Contractions of a segment of bowel result in alterations of its blood flow. However, the precise temporal and spacial relationships between contractions and mucosal blood flow are unknown. Rats were fitted with strain gauge force transducers and implanted with silver wire electrodes into the muscularis externa of the stomach. In vivo microscopic observation of motility and of the gastric mucosal blood flow was performed during electrical field-stimulated contractions. Contractions originated in the midcorpus, were 0.237 +/- 0.018 cm wide, traveled along the corpus at 0.133 +/- 0.024 cm/s, and had a duration of 5.9 +/- 0.1 s. Antral contractions were 0.174 +/- 0.032 cm wide, traveled at 0.070 +/- 0.009 cm/s, and had a duration of 5.6 +/- 0.7 s. During the contraction, capillary flow velocity in the corpus decreased from a basal value of 410 +/- 105 to 206 +/- 104 microns/s at the peak of a contraction. Five seconds after the contraction was released hyperemia was observed with the flow velocity increasing to 570 +/- 102 microns/s. In the antrum, flow stopped completely during the contraction irrespective of the initial flow velocity and no hyperemia occurred with release of the contraction; rather, flow velocity slowly returned to baseline values. In both regions the flow reductions were in phase with the contractions as measured by the force transducers. These studies provide direct evidence that strong gastric contractions can effectively reduce or stop gastric mucosal blood flow.
Mild head injury can be followed by a triad of emotional, cognitive and somatic complaints (Evans 1992; Brown,Fann, and Grant 1994). Prior head injuries, substance abuse, as well as somatization and posttraumatic stress disorder (PTSD) symptoms are factors which render difficult the assignment of a specific constellation of symptoms fully attributable to the litigated head trauma. There is also a high base rate in the normal population of having suffered a minor head trauma without lasting consequences (Evans 1992; Mittenberg and Strauman 2000). Some suggest that persisting symptoms in the context of a mild head injury and litigation are predominantly the consequence of financial incentives (Binder and Rohling 1996).
The effects of tailshock on gastric contractility and lesions were investigated in rats exposed to 100 1-mA tailshocks while confined inside plastic tubes. A light preceded each shock in one group and was randomly presented with respect to shock in the other. Following the session, animals were given 3 hr of rest before being sacrificed. Contractility of the corpus of the stomach was measured by means of chronically implanted extraluminal force transducers. Contractility was measured in 10-min blocks and analyzed by computer. Lesions were quantified by inspection; quantitative histology was performed on corpus and antrum sections. Signaled (n = 13) and unsignaled (n = 17) shock stimulated high-amplitude gastric contractions in fasted rats, which continued for 2 hr after the shock session. Cumulative contractile activity (1.5-hr shock plus 2-hr rest) in shocked animals was twice that in restrained and unrestrained control animals (n = 19, p less than .05), and contractile activity had a 30%-40% greater average amplitude than after a meal. Compared with unrestrained controls, shocked rats had visibly more mucosal injury (2.2 +/- 0.5 mm2 vs. 0.1 +/- 0 mm2). Larger cumulative contractile activity was associated with a larger area of erosions (r = .36, p less than .05). Frequency and duration of contractions did not distinguish between shocked and unshocked groups. We conclude that in rats, signaled and unsignaled tailshock stimulates persistent, high-amplitude gastric contractions and is associated with injury of the mucosa of the stomach.
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