Nine pregnant, nonlactating cows were used to monitor liver triglycerides before and after parturition. Estimates were made of the contribution of depressed feed intake and parturition to plasma NEFA concentrations and development of fatty liver. Liver biopsies and plasma samples were obtained on d 19, 10, 5, 3, and 1 prior to calving and on d 1, 7, 14, and 21 after calving. Depression of DMI started on d 2 prior to calving and was 40% of DMI on d 3 prior to depression of feed intake. Elevation of plasma NEFA concentrations started prior to DMI depression, on d 5 before parturition. Liver triglyceride infiltration did not occur until the concentration of plasma NEFA was maximized on d 1 after calving. This result implicated the acute rise in NEFA at calving as a contributing factor to triglyceride accumulation in the liver. The increasing plasma glucose and decreasing plasma BHBA prior to calving may have reflected metabolic changes toward gluconeogenesis. Liver glycogen decreased 70% during the final 19 d prior to calving. Hepatic triglyceride infiltration (7.7% DM basis) on d 1 post-partum and duration of DMI depression prepartum were less severe than those observed in previous studies. Frequent liver biopsies did not affect DMI.
The objective of this study was to examine the effects of two different denervation procedures on the distribution of nerve fibers and neurotransmitter levels in the rat jejunum. Extrinsic nerves were eliminated by crushing the mesenteric pedicle to a segment of jejunum. The myenteric plexus and extrinsic nerves were eliminated by serosal application of the cationic surfactant benzyldimethyltetradecylammonium chloride (BAC). The effects of these two denervation procedures were evaluated at 15 and 45 days. The level of norepinephrine in whole segments of jejunum was initially reduced by more than 76% after both denervation procedures, but by 45 days the level of norepinephrine was the same as in control tissue. Tyrosine hydroxylase (noradrenergic nerve marker) immunostaining was absent at 15 days, but returned by 45 days. However, the pattern of noradrenergic innervating axons was altered in the segment deprived of myenteric neurons. Immunohistochemical studies showed protein gene product 9.5 (PGP 9.5)-immunoreactive fibers in whole-mount preparations of the circular smooth muscle in the absence of the myenteric plexus and extrinsic nerves. At 45 days, the number of nerve fibers in the circular smooth muscle increased. Vasoactive intestinal polypeptide (VIP)-immunoreactive fibers, a subset of the PGP 9.5 nerve fibers, were present in the circular smooth muscle at both time points examined. Choline acetyltransferase (CAT) activity and VIP and leucine enkephalin levels were measured in separated smooth muscle and submucosa-mucosal layers of the denervated jejunum. VIP and leucine-enkephalin levels were no different from control in tissue that was extrinsically denervated alone. However, the levels of these peptides were elevated two-fold in the smooth muscle 15 and 45 days after myenteric and extrinsic denervation. In the submucosa-mucosa, VIP and leucine enkephalin levels also were elevated two-fold at 15 days, but comparable to control at 45 days. CAT activity was equal to control in the smooth muscle but elevated two-fold in the submucosa-mucosa at both times. These results provide evidence for innervation of the circular smooth muscle by the submucosal plexus. Moreover, these nerve fibers originating from the submucosal plexus proliferate in the absence of the myenteric plexus. Furthermore, the myenteric neurons appear to be essential for normal innervation of the smooth muscle by the sympathetic nerve fibers. It is speculated that the sprouting of the submucosal plexus induced by myenteric plexus ablation is mediated by increased production of trophic factors in the hyperplastic smooth muscle.
The objective of this research is to examine the relationship between intestinal smooth muscle cell proliferation and polyamine metabolism. Proliferation of muscle is induced by serosal application of benzyldimethyltetradecylammonium chloride (BAC) to a segment of rat jejunum. This treatment destroys all of the longitudinal muscle, one-half of the circular muscle, and the myenteric and extrinsic nerves. The remaining muscle cells undergo mitosis and, by 15 days, the number of muscle cells is increased in both the longitudinal and circular muscle layers. Within 12 h after BAC treatment, there is an increase in the activity of ornithine decarboxylase (ODC) that returns to preinjury levels by 4 days. The smooth muscle content of the three polyamines putrescine, spermidine, and spermine is increased 6 h after injury, returning to preinjury levels within 1 day. DL-alpha-Difluoromethylornithine (DFMO), an irreversible inhibitor of ODC, prevents the transient increases in both ODC activity and the three polyamines in the smooth muscle. In addition to preventing the transient increases in the three polyamines, DMFO has different effects on smooth muscle content of putrescine, spermidine, and spermine. Putrescine content is permanently depleted by DFMO. Spermidine and spermine content is initially decreased within 24 h by DFMO administration. In contrast to the persistent depletion of putrescine by DFMO, spermidine and spermine return to preinjury levels by 2 days. The maximal peak in DNA synthesis occurs 2 days after injury. In DFMO-administered animals, the maximal DNA synthesis occurs 5 days after injury. The increases in smooth muscle wet weight and DNA content 15 days after injury are not affected by DFMO.(ABSTRACT TRUNCATED AT 250 WORDS)
Chronic absence of myenteric neurons from a 5-cm segment of rat jejunum causes alterations in myoelectric activity. Spike potentials characteristic of phase III activity of the migrating motor complex (MMC) are present; however, the number of propagating spike potentials through the myenterically denervated region is reduced. The objective of this study was to examine the effect of the regional loss of myenteric neurons on gastrointestinal transit of a solid marker in the fasted rat. The rate of gastric emptying was not affected by the absence of the myenteric plexus in a 5-cm segment of the jejunum. However, 15 days after either myenteric denervation or vehicle treatment of a segment of jejunum, a more cephalad distribution and decreased rate of intestinal propulsion of the solid marker was observed in the small intestine. This delay in small intestinal transit observed at 15 days was not seen at 48 and 120 days. The decrease in transit at 15 days can be attributed to the handling of the bowel during the surgical procedure. The mouth-to-cecum transit time (MCT) was also not affected by chronic absence of the myenteric plexus. Furthermore, the MCT indicated that bacterial overgrowth, a common manifestation when gut motility is disrupted, did not occur in the small intestine after the experimental destruction of the myenteric plexus. The results of this study indicate that the regional loss of the myenteric plexus does not impair gastrointestinal transit in the fasted rat.(ABSTRACT TRUNCATED AT 250 WORDS)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.