Microvessels in the cheek pouch of the hamster were investigated to determine their structural, reactivity, and permeability characteristics after the induction of diabetes. To induce diabetes, hamsters were injected with streptozotocin (50 mg/kg body wt./day, i.p., for 3 days). Vehicle-injected, age-matched hamsters were the controls. Diabetic hamsters were characterized by elevated serum glucose (greater than 300 mg/dl) and triglycerides and decreased serum insulin (50%). Microvascular studies were completed on cheek pouch microvessels suffused with Ringer's solution (37 degrees C, pH 7.4) bubbled with 95% N2-5% CO2. Vascular dimensions and reactivity of selected arterioles and venules to microapplications of norepinephrine were determined with a video micrometer using intravital microscopy. Restrictiveness of the microvascular membranes to fluorescein-labeled dextran fractions (mol wt: 150,000; 40,000; 20,000 daltons) was measured by determining the number of leaky sites. Stimulation of membrane permeability by histamine was investigated. There were no major alterations in arteriolar lumen and wall diameters, whereas venular lumen diameters were increased in hamsters diabetic for two months. Likewise, arteriolar responses to norepinephrine were not altered by diabetes; however, venular responses were decreased at two months. The restrictiveness of the vascular membrane to various dextran fractions was dramatically decreased in the diabetic animals at two months. Histamine did not alter microvascular leakage in the diabetic as it did in the normal hamsters. These studies indicate that microvascular alterations, venular dilation, and increased permeability to large molecules occur in the diabetic hamster within two months after the induction of diabetes.
Postresection villus hyperplasia is a major compensatory mechanism in the short-bowel patient. Substances capable of augmenting postresection mucosal hyperplasia could have therapeutic implications. Human growth hormone (hGH) and human growth hormone releasing factor (hGHRF) stimulate growth of the gastrointestinal tract; however, the diabetogenic actions of growth hormone limit its usefulness in clinical practice. Plerocercoid larvae of the tapeworm Spirometra mansonoides produce an analog of hGH void of diabetogenic side effects. We assessed effects of plerocercoid growth factor (PGF) on mucosal adaptation following 70% proximal jejunoileal resection in young rats. Mucosal weight, DNA, protein, and total sucrase activity per centimeter of bowel were increased in resected PGF-treated animals compared to resected controls. We conclude PGF augments intrinsic postresection mucosal hyperplasia following extensive intestinal resection.
The only observed morphological difference between Spirometra erinacei and S. mansonoides is the uterine shape of the mature proglottid. Two species of worms are thought to be evolutionarily closely related. Biomolecular comparison of the two worms by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis was conducted to observe the genetic distance. The 28s rDNA, mitochondrial cytochrome c oxidase subunit I (mCOI), and ribosomal internal transcribed spacer 1 (ITS1) fragments were obtained from the worms by PCR. The PCR products were cleaved by 5 four-base pair restriction enzyme combinations (Msp I, Hae III, Alu I, Cfo I, Rsa I), electrophoresed and analyzed with PAUP 3.1.1. The fragment patterns of 28S rDNA and ITS1 demonstrated that two worms were in identical systematic tree with bootstrap number 94 and 100, respectively. As for mCOI, bootstrap number was 74 in a different tree. Above results are indicative of recent common ancestry between S. erinacei and S. mansonoides.
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.