Laparoscopic repair of a small bowel herniation through a broad ligament defect.

A 44-year-old female presented with a diagnosis of intestinal obstruction from unknown origin. Laparoscopy revealed herniation of small bowel trough a defect in the left broad ligament. After reduction, the defect was corrected laparoscopically. The post operative recovery was uneventful.

Centrally administered insulin potentiates the pressor response to angiotensin II.

The aim of the present study was to determine if insulin can modulate the pressor response to angiotensin II at brain level in normotensive rats. Anaesthetized male rats were intracerebroventricularly infused with insulin (12 mU/h, n=15) or Ringer's solution as vehicle (n=15) for 2 h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n=10) or vehicle (n=5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In other subset of animals, PD98059 (MAPK inhibitor) or vehicle were intracerebroventricularly administered previously to insulin perfusion for 2 h and changes in MAP in response to intracerebroventricular angiotensin II (5 pmol) injection were evaluated for 10 min (n=6 for each group). Angiotensin II did not modify MAP in vehicle pre-treated rats, but increased MAP in insulin pre-treated animals. Insulin significantly increased Akt phosphorylation, but no changes were observed after angiotensin II injection in vehicle-pretreated animals. Angiotensin II or insulin infusion increased in more than two fold phospho-ERK 1/2 hypothalamic levels. Animals that received insulin infusion followed by Ang II injection presented 4.5 higher values than those which received vehicle, and nearly twice than those who received Ang II without insulin pre-treatment. PD98059 administration abolished the blood pressure response exerted by angiotensin II in insulin pre-treated rats. In conclusion, centrally administered insulin potentiates the pressor effects to angiotensin II, suggesting a novel mechanism, possibly involving MAPK activation, by which insulin influences blood pressure control at central level.

Chronic infusion of angiotensin-(1-7) improves insulin resistance and hypertension induced by a high-fructose diet in rats.

The current study was undertaken to determine whether Ang-(1-7) is effective in improving metabolic parameters in fructose-fed rats (FFR), a model of metabolic syndrome. Six-week-old male Sprague-Dawley rats were fed either normal rat chow (control) or the same diet plus 10% fructose in drinking water. For the last 2 wk of a 6-wk period of either diet, control and FFR were implanted with subcutaneous osmotic pumps that delivered Ang-(1-7) (100 ng.kg(-1).min(-1)). A subgroup of each group of animals (control or FFR) underwent a sham surgery. We measured systolic blood pressure (SBP) together with plasma levels of insulin, triglycerides, and glucose. A glucose tolerance test (GTT) was performed, with plasma insulin levels determined before and 15 and 120 min after glucose administration. In addition, we evaluated insulin signaling through the IR/IRS-1/PI3K/Akt pathway as well as the phosphorylation levels of IRS-1 at inhibitory site Ser(307) in skeletal muscle and adipose tissue. FFR displayed hypertriglyceridemia, hyperinsulinemia, increased SBP, and an exaggerated release of insulin during a GTT, together with decreased activation of insulin signaling through the IR/IRS-1/PI3K/Akt pathway in skeletal muscle, liver, and adipose tissue, as well as increased levels of IRS-1 phospho-Ser(307) in skeletal muscle and adipose tissue, alterations that correlated with increased activation of the kinases mTOR and JNK. Chronic Ang-(1-7) treatment resulted in normalization of all alterations. These results show that Ang-(1-7) ameliorates insulin resistance in a model of metabolic syndrome via a mechanism that could involve the modulation of insulin signaling.