiring an emergency intraaortic balloon pump in five. Procedural success was achieved in all 28 patients in Group 1 and in 118 in Group 2 (p = 0.07). Slow flow occurred in 18% and 17% of Group 1 and 2 patients, respectively. Among patients with slow flow, non-Q wave myocardial infarction occurred only in Group 2 (0% vs. 27%). On multivariate analysis, elective intraaortic balloon pump placement was the only variable to correlate with a successful procedure uncomplicated by hypotension (p < 0.05). Hospital stay and vascular complications were similar in both groups. CONCLUSIONS: Elective placement of an intraaortic balloon pump before coronary rotational atherectomy in selected high risk patients promotes both procedural hemodynamic stability and a successful outcome.

Aged↗

PubMed1995

Do increases in markers of vagal activity imply protection from sudden death? The case of scopolamine.

BACKGROUND: Low-dose scopolamine increases heart rate variability (HRV) in patients with a prior myocardial infarction (MI). This observation, combined with the evidence that elevated cardiac vagal activity during acute myocardial ischemia is antifibrillatory, has generated the hypothesis that scopolamine might be protective after MI. We tested low-dose scopolamine in a clinically relevant experimental preparation for sudden death in which other vagomimetic interventions are effective. METHODS AND RESULTS: Nineteen mongrel dogs that survived an anterior MI were used in the study. Occurrence or lack of ventricular fibrillation (VF) due to acute myocardial ischemia during submaximal exercise identified dogs at high and low risk for sudden death. Dose-response curves performed in 12 dogs at high (n = 6) and low (n = 6) risk showed that scopolamine at 3 micrograms/kg exerts the greatest effect on HRV. A second group of 7 high-risk dogs were exposed to an exercise-and-ischemia test after treatment with scopolamine (3 micrograms/kg i.v.). Scopolamine increased the standard deviation of RR intervals by 41%, increased the high-frequency band of spectral analysis by 48%, and decreased resting heart rate by 14%. Despite the increase in markers of vagal activity, VF recurred during the exercise-and-ischemia test in 6 dogs (86%). CONCLUSIONS: The significant increase in HRV induced by acute scopolamine did not result in a decreased risk for VF due to acute myocardial ischemia in association with sympathetic activation. Caution must be applied when extrapolating the potential antifibrillatory activity of an intervention from its influence on autonomic markers.

Animals↗

PubMed1995

K+ channel blockade in the prevention of ventricular fibrillation in dogs with acute ischemia and enhanced sympathetic activity.

The value of K+ channel blockade in preventing lethal arrhythmias, and specifically those triggered by acute myocardial ischemia and sympathetic hyperactivity, remains unproven. To address this issue, we tested the antifibrillatory effect of d-sotalol, and Ikr blocker, d,l-sotalol, its racemic compound which blocks Ikr, and beta-adrenoreceptors, and propranolol. Ten dogs with a healed anterior myocardial infarction (MI) had ventricular fibrillation (VF) during a 2-min occlusion of the circumflex coronary artery performed toward the end of a submaximal exercise stress test. In successive trials in the same animals, d-sotalol (three injections of 8 mg/kg, one every 12 h), d,l-sotalol (8 mg/kg), and propranolol (1 mg/kg) were tested. All three interventions significantly reduced heart rate (HR) response to exercise, but only d,l-sotalol and propranolol also blunted the reflex HR increase during acute myocardial ischemia. With d-sotalol, HR at 30 s of coronary occlusion was similar (253 +/- 28 beats/min) to that observed in the control tests (259 +/- 35 beats/min). d-Sotalol prevented recurrence of VF in only 1 of 10 dogs tested. One dog was lost to the continuation of the study after occurrence of VF with d-sotalol. Six of 9 dogs (67%) tested with d,l-sotalol and 5 (56%) of the same 9 dogs tested with propranolol were protected from VF. d-Sotalol does not reduce risk of VF during acute myocardial ischemia associated with sympathetic hyperactivity, and lethal events can be prevented by antiadrenergic interventions.

Animals↗

PubMed1994

Responses of feline raphespinal neurons to urinary bladder distension.

Effects of distending the urinary bladder were studied on extracellular activity of 77 raphespinal neurons in 19 alpha-chloralose anesthetized cats. Neurons were activated antidromically from thoracic spinal cord; recording sites were located in nucleus raphe magnus (NRM). Mean conduction velocity was 48 +/- 2 m/s. Urinary bladder distension (UBD) increased activity in 12 cells and decreased activity in 17 cells. Spontaneous bladder contractions also affected activity in raphespinal neurons responsive to UBD. Noxious pinch stimulus applied to proximal hindlimbs or forelimbs either increased or decreased activity in 28 raphespinal neurons. No cells were excited both by UBD and pinching of skin and deep tissues of the limbs. Thus, excitatory viscerosomatic convergence was not observed with the stimuli tested in raphespinal neurons examined in this study. Urinary bladder input to descending projection neurons in NRM might participate in descending modulation of dorsal horn neurons. In addition, micturition reflexes might be affected by urinary bladder input to these neurons.

Afferent Pathways↗