Mechanical stimulation is not responsible for activation of gastrointestinal afferents during ischemia

1997 ◽  
Vol 272 (1) ◽  
pp. H99-H106 ◽  
Author(s):  
H. L. Pan ◽  
Z. B. Zeisse ◽  
J. C. Longhurst
Keyword(s):  
Gastrointestinal Motility ◽  
Mechanical Stimulation ◽  
Single Unit ◽  
Intraluminal Pressure ◽  
Mechanical Activity ◽  
Single Unit Activity ◽  
C Fiber ◽  
Afferent Discharge ◽  
The Right

Abdominal ischemia reflexly excites the cardiovascular system through activation of visceral sympathetic afferents. Although a number of ischemic metabolites are known to stimulate sympathetic afferents, the contribution of mechanical stimulation to activation of afferents during abdominal ischemia remains uncertain. Thus the present study examined the role of changes in motility in activation of gastrointestinal afferents during ischemia. Single-unit activity of C fiber afferents located on the stomach, duodenum, jejunum, or colon was recorded from the right sympathetic chain of anesthetized cats during 15 min of ischemia. Intraluminal pressure, as a reflection of local mechanical activity, was measured by an open catheter placed in the lumen of the gastrointestinal tract. The results show that gastrointestinal motility was mainly inhibited during abdominal ischemia. Changes in intraluminal pressure did not correlate with afferent discharge activity during ischemia (r = -0.32, n = 10). Furthermore, discharge frequency of gastrointestinal afferents during ischemia was not altered significantly by topical application of 100 micrograms/ml of atropine (3.98 +/- 0.62 to 3.83 +/- 0.59 imp/s, n = 12), which profoundly inhibited local gastrointestinal motility. Collectively, these data indicate that gastrointestinal motility changes during abdominal ischemia do not contribute to activation of gastrointestinal sympathetic C fiber afferents.

Activation of visceral afferents by bradykinin and ischemia: independent roles of PKC and prostaglandins

1999 ◽  
Vol 276 (6) ◽  
pp. H1884-H1891 ◽  
Author(s):  
Zhi-Ling Guo ◽  
J. David Symons ◽  
John C. Longhurst
Keyword(s):  
Single Unit ◽  
Visceral Afferents ◽  
Single Unit Activity ◽  
Afferent Activity ◽  
C Fibers ◽  
Kinase C ◽  
Afferent Activation ◽  
C Fiber ◽  
The Right ◽  
Afferent Response

We have shown that the cyclooxygenase (COX) and protein kinase C (PKC) systems both contribute to afferent activation in response to bradykinin (BK) and abdominal ischemia. Because the contribution from PKC to C fiber activation may depend, in part, on prostaglandin production, we hypothesized that an intact COX system is required for PKC-induced activation of ischemically sensitive abdominal visceral afferents by BK and abdominal ischemia. Single-unit activity of abdominal visceral C fibers was recorded from the right thoracic sympathetic chain of anesthetized cats. Three repeated injections of BK (1–2 μg/kg ia) produced similar increases in afferent activity from the baseline of 1.32 ± 0.24, 1.37 ± 0.32, and 1.41 ± 0.24 impulses/s ( n = 5). In another group of animals ( n = 5), the second and third BK injections were performed after COX inhibition (indomethacin; 5 mg/kg iv) and then combined COX + PKC inhibition [PKC-(19—36), 20 μg/kg iv], respectively. Inhibition of COX reduced ( P < 0.05) the afferent response to BK (0.59 ± 0.12 impulses/s) compared with the unblocked condition (1.14 ± 0.27 impulses/s), whereas combined COX + PKC inhibition further attenuated the increase from baseline (0.18 ± 0.09 impulses/s; P < 0.05). Similar results were obtained in a third group of cats when the antagonists were administered in reverse order ( n = 7). In a fourth group of cats ( n = 9) that were pretreated with indomethacin, ischemia increased afferent activity (0.78 ± 0.17 impulses/s). However, neural activity was attenuated (0.51 ± 0.14 impulses/s; P < 0.05) during a second bout of ischemia in the presence of indomethacin + PKC-(19—36). These results suggest that the contribution from PKC to the activation of ischemically sensitive C fibers, particularly by BK, does not require an intact cyclooxygenase system.

Effects of ouabain on neuronal thermosensitivity in hypothalamic tissue slices

1989 ◽  
Vol 257 (1) ◽  
pp. R21-R28
Author(s):  
M. C. Curras ◽  
J. A. Boulant
Keyword(s):  
Firing Rate ◽  
Neuronal Activity ◽  
Unit Activity ◽  
Single Unit ◽  
Single Unit Activity ◽  
Tissue Slices ◽  
Temperature Changes ◽  
Cold Sensitive ◽  
Hypothalamic Tissue

To determine the role of the electrogenic Na+-K+ pump in neuronal thermosensitivity, single-unit activity was recorded in rat hypothalamic tissue slices before, during, and after perfusions containing 10(-5) or 10(-6) M ouabain, a specific pump inhibitor. Most neurons were recorded in the preoptic-anterior hypothalamus. Some neurons were also tested with high magnesium-low calcium perfusions to determine ouabain's effects on neuronal activity during synaptic blockade. When the neurons were characterized according to thermosensitivity, 24% were warm sensitive, 8% were cold sensitive, and 68% were temperature insensitive. Ouabain increased the firing rate of 60% of all neurons. Ouabain did not reduce the thermosensitivity of cold-sensitive and warm-sensitive neurons; however, temperature-insensitive neurons became more warm sensitive during ouabain perfusion. This increase in warm sensitivity did not occur with ouabain plus high Mg2+-low Ca2+ perfusion, suggesting that Ca2+ is important in this response. These results indicate that the Na-K pump is not responsible for the thermosensitivity of hypothalamic cold-sensitive or warm-sensitive neurons; however, this pump may be actively employed by many neurons that remain insensitive to temperature changes.

Signal transduction in activation of ischemically sensitive abdominal visceral afferents: role of PKC

1998 ◽  
Vol 275 (3) ◽  
pp. H1024-H1031 ◽  
Author(s):  
Zhi-Ling Guo ◽  
Liang-Wu Fu ◽  
J. David Symons ◽  
John C. Longhurst
Keyword(s):  
Signal Transduction ◽  
Impulse Activity ◽  
Visceral Afferents ◽  
C Fibers ◽  
Kinase C ◽  
C Fiber ◽  
Afferent Nerve Endings ◽  
The Right ◽  
Stimulation Of

Abdominal ischemia reflexly activates the cardiovascular system by stimulating abdominal visceral afferent nerve endings. Whereas many ischemic metabolites responsible for activating these nerves have been identified (e.g., bradykinin), their precise mechanism of action is unclear. Protein kinase C (PKC) is an important part of the signal transduction process underlying the action of metabolites such as bradykinin and is a regulator of neuronal activity. Therefore, we hypothesized that PKC contributes to stimulation of ischemically sensitive abdominal visceral afferents. Single-unit activity was recorded from the right thoracic sympathetic chain of anesthetized cats. Exogenous activation of PKC using phorbol 12,13-dibutyrate (PDBu, 5 μg/kg ia) increased the impulse activity of ischemically sensitve C-fiber afferents from 0.04 ± 0.01 to 0.67 ± 0.23 impulses/s ( n = 11; P < 0.05). The influence of endogenous activation of PKC also was evaluated during 10 min of mesenteric ischemia. Inhibition of PKC using PKC-(19—36) (20 μg/kg iv) reduced ischemia-induced increases in afferent activity from 0.46 ± 0.11 to 0.19 ± 0.08 impulses/s ( n = 7, P < 0.05). Moreover, PKC-(19—36) (20 μg/kg iv) reduced the response of ischemically sensitive C fibers to bradykinin (0.5–1.0 μg/kg ia) from 1.18 ± 0.20 to 0.66 ± 0.14 impulses/s ( n = 13, P < 0.05). These results indicate that PKC contributes to activation of abdominal visceral afferents during ischemia and specifically to part of the bradykinin-induced activation of these afferents.

Receptive Field Properties of Unmyelinated Tactile Afferents in the Human Skin

2003 ◽  
Vol 89 (3) ◽  
pp. 1567-1575 ◽  
Author(s):  
Johan Wessberg ◽  
Håkan Olausson ◽  
Katarina Wiklund Fernström ◽  
Åke B. Vallbo
Keyword(s):  
Single Unit ◽  
Receptive Fields ◽  
Single Unit Activity ◽  
Affiliative Behavior ◽  
Scanning Method ◽  
Conduction Velocities ◽  
The Individual ◽  
Skin To Skin ◽  
Field Area

We recorded, with the microneurography technique, single-unit impulses from nine cutaneous mechanoreceptive afferents with conduction velocities in the C range and receptive fields in the hairy skin of the forearm. The units responded with high impulse rates to light touch and had low monofilament thresholds. The geography of receptive fields was explored with a scanning method: a lightweight probe with a small and rounded tip was made to scan the field area in a series of closely adjacent tracks while single-unit activity was recorded. The fields of the nine units varied considerably in size as well as complexity. The individual field consisted of one to nine small responsive spots distributed over an area of 1–35 mm2 when explored with a moving indentation of 5 mN. The fields were roughly round or oval in shape with no preferred orientation. The size of the response differed between individual sensitive spots in a field, suggesting a highly nonuniform terminal organization. The properties of the fields seem consistent with a role of tactile C afferents to provide information about pleasant touch and skin-to-skin contacts to central structures controlling emotions and affiliative behavior.

Role of cAMP in activation of ischemically sensitive abdominal visceral afferents

2000 ◽  
Vol 278 (3) ◽  
pp. H843-H852 ◽  
Author(s):  
Zhi-Ling Guo ◽  
John C. Longhurst
Keyword(s):  
Adenylate Cyclase ◽  
Repeated Administration ◽  
Visceral Afferents ◽  
Control Group ◽  
Single Unit Activity ◽  
Time Control ◽  
C Fibers ◽  
Camp System ◽  
The Right

A number of metabolites produced during abdominal ischemia can stimulate and/or sensitize visceral afferents. The precise mechanisms whereby these metabolites act are uncertain. Other studies have shown that the adenylate cyclase-cAMP system may be involved in the activation of sensory neurons. Therefore, we hypothesized that cAMP contributes to the activation of ischemically sensitive abdominal visceral afferents. Single-unit activity of abdominal visceral C fibers was recorded from the right thoracic sympathetic chain in anesthetized cats before and during 7 min of abdominal ischemia. Forty-six percent of ischemically sensitive C fibers responded to intra-arterial injection of 8-bromo-cAMP (0.35–1.0 mg/kg), an analog of cAMP, with responses during ischemia increasing from 0.50 ± 0.06 to 0.84 ± 0.08 impulses/s ( P < 0.05, n = 11 C fibers). Conversely, an inhibitor of adenylate cyclase, 2′,5′-dideoxyadenosine (DDA; 0.1 mg/kg iv), attenuated ischemia-induced increase in activity of afferents from 0.66 ± 0.10 to 0.34 ± 0.09 impulses/s ( P < 0.05; n = 8). Furthermore, whereas exogenous PGE2 (3–4 μg/kg ia) augmented the ischemia-induced increase in activity of afferents ( P < 0.05, n = 10), treatment with DDA (0.1 mg/kg iv) substantially reduced the increase in discharge activity of afferents during ischemia, which was augmented by PGE2 (1.45 ± 0.24 vs. 0.70 ± 0.09 impulses/s, −DDA vs. +DDA; P < 0.05) in six fibers. A time control group ( n = 4), however, demonstrated similar increases in the activity of afferents with repeated administration of PGE2. These data suggest that cAMP contributes to the activation of abdominal visceral afferents during ischemia, particularly to the action of PGs on activation and/or sensitization of these endings.

Differential effect of 5- and 15-lipoxygenase products on ischemically sensitive abdominal visceral afferents

1995 ◽  
Vol 269 (1) ◽  
pp. H96-H105 ◽  
Author(s):  
H. L. Pan ◽  
G. L. Stahl ◽  
J. C. Longhurst
Keyword(s):  
Receptive Field ◽  
Impulse Activity ◽  
Leukotriene B4 ◽  
Visceral Afferents ◽  
Single Unit Activity ◽  
Tetraenoic Acid ◽  
Mechanical Threshold ◽  
Lipoxygenase Products ◽  
C Fiber ◽  
The Right

The effects of 5- and 15-lipoxygenase products, leukotriene B4 (LTB4) and (8R,15S)-dihydroxyeicosa(5E-9,11,13Z)tetraenoic acid (8R,15S-diHETE), on ischemically sensitive abdominal visceral C fiber afferents were evaluated, because this system is important in sensitizing cutaneous afferents. Single-unit activity of abdominal visceral C fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 5 min of ischemia. Inhibition of 5-lipoxygenase with WY-50295 tromethamine (5 mg/kg iv) augmented the impulse activity from 0.48 +/- 0.15 to 0.79 +/- 0.24 impulses/s (P < 0.05) in seven ischemically sensitive afferents. Conversely, topical application of LTB4 (125 ng) directly onto the receptive field attenuated impulse activity of 10 ischemically sensitive C fiber afferents from 0.82 +/- 0.23 to 0.42 +/- 0.10 impulses/s (P < 0.05). In additional cats, application of 8R,15S-diHETE (125 ng) onto the receptive field augmented the impulse activity of nine ischemically sensitive C fiber afferents (from 0.48 +/- 0.15 to 0.70 +/- 0.15 impulses/s, P < 0.05) and significantly decreased the mechanical threshold of these nine afferents, whereas application of 8S,15S-diHETE (125 ng), a stereoisomer of 8R,15S-diHETE, attenuated the impulse activity from 0.77 +/- 0.48 to 0.45 +/- 0.13 impulses/s (P < 0.05) in six additional ischemically sensitive C fiber afferents. In animals pretreated with aspirin (50 mg/kg iv, n = 6) or 8S,15S-diHETE (125 ng, n = 6), WY-50295 tromethamine (5 mg/kg iv) still potentiated the impulse activity of ischemically sensitive C fiber afferents. These data indicate that 8R,15S-diHETE interacts with stereospecific receptors to sensitize, whereas LTB4 reduces, the response of abdominal visceral afferents to ischemia. Furthermore the data suggest that the augmented response of afferents to abdominal ischemia after inhibition of 5-lipoxygenase is, at least in part, independent of shunting to the cyclooxygenase or 15-lipoxygenase system.

scholarly journals Opposite responses to lidocaine between intrapulmonary mechanical and chemical sensors

2009 ◽  
Vol 297 (3) ◽  
pp. R853-R858 ◽  
Author(s):  
Huafeng Li ◽  
Lei Du ◽  
Peyman Otmishi ◽  
Yuwen He ◽  
Juan Guardiola ◽  
...  
Keyword(s):  
Pulmonary Circulation ◽  
Systemic Circulation ◽  
Left Ventricular ◽  
High Threshold ◽  
Single Unit Activity ◽  
Mechanically Ventilated ◽  
C Fiber ◽  
Lidocaine Injection ◽  
Bioactive Agents ◽  
The Right

We attempted to determine whether intrapulmonary sensory receptors are nourished by the pulmonary or the systemic circulation. Single-unit activity from the cervical vagus nerve was recorded in anesthetized, open chest, mechanically ventilated rabbits, comparing responses to right or left ventricular injection of 2% lidocaine (at 4 mg/kg). Airway mechanosenors [slowly adapting receptor (SARs) and rapidly adapting receptors] were inhibited by lidocaine, whereas chemosensors (C-fiber receptors and high-threshold Aδ-receptors) were stimulated. Furthermore, all types of airway sensors were perfused preferentially by the pulmonary circulation. For example, 14 of the 15 tested SARs ceased discharge at 4.1 ± 0.6 s after lidocaine injection into the right ventricle. The blocking effect lasted 35 ± 6.2 s. In contrast, none of the 15 SARs ceased their activity after lidocaine injection into the left ventricle. Our data show that intrapulmonary sensors are mainly nourished by the pulmonary circulation. Their very short latency indicates that these sensors receive ample blood supply. Thus, intrapulmonary sensors rely on the pulmonary circulation to detect bioactive agents in the blood.

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