Lateral cecal arterial blood flow, carotid arterial pressure, heart rate, and mechanical activity of the circular and longitudinal muscle layers of the cecal body were measured in 7 conscious healthy horses during IV infusion of physiologic saline solution for 60 minutes (control), during a 60-minute IV infusion of dopamine (at dosages of 1, 2.5, and 5 microgram/kg/min), and for 60 minutes after IV infusion of dopamine. The mean values for lateral cecal arterial blood flow during IV infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min were not significantly different from the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. The mean values for lateral cecal arterial blood flow, however, were significantly greater during IV infusion of dopamine at a dosage of 5 microgram/kg/min than the mean values for lateral cecal arterial blood flow during IV infusion of saline solution. Intravenous infusion of dopamine at 1 and 2.5 microgram/kg/min did not significantly change the mean values for carotid arterial pressure. In contrast, the mean values for carotid arterial pressure were significantly less during IV infusion of dopamine at dosages of 2.5 and 5 microgram/kg/min than during infusion of saline solution. The mean values for heart rate were not significantly altered by infusion of dopamine at a dosage of either 1 or 2.5 microgram/kg/min, but infusion of dopamine at a dosage of 5 microgram/kg/min significantly increased heart rate. Intravenous infusion of dopamine at dosages of either 1 or 5 microgram/kg/min did not significantly change the mechanical activity of the circular muscle layer of the cecal body, as measured by the area under the strain gauge deflection curve. Conversely, the mechanical avtivity of the circular muscle layer of the cecal body was significantly reduced by IV infusion of dopamine at a dosage of 2.5 microgram/kg/min. This reduction of circular muscle mechanical activity by dopamine infusion was attributable to a significant decrease in the total duration of contractions. The mechanical activity of the longitudinal muscle layer was not significantly altered by infusion of dopamine at any dose. These results suggest that IV infusion of dopamine at a dosage of 5 microgram/kg/min increased lateral cecal arterial blood flow by either increasing cardiac output or dilating the lateral cecal artery, an effect most likely mediated by dopaminergic or beta-adrenergic receptors. In addition, dopamine had a biphasic effect on contractile activity of the equine cecum.

Effects of xylazine HCl (0.5 mg/kg of body weight, IV) and/or butorphanol tartrate (0.04 mg/kg, IV) or neostigmine methylsulfate (0.022 mg/kg, IV) on myoelectric activity of the cecum and right ventral colon were studied in 4 conscious female ponies. Eight bipolar Ag/AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and right ventral colon (2 electrodes). Recordings began 30 minutes before and continued for 90 minutes after drug administration. Each drug or drug combination was studied on 2 occasions in each pony. Two major patterns of coordinated spike bursts were identified. A series of coordinated spike bursts began at the cecal base and was conducted to the cecal apex (pattern I). A series of coordinated spike bursts began at the cecal apex, traversed the cecum, cecocolic orifice, and right ventral colon and was termed a progressive pattern (pattern II). Xylazine administration caused a significant decrease in patterns I and II for 20 minutes (P less than 0.05). Butorphanol tartrate administration caused a significant decrease in the progressive pattern for 10 minutes (P less 0.05) without affecting the orally directed pattern. Administration of the combination of xylazine/butorphanol significantly decreased the frequency of pattern I for 40 minutes (P less than 0.05) and pattern II for 30 minutes (P less than 0.05). Neostigmine administration caused a significant increase in the frequency of pattern II for 30 minutes (P less than 0.05) without affecting pattern I (P greater than 0.05). Changes in conduction velocity of pattern I or II or the duration of spiking activity were not significantly different because of any treatment.

Five 5 to 6 month old horses were surgically prepared with silver electrodes sutured to the serosa of gastric antrum, duodenum and proximal portions of the jejunum. Normal migrating motility complex (MMC) periodicity was determined during daytime hours in horses that were fed and horses from which food was withheld for 24 hours. Periodicity was defined as time span from the end of one period of regular spike activity (RSA) to the end of the next RSA in the MMC. The periodicity was 120.5 +/- 9.5 (SEM) minutes in horses from which food was withheld, and was 125.7 +/- 20.3 minutes in horses fed hay free choice. Coincident with each duodenal RSA, antral spike activity ceased. Xylazine (0.25 and 0.5 mg/kg), given IV during the period of intermittent spike activity of the MMC to either fed or unfed horses induced, within 2 minutes, a RSA complex in the duodenum that migrated to the proximal portion of the jejunum. This was followed by a period of no spike activity of normal duration, which proceeded on to a period of intermittent spike activity of varying duration to complete the MMC cycle. Pretreatment IV administration of an alpha 2-adrenergic antagonist, tolazoline (1 mg/kg) also provoked a RSA complex, but blocked the xylazine effect. The results indicated that xylazine resets the duodenal MMC in the horse, but does not seriously disrupt proximal gastrointestinal tract motility, and that control of MMC periodicity in this region probably involves more than alpha 2-adrenergic receptors.

The myoelectric activity of the cecum and right ventral colon (RVC) was studied in 4 female ponies. Eight, bipolar Ag-AgCl electrodes were sequentially placed on the seromuscular layer of the cecum (6 electrodes) and RVC (2 electrodes), and recordings were begun 14 days after surgery. The myoelectric activity for each pony was recorded during 12, 60-minute recording sessions done during the interdigestive period (3 to 7 hours after the morning feeding). Coordinated series of spike bursts were recognized as independent motility patterns in the cecum and in the RVC. Local haustra-haustra myoelectric activity involving approximately 40 cm of the cecal body (0.45 +/- 0.03 spike bursts/min) were detected. A series of spike bursts started at the cecal apex and progressed to, but stopped at, the caudal cecal base (0.04 +/- 0.03 spike bursts/min). Infrequently, a series of spike bursts started at the apex and progressed to the cranial cecal base (0.09 +/- 0.01 spike bursts/min). More commonly, a series of spike bursts with a conduction velocity of 3.8 +/- 0.07 cm/s, began in the cranial base and progressed orally to the cecal apex (0.46 +/- 0.03 spike bursts/min). Spike bursts conducted aborally (propulsion) beginning at the origin of the RVC (0.05 +/- 0.07 spike bursts/min) and spike bursts conducted orally (retropulsion; 0.15 +/- 0.02 spike bursts/min) were seen independent of cecal myoelectric activity. A progessive series of coordinated spike bursts, which began at the cecal apex, were conducted through the cecolic orifice and continued into the RVC (0.42 +/- 0.02 spike bursts/min), representing the only pattern common to the cecum and RVC. This pattern, associated with a loud rush of ingesta heard on auscultation, had a conduction velocity of 5.65 +/- 0.12 cm/s and was always generated in the cecal body, near the apex. An apparent electrical pace-maker area was proposed in this area. Duration of spiking activity during the progressive pattern was significantly (P = 0.0001) greater at electrodes 7 and 8 in the RVC than at any electrode locus in the cecum. Coordinated orally directed spike bursts were detected frequently in the cecum before and after the progressive pattern, indicating a complex sequence of motility patterns may exist.