Misoprostol use in obstetrics

This study is a bibliographic review in order to overview the use, indications and contraindications of misoprostol in obstetrics. Thirty three academic articles in Portuguese, Spanish, and English in the range 2005 to 2014 wer collected and analysed. Misoprostol is a methyl analogue of PGE1 and has anti-secretory action and protective properties of the mucosa, and cause increased uterine contractility, induce the development of contractions and cause cervical effacement, facilitating the expansion necessary to carry out obstetric procedures. It is an important drug in obstetric practice and is indicated for treatment of missed abortion, labor induction, shortens the operatory time in situations where the cervix has no dilation, reduce the frequency of complications and caesarean indications, and can be used in prophylaxis of post-partum hemorrhage. Attention should be paid to its misuse as an abortifacient and the existence of reports of congenital malformations, especially the Moebius Syndrome. It is a stable product, safe, effective, inexpensive and easy management, ensuring broad employability of its clinical use in current obstetrics.

A COMPARATIVE STUDY ON MONOTHERAPY AND COMBINATION THERAPY OF PANTOPRAZOLE WITH PREGABALIN AGAINST SURGICAL ESOPHAGITIS

The objective of this study was to evaluate the effect of pantoprazole and pregabalin on experimental esophagitis in albino rats. The groups of rats fasted for 24 hours and were subjected to pylorus and forestomach ligation. Rats of different groups received normal saline (3 ml/kg, po; sham control), pantoprazole (30 mg/kg, po), pregabalin (30 mg/kg, po) and their combinations along with a parallel toxic control group. Animals were sacrificed after 8 h and evaluated for the gastric pH, total acidity, free acidity and esophagitis index. The morphological changes were scrutinized by digital microscopy. The beneficial effect of pantoprazole and pregabalin against GERD could be attributed to the anti-secretory action of pantoprazole and reduction in the tracheal lower esophageal sphincter release rate by pregabalin. Combination therapy of gamma-aminobutyric acid derivative promotes proton pump inhibitor based healing of reflux esophagitis in animal model. Keywords: Esophagitis, Pantoprazole, Pregabalin, Pylorus ligation, Gamma-aminobutyric acid.

An experimental evaluation of gastro protective activity of paracetamol on ulcerogenicity of some NSAIDs in albino rats

Background: Fixed dose combinations (FDCs) of NSAIDs are commonly prescribed and extensively sold over the counter. An indiscriminate usage of them leads to toxicity, mainly involving gastrointestinal system. Paracetamol appears to have controversial reputation regarding its gastro protective action. In this background, the study was planned to evaluate gastro protective effect of paracetamol on the ulcerogenicity of some relatively new NSAIDs in their therapeutic and sub therapeutic doses.Methods: Gatric toxicity and gastric juice analysis- Pyloric ligation method was adopted for assessing the ulcer index of 3 NSAIDs namely aceclofenac, nimesulide and lornoxicam individually and in combination with paracetamol. Gastric juice collected was subjected for total juice volume, free acidity, combined acidity and total acid output.Results: Paracetamol produced non significant gastric damage similar to that of control. When co administered with therapeutic doses of aceclofenac, nimesulide and lornoxicam, there was significant decrease in their gastric toxicity in a uniform manner and the ulcerogenicity of these NSAIDs in sub therapeutic doses was not affected by paracetamol. This upholds the uniform gastro protective activity of paracetamol in this study and this could be explained by its anti acid secretory action on gastric juice.Conclusions: Paracetamol, itself has least gastric damaging property. When co administered with other NSAIDs, their toxicity is rather reduced than enhancing the mucosal damage by them. Thus FDCs of various NSAIDs available in market are partially justifiable.

The influence of TNFα and IL-8 on secretory action of neutrophils isolated from heifers in the course of bovine respiratory disease

The goal of this study was to give insight into the lesser known action of neutrophils in the course of bovine respiratory disease (BRD). Neutrophils are principally involved in resistance to infection but under certain conditions these cells participate in lung injury. TNFα and IL-8, primary cytokines which play an essential role in neutrophil activation during the inflammatory process, may lead not only to host defence reaction but also to destructive responses. Neutrophil constituents, such as elastase, myeloperoxidase (MPO), alkaline phosphatase (ALKP) and superoxide among others, contribute to tissue destruction. Also, 5-oxo-eicosatetraenoic acid (5-oxo-ETE), the potent activator of neutrophil chemotaxis and degranulation, can cause lung injury. This study revealed that neutrophils under the influence of TNFα exacerbated the release of elastase, MPO, ALKP and superoxide. IL-8, in turn, triggered those neutrophils which were isolated from heifers suffering from BRD, and released elastase, ALKP and 5-oxo-ETE, but not MPO or superoxide (O 2− ). The most pronounced degranulative response was observed in the acute form of BRD and a lesser response was seen in the chronic form. The secretory action of neutrophils varied not only depending on the form and phase of the disease but it also diminished successively during recovery.

Regulation of ecdysis-triggering hormone release by eclosion hormone.

Ecdysis behavior in the tobacco hornworm Manduca sexta (Lepidoptera: Sphingidae) is triggered through reciprocal peptide signaling between the central nervous system and the epitracheal endocrine system. Recent evidence indicates that eclosion hormone may initiate endocrine events leading to ecdysis through its action on epitracheal glands to cause the release of ecdysis-triggering hormone (ETH). Here, we report that direct exposure of epitracheal glands to eclosion hormone in vitro leads to secretion of ETH. The threshold concentration of eclosion hormone needed to evoke release of ETH is approximately 3 pmol l-1. Eclosion hormone also induces elevation of cyclic GMP, but not cAMP, concentration in epitracheal glands at concentrations similar to those causing release of ETH. Both cGMP and 8-Br-cGMP mimic the secretory action of eclosion hormone. The sensitivity of the secretory response to eclosion hormone occurs during a narrow window of development, beginning approximately 8 h prior to pupal ecdysis. However, eclosion hormone can cause elevation of cGMP levels in epitracheal glands long before they acquire competence to release ETH, showing that the initial portion of the signal transduction cascade is in place early in development, but that the absence of a downstream step in the cascade prevents secretion. Measurements of cGMP levels in epitracheal glands during the ecdysis sequence show a sudden elevation some 30 min after the onset of pre-ecdysis, well after ETH secretion has been initiated. ETH secretion can therefore be viewed as a two-step process, beginning at pre-ecdysis when cGMP levels are relatively low, followed by a massive release resulting from a logarithmic elevation of cGMP levels.