Coordination of the myoelectrical activity of the large and small intestine

Coordination of the myoelectrical activity of the large and small intestine was studied. Pacemaker cells of intestine are predominantly located at the proximal divisions of large and small intestine and have an increased spontaneous slow-wave activity, which ensures the distribution of excitation in smooth muscle underlying intestines. Due to the ileocecal coordination by sequential motor activity of small and large intestine is provided. The distal direction gradient of slow waves frequency reduction was established. Pacemaker cells possess certain structural specificity and is specialized in the spontaneous bioelectric activity.     

Ontogeny of fasting small intestinal motor activity in the human infant.

A clearly defined progression of fasting small intestinal motor development is seen in the human infant from disorganised low amplitude motor activity before 31 weeks gestation through an intermediate phase of increasing motor organisation and amplitude to the development of a normal cyclical pattern of motor activity with clearly defined phase I, II, and III activity between 37 weeks gestation and term. With increasing maturity smooth muscle contractility [gastric antral pressure (5-30 mmHg), average duodenal pressure (2-12 mmHg)], propagation and slow wave frequency (10.5-12.5 cpm) all increased in a significant fashion (p less than 0.01). The stage of development of fasting motor activity in the small intestine of the preterm infant can now be readily predicted from the gestational age of the infant.     

Relation between oxidative metabolism and slow rhythmic potentials in mammalian intestinal muscle.

Intact muscle layers separated from the small intestine of the cat were mounted in a specially designed chamber to measure electrical slow waves and NADH fluorescence simultaneously. Cooling the muscle to 17 degrees eliminated slow waves and simultaneously increased the level of fluorescence. Likewise, superfusing the muscle with a N2-bubbled glucose-free Krebs solution decreased the amplitude of slow waves and concomitantly increased fluorescence emission. In both cases, return to normal conditions reversed the effects on both slow waves and fluorescence. When signals were averaged over 30-70 slow waves, a pattern emerged with the fluorescence oscillations in phase with the electric oscillations. The NADH:NAD+ ratio reached a maximum at the most depolarized point of the slow waves and a minimum at the most polarized point between slow waves. This indicates maximum ATP utilization during the repolarization process. The correlation between redox oscillations and electrical slow wave generation is associated with cell metabolism.     

ATP regulation of the slow calcium channels in vascular smooth muscle cells of guinea pig mesenteric artery

Effects of intracellularly perfused ATP, and extracellularly applied cyanide and 2-deoxy-D-glucose, on fast and slow Ca2+ channel currents of isolated single vascular smooth muscle cells were investigated by a whole-cell voltage-clamp method combined with an intracellular perfusion technique. Single smooth muscle cells were prepared by collagenase treatment from guinea pig small mesenteric arteries (diameter of less than 300 micron). With Cs+-rich solution in the pipette and isotonic Ba2+ solution (100 mM) in the bath, depolarizing pulses evoked two types of the Ca2+ channel current. Depolarizing pulses from the holding potential of -80 mV to over -30 mV evoked a fast Ca2+ channel current. This fast component was inhibited by shifting the holding potential in a positive direction. With a holding potential of -40 mV, the fast component was almost inhibited. In contrast, the slow current was evoked by command potentials to above -10 mV, and its full amplitude was preserved at the holding potential of -40 mV. Without ATP in the pipette, the fast current was dominant. Increase in the ATP concentration in the pipette (0.3 to 5 mM) enhanced the slow current but did not affect the fast current. Maximum enhancement of the slow current was observed at 5 mM ATP. Increase in ATP concentration, however, did not modify the shape of the current trace and the steady state inactivation curve of the slow current. Maximum amplitudes of the fast current and slow current recorded with 5 mM ATP averaged 17.4 pA (SD of 10.4 pA, n = 30; observed at -10 mV to +10 mV) and 141.8 pA (SD of 27.1 pA, n = 30; observed at +30 mV to +40 mV), respectively. Presence of CN- and 2-deoxy-D-glucose (without glucose) in the bath, and absence of ATP in the pipette, abolished the slow current within 10 minutes; in contrast, it took more than 10 minutes to depress the fast current. The inhibitory effect of CN- and 2-deoxy-D-glucose on the slow current was reduced by intracellular application of ATP. In summary, the activation of the slow Ca2+ channel required physiological concentration of ATP, whereas the fast channel current was preserved, even under ATP-free conditions. These results indicate that only the slow current is a metabolically dependent Ca2+ channel current in these vascular smooth muscle cells.     

In Vivo Gastric and Intestinal Slow Waves in W/W<Superscript>v</Superscript> Mice

The aim was to investigate whether there are regular gastric and intestinal slow waves in conscious W/W^v mice. Eleven W/W^v mice and 11 wild-type mice were implanted with two pairs of electrodes in the stomach and small intestine. Gastrointestinal slow waves were recorded both under anesthesia and in the conscious state. Atropine and verapamil were given separately to an additional 10 W/W^v mice. Results were as follows. (1) The conscious W/W^v mice showed lower rhythmic slow waves in the small intestine (77.1 vs 93.5%; P < 0.001). However, the frequency (10.7 vs 18.8 cpm; P < 0.0001) and the antregrade propagation of intestinal slow waves in W/W^v mice were significantly lower than in the controls. In the stomach, regular slow waves were recorded in both groups, with no difference between the two groups. (2) Anesthesia significantly impaired both gastric and intestinal slow waves in both groups. (3) Atropine and verapamil had no effects on the rhythmicity of intestinal slow waves. We conclude that ICC-MY may not be the sole pacemaker cells for slow waves in the small intestine.There may be some abnormality of smooth muscle cells in W/W^v mice that causes a reduction in the frequency, rhythmicity, and antegrade propagation of slow waves.Xiaohua Hou is a Visiting Scientist from the Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.     

Serotonin regulation of motor function of the small intestine

The review described serotonergic regulation of motor function of the small intestine. Motor neurons of the enteric nervous system and cells--pacemakers (cells of Cajal) play an important role in the regulation of motor activity of the small intestine. Activated serotonin receptors expressed by neuronal and effector cells initiate the phase II and III of the migrating motor complex (MMC), changes the duration of the cycle and frequency of MMC. Serotonin, acting on 5-HT(2B) -, 5-HT(3) - and 5-HT(4)-receptors expressed by the Cajal cell, regulate the frequency of slow waves and amplitude of electromotor activity of the small intestine.     

Bursts of non-deglutitive simultaneous contractions may be a normal oesophageal motility pattern.

The frequency and characteristics of non-deglutitive motor activity of the human oesophagus and its relation to motility patterns in the antrum and upper small intestine were studied in 25 fasted healthy subjects. Motility of the oesophagus, antrum, and upper small intestine was recorded by means of a manometric perfused catheter system. The most striking non-deglutitive motility pattern consisted of repetitive bursts of non-sequential pressure peaks occurring in the smooth muscle portion of the oesophagus. The mean number of pressure peaks per burst was 2.7 (SD 2) waves with a mean amplitude of 19.5 (SD 9.9) mm Hg and a duration of 3.09 (SD 0.22) seconds. The highest amplitude was 80 mm Hg and the longest burst consisted of 13 repetitive waves. The bursts were recorded up to a distance of 15-20 cm above the lower oesophageal sphincter. Ninety five per cent of the bursts occurred during a 15 minute period before the onset of phase 3 of the migrating motor complex in the antral or upper small intestinal area, or during the lower oesophageal sphincter component of the migrating motor complex. In conclusion, spontaneous bursts of non-sequential pressure peaks occurred in the smooth muscle part of the human oesophagus in relation to phase 3 of the migrating motor complex. They represent the oesophageal body component of phase 3 of the migrating motor complex and are not a sign of oesophageal motor abnormalities.     

Disruption of interstitial cells of Cajal networks after massive small bowel resection

AIM: To investigate the disruptions of interstitial cells of Cajal (ICC) in the remaining bowel in rats after massive small bowel resection (mSBR). METHODS: Thirty male Sprague-Dawley rats fitting entry criteria were divided randomly into three experimental groups (n = 10 each): Group A rats underwent bowel transection and re-anastomosis (sham) and tissue samples were harvested at day 7 post-surgery. Group B and C rats underwent 80% small bowel resection with tissue harvested from Group B rats at day 7 post-surgery, and from Group C rats at day 14 postsurgery. The distribution of ICC at the site of the resid-ual small bowel was evaluated by immunohistochemical analysis of small intestine samples. The ultrastructural changes of ICC in the remnant ileum of model rats 7 and 14 d after mSBR were analyzed by transmission electron microscopy. Intracellular recordings of slow wave oscillations were used to evaluate electrical pacemaking. The protein expression of c-kit, ICC phenotypic markers, and membrane-bound stem cell factor (mSCF) in intestinal smooth muscle of each group were detected by Western blotting. RESULTS: After mSBR, immunohistochemical analysis indicated that the number of c-kit-positive cells was dramatically decreased in Group B rats compared with sham tissues. Significant ultrastructural changes in ICC with associated smooth muscle hypertrophy were also observed. Disordered spontaneous rhythmic contractions with reduced amplitude (8.5 ± 1.4 mV vs 24.8 ± 1.3 mV, P = 0.037) and increased slow wave frequency (39.5 ± 2.1 cycles/min vs 33.0 ± 1.3 cycles/min, P = 0.044) were found in the residual intestinal smooth muscle 7 d post mSBR. The contractile function and electrical activity of intestinal circular smooth muscle returned to normal levels at 14 d post mSBR (amplitude, 14.9 ± 1.6 mV vs 24.8 ± 1.3 mV; frequency, 30.7 ± 1.7 cycles/min vs 33.0 ± 1.3 cycles/min). The expression of Mscf and c-kit protein was decreased at 7 d (P = 0.026), but gradually returned to normal levels at 14 d. The ICC and     

Sensing and pacing with floating electrodes in the right atrium and right atrial appendage

Unipolar and bipolar floating atrial electrograms from 58 pacemaker patients were recorded and compared. Twenty-four floating unipolar electrodes and 29 floating bipolar electrodes were used at mid-right atrial level and five orthogonal atrial J leads within the right atrial appendage. Each signal was analyzed in the time domain: peak to peak deflection of P wave and QRS complex, duration of P wave and QRS complex and slew rate; and in the frequency domain: maximum of the energy spectrum and frequency at which a decrease of 3 dB from the maximal amplitude occurred. Atrial P (1.31 +/- 0.94 mV, mean +/- SD) and QRS (1.0 +/- 0.56 mV) waves from unipolar floating electrodes were comparable, whereas they were significantly different from bipolar floating electrodes (1.15 +/- 0.77 mV and 0.25 +/- 0.39 mV). Amplitudes of P waves from orthogonal J leads were largest (3.1 +/- 2.6 mV) and QRS complexes (0.21 +/- 0.13 mV) smallest. The P waves had the highest frequency content (17.1 +/- 19.4 Hz). It is concluded that atrial electrograms from orthogonal electrodes (bipolar or orthogonal J) offer superior sensing characteristics because of the large amplitude P wave and discriminating power between P and QRS waves (P/QRS voltage 15:1). An orthogonal J lead can thus be used for P synchronous pacing at the atrial level, whereas an orthogonal ventricular lead can be used for rate-response pacing systems.     

急性缺氧对大鼠肺动脉平滑肌细胞电压门控钾通道电流的影响

目的：研究急性缺氧对大鼠肺动脉平滑肌细胞电压门控钾通道（Kv）电流的影响。方法：雄性SD大鼠20只随机分为常氧对照组和急性缺氧组（各10只）。急性缺氧组大鼠在低氧仓中缺氧停留8h后进行实验。应用全细胞膜片钳技术记录肺动脉平滑肌细胞电压门控钾通道电流（Ik）。结果：急性缺氧显著降低大鼠肺动脉平滑肌细胞的Ik密度。在大鼠肺动脉平滑肌细胞静息膜电位-60mV至-10mV时,急性缺氧降低大鼠肺动脉平滑肌细胞的IK密度不明显（P〉0．05）。在0mV时,大鼠肺动脉平滑肌细胞的峰值Ik密度显著下降[从（38．1±5．2）pA／pF→（9．82±2．1）pA／pF,P〈0．05）],此后随着细胞静息膜电位的增加,平滑肌细胞的Ik密度下降幅度逐渐增加（P〈0．05）;从＋30mV至＋60mV时,平滑肌细胞的Ik密度下降幅度更大（P〈0．01）。在＋60mV时,IK密度峰值从（135．4±16．5）pA／pF降到（73．1±10．6）pA／pF,降幅达（46．8±3．3）％。结论：急性缺氧可降低肺动脉平滑肌细胞Kv电流,导致肺血管缺氧性收缩。     

Evidence for a differential cellular distribution of inward rectifier K channels in the rat isolated mesenteric artery

The distribution of functionally active, inwardly rectifying K (K(IR)) channels was investigated in the rat small mesenteric artery using both freshly isolated smooth muscle and endothelial cells and small arterial segments. In Ca(2+)-free solution, endothelial cells displayed a K(IR) current with a maximum amplitude of 190 +/- 16 pA at -150 mV and sensitivity to block with 30 microM Ba(2+) (n = 7). In smooth muscle cells, outward K current was activated at around -47 +/- 3 mV, but there was no evidence of K(IR) current (n = 6). Furthermore, raising extracellular [K(+)] to either 60 or 140 mM, or applying the alpha(1)-adrenoceptor agonist phenylephrine (PE; 30 microM), failed to reveal an inwardly rectifying current in the smooth muscle cells, although PE did stimulate an iberiotoxin-sensitive outward K current (n = 4). Exogenous K(+) (10.8-16.8 mM) both relaxed and repolarized endothelium-denuded segments of the mesenteric artery contracted with PE. These effects were depressed by 100 microM ouabain but unaffected by either 30 microM BaCl(2) or 3 microM glibenclamide. These data suggest that functional, inwardly rectifying Ba(2+)-sensitive channels are restricted to the endothelial cell layer in the rat small mesenteric artery.     

Comparative study in the effect of C-type natriuretic peptide on gastric motility in various animals

AIM: To investigate the effect of natriuretic peptides on gastric motility in various animals, and the effect of C-type natriuretic peptide (CNP) on spontaneous contraction of gastric smooth muscle in rat, guinea-pig and human in vitro was compared.METHODS: Spontaneous contraction of gastric smooth muscle was recorded by four channel physiograph.RESULTS: In the guinea-pig and rat gastric antral circular smooth muscle, CNP markedly decreased the amplitude of spontaneous contraction but it didn't affect the frequency,however, the contractile activity was completely inhibited by CNP in gastric antral longitudinal smooth muscle. In the human gastric antral circular and longitudinal smooth musie, CNP completely inhibited spontaneous contraction. In the circular smooth muscle of guinea-pig and rat gastric fundus,CNP obviously decreased the amplitude of spontaneous contraction but it didn't affect the frequency, however, the contractile activity was completely inhibited by CNP in smooth muscle of fundus longitudinal. In the circular and longitudinal smooth muscle of guinea-pig gastric body, CNP at first induced a relaxation and then an increase in amplitude of spontaneous contraction (rebound contraction), but the frequency was not changed. After the circular smooth muscle of gastric body was pretreated with atropine, an M receptor blocker, the rebound contraction was abolished; In circular and longitudinal smooth muscle of rat gastric body, CNP induced a transient and slight relaxation and successively followed by the recovery in amplitude of spontaneous contraction but it also didn't affect the frequency. After the smooth muscle was pretreated with atropine, the transient and slight relaxation was replaced by long term and complete inhibition; The percentage of CNP-induced inhibition was 76.77±6.21% (fundus), 67.21±5.32 % (body) and 58.23±6.21% (antral) in the gastric circular muscle, however, the inhibitory percentage was 100±0.00 % (fundus), 68.66±3.55 % (body) and 100±0.00 % (antrum) in the gastric longitudinal smooth muscle of guinea-pigs; In the rat, the percentage of CNP-induced inhibition was 95.87±4.12 %(fundus), 94.91±5.08 % (body) and 66.32±7.32 % (antrum)in the gastric circular smooth muscle, but in the longitudinal smooth muscle, CNP completely inhibited the spontaneous contraction. Using LY83583, a guanylate cyclase inhibitor, and zaparinast as a phosphoesterase inhibitor to inhibit the generation of cGMP, the effect of CNP on the spontaneous contraction was markedly weakened by LY83583, however, the inhibitory effect was enhanced by zaparinast.CONCLUSION: (1) CNP can obviously inhibit the spontaneous contraction of gastric antral circular and longitudinal smooth muscle in the rat, guinea-pig and human.The order of inhibitory potency is human ＞rat＞ guinea-pig.(2) In the same animals, the inhibitory effect of CNP on spontaneous contraction is the most powerful in fundus and the weakest in antrum, in the same position, the inhibitory effect on the circular smooth muscle is more powerful than that on longitudinal smooth muscle. (3) The inhibitory effect of CNP on spontaneous contraction in the gastric smooth muscle is mediated by a cGMP dependent pathway.     

Intracellular studies of electrical membrane properties of opossum esophageal circular smooth muscle

It has been suggested that regional differences in membrane properties of circular esophageal smooth muscle play an important role in the mechanism of esophageal peristalsis. The purpose of this study was to examine both the passive and active membrane properties of circular smooth muscle at proximal and distal esophageal sites so as to delineate the role of myogenic properties in the intramural mechanism of peristalsis. Intracellular recordings were made in circular muscle strips taken from proximal (8 cm above the gastroesophageal junction) and distal (2 cm above the gastroesophageal junction) sites in 10 opossums using the partition method of Abe and Tomita. At both esophageal sites, determinations were made of resting membrane potentials, time constants, space constants, thresholds for action potentials, action potential amplitudes, rates of rise of action potentials, and action potential durations at half-amplitude. The values for these parameters at the proximal and distal sites, respectively, were as follows: mean resting membrane potential, 49.7 +/- 0.24 and 49.5 +/- 0.3 mV; length constant, 4.0 +/- 0.4 and 3.8 +/- 0.4 mm; time constant, 513 +/- 49 and 456 +/- 53 ms; threshold for action potentials, 9.3 +/- 0.4 and 8.8 +/- 0.3 mV; amplitude of action potentials, 36.0 +/- 5.2 and 35.3 +/- 1.7 mV; rate of rise of action potentials, 2.3 +/- 0.3 and 2.6 +/- 0.4 mV/ms; duration of action potentials at half-amplitude, 5.0 +/- 1.2 and 4.1 +/- 0.4 ms; and the conduction velocity for evoked potentials, 3.9 +/- 0.3 and 3.8 +/- 0.4 cm/s. Our studies show that there are no differences between proximal and distal esophageal sites in any of these determinations. These studies also show that regional differences in the electrical membrane properties of circular smooth muscle do not account for esophageal peristalsis.     

Action potential generation in reaggregates of rat aortic smooth muscle cells in primary culture.

Cultured vascular smooth muscle cells were prepared from adult rat aortas. The cells were dispersed by collagenase/elastase, and allowed to reaggregate into small spheres (50-200 micron in diameter) by plating on to cellophane. These primary cultures were incubated for 5-14 days, and then impaled with microelectrodes. The mean resting potential was -55 mV, and the mean input resistance was 9.0 M omega. The cells were quiescent, electrically and mechanically, and electrical stimulation usually did not elicit responses. However, addition of Ba++ (1 mM) or tetraehtylammonium ion (TEA; 5-15 mM) induced excitability (with accompanying contractions), either as spontaneous action potentials or by allowing responses to electrical stimulation. The cells became partially depolarized (e.g., to -36 mV) by these agents, and the input resistance increased. The frequency of spontaneous firing of the Ba++-induced spikes was affected by polarizing current pulses, as expected for pacemaker behavior. Elevation of Ca++ in the bathing solution increased the amplitude (overshoot) of the action potentials, and the spikes were blocked by verapamil (10(-5) M). Electron microscopy showed that the reaggregates consisted of a tight packing of elongated small-diameter cells, some of which exhibited thick and thin myofilaments and 'dense bodies'; many cells possessed surface caveolae. The results of this study demonstrate that reaggregates of arterial smooth muscle in primary culture can maintain functional and morphological characteristics of intact arterial smooth muscle, and therefore provide a useful preparation for the study of vascular smooth muscle function and control.     

Evidence for voltage-dependent block of cardiac sodium channels by tetrodotoxin

The effects of tetrodotoxin (TTX) on cardiac sodium channels in guinea-pig ventricular muscle were investigated. Membrane potential was controlled using a single sucrose gap voltage clamp method, and the maximum upstroke velocity of the ventricular action potential (Vmax) was used as an indicator of drug-free sodium channels. Reduction of Vmax by TTX was found to be both voltage- and time-dependent, similar to the effects of many local anesthetic drugs, with the exception that TTX concentrations high enough to produce significant use-dependent block (e.g. 2 microM), also produced significant tonic block, even at potentials negative to -85 mV. The mechanism underlying use-dependent block was determined by defining the time course of block development at potentials between -40 and +20 mV, and the time course of recovery at -85 mV. In 2 microM TTX, the time course of block development at +20 mV contained two phases, a fast phase (tau less than 3 ms) having a mean amplitude of 8.1 +/- 3.2% of control Vmax, and a slow phase (tau = 429 +/- 43 ms) having an amplitude of 35 +/- 2% of control Vmax (n = 5). Recovery from use-dependent block at -85 mV occurred with a time constant of 324 +/- 58 ms (n = 5). The effects of TTX could be well-described by a modulated receptor model with an estimated 12 mV drug-induced shift of inactivation, and state-dependent dissociation constants of 10, 4 and 0.3 microM for rested, activated and inactivated channels. These same drug rate constants could also be used to adequately simulate the reported effects of TTX on plateau sodium currents in a variant model with slow inactivation kinetics.     

Stability of far field R wave signals in different conditions.

AIMS: The presence of far field R wave sensing (FFRS) is usually evaluated in patients with dual chamber pacemakers in supine position. To check if this approach is valid, we tested whether FFRS is consistent both in terms of amplitude threshold and timing characteristics in different daily life conditions. METHODS AND RESULTS: In 42 patients with a DDD pacemaker, the presence, amplitude threshold and timing parameters of FFRS were therefore determined, with patients supine, standing and at peak exercise. Measurements were made of paced and sensed R waves, in unipolar and bipolar sensing configurations (at peak exercise only paced R waves and bipolar sensing). After paced R waves (bipolar sensing) amplitude thresholds/time of FFRS after V pace were 0.32+/-0.18 mV/119-139 ms (supine), 0.32+/-0.16 mV/114-130 ms (upright) and 0.27+/-0.13 mV/121-136 ms (exercise) - with unipolar sensing, this was 0.49+/-0.27 mV/101-150 ms (supine), 0.51+/-0.29 mV/100-144 ms (upright). After sensed R waves (bipolar sensing) amplitude thresholds/time of FFRS after V sense were 0.27+/-0.18 mV/24-42 ms (supine), 0.29+/-0.16 mV/18 to 41 ms (upright) - with unipolar sensing, thresholds were 0.59+/-0.32 mV/3-50 ms (supine), 0.59+/-0.36 mV/2-58 ms (upright). CONCLUSION: given the lower FFRS thresholds with bipolar sensing, bipolar sensing is superior in avoiding FFRS compared with unipolar sensing. No differences were found in terms of amplitude thresholds and timing characteristics with patients supine, standing and at peak exercise. Thus, measurements made in the supine position are basically sufficient to predict the presence/absence of FFRS under different conditions.     

Electrophysiological basis of arteriolar vasomotion in vivo

We tested the hypothesis that cyclic changes in membrane potential (E(m)) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (approximately 3 min(-1)) were preceded (approximately 3 s) by oscillations in E(m) of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E(m) were resolved into six phases: (1) a period (6 +/- 2 s) at the most negative E(m) observed during vasomotion (-46 +/- 2 mV) correlating (r = 0.87, p < 0.01) with time (8 +/- 2 s) at the largest diameter observed during vasomotion (41 +/- 2 microm); (2) a slow depolarization (1.8 +/- 0.2 mV s(-1)) with no diameter change; (3) a fast (9.1 +/- 0.8 mV s(-1)) depolarization (to -28 +/- 2 mV) and constriction; (4) a transient partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarization (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) at the smallest diameter (27 +/- 2 microm) during vasomotion; (6) a slow repolarization (2.5 +/- 0.2 mV s(-1)) and relaxation. The absolute change in E(m) correlated (r = 0.60, p < 0.01) with the most negative E(m). Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO(2) caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E(m) of SMC and EC corresponding with cation fluxes across plasma membranes.     

Effect of areca on contraction of colonic muscle strips in rats

AIM: To investigate the effects of areca on the contractileactivity of isolated colonic muscle strips in rats andmechanism involved.METHODS: Each strip (LMPC, longitudinal muscle ofproximal colon; CMPC, circular muscle of proximal colon;LMDC, longitudinal muscle of distal colon; CMlC, circularmuscle of distal colon. ) was suspended in a tissue chambercontaining 5 mL Krebs solution (37 ℃), bubbledcontinuously with 950 mL@ L-1 O2 and 50 mL@ L-1 CO2 . Themean contractile amplitude (A), the resting tension (T),and the contractile frequency (F) were simultaneouslyrecorded on recorders.RESULTS: Arsca dose dependently increased the meancontractile amplitude, the resting tension of proximal anddistal colonic smooth muscle strips in rats ( P ＜ 0.05). Italso partly increased the contractile frequency of colonicsmooth muscle strips in rats ( P ＜ 0.05). The effects werepartly inhibited by atropine (the resting tension of LMPCdecreased from 0. 44 ± 0. 12 to 0. 17 ± 0.03; the restingtension of LMDC decreased from 0.71 ± 0.14 to 0.03 ± 0.01;the mean contractile amplitude of LMPC increased from -45.8 ± 7.2 to -30.5 ± 2.9; the motility index of CMDC decreasedfrom 86.6± 17.3 to 32.8 ± 9.3; P＜ 0.05 vs areca), but theeffects were not inhibited by hexamethonium (P＞ 0.05).CONCLUSION: Areca stimulated the motility of isolatedcolonic smooth muscle strips in rats. The stimulation ofareca might be relevant with M reoeptor partly.     

Intracellular electrical activity in circular muscle of canine colon

In vivo and extracellular in vitro studies of colon muscle have led to a great deal of disagreement on the characteristics of slow wave activity. As intracellular recordings of electrical activity in single cells give clear records which are easier to analyse, we used this method to study the slow wave activity of the circular muscle of three different parts of the canine colon. Mucosa was removed from segments of proximal, mid and distal canine colon and specimens from each segment were mounted in an organ bath perfused with oxygenated Krebs' solution. Membrane potential, amplitude and frequency of slow waves were measured using intracellular electrodes. Slow wave activity was present at a single, continuous frequency of 4-6 cpm in the circular muscle at all the sites studied in canine colon. There was no significant frequency gradient along the colon: the membrane potential and amplitude of slow waves did not differ significantly in the three parts of the colon.     

Opioids inhibit neuromuscular transmission in circular muscle of human and baboon jejunum.

Intracellular recording techniques were used to study the effects of methionine enkephalin and dynorphin(1-13) on normal circular smooth muscle of human and baboon jejunum. Tetrodotoxin-sensitive inhibitory junction potentials had a mean (+/- SEM) amplitude of 21 +/- 3.3 mV in human jejunum and 24.1 +/- 1.3 mV in baboon jejunum. In both species, exogenously added methionine enkephalin and dynorphin (1-13) decreased inhibitory junction potentials amplitude in a dose-dependent manner with methionine enkephalin being more potent. Both opioid peptides acted on receptors located on axons of intrinsic inhibitory nerves. The effects of both methionine enkephalin and dynorphin(1-13) were blocked by ICI-174,864, a selective delta-receptor antagonist. The selective delta agonist, cyclic [D-penicillamine2, D-penicillamine5]enkephalin, and the selective mu agonist, Try-Pro-NMePhe-D-Pro-NH2, (each 10 mumol/L) decreased inhibitory junction potential amplitude by 79% +/- 6.9% and 61% +/- 4.8%, respectively. The selective kappa agonist, [trans-3,4-dichloro-N-methyl-N-(2-91-pyrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate, (10 mumol/L) had no effect. Although direct postsynaptic opioid receptor blockade of the inhibitory neurotransmitter on the smooth muscle cell has not been ruled out, the authors believe these data suggest that delta and mu receptors were present on inhibitory motor nerves innervating the circular muscle and that methionine enkephalin and dynorphin(1-13) decreased release of inhibitory neurotransmitter(s) by acting on delta receptors.