zea perennis/hemorrhage

Studies concerning with pathogenesis of gastric hemorrhage and mucosal ulceration produced in atherosclerotic rats are lacking. The aim of this study is to examine the role of gastric acid back-diffusion, mast cell histamine release, lipid peroxide (LPO) generation and mucosal microvascular

Though cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) has been recognized for over half a century, it remains a major complication in patients with SAH. Clinical studies have shown that elevated levels of endothelin-1 (ET-1) are present in the cerebrospinal fluid of patients with

The constituents of the roots bleeding sap are an important index characteristic of roots activity and roots-shoots relationship. To compare the differences between the constituents of roots bleeding sap from maize and soybean plants, roots bleeding saps were collected from maize (Zea mays L.

OBJECTIVE Administration of female sex steroids in males after trauma-hemorrhage has salutary effects on the depressed immune responses. METHODS Randomized laboratory experiment. METHODS Male C3H/HeN mice were subjected to midline laparotomy and hemorrhagic shock (35+/-5 mm Hg for 90 minutes, then

OBJECTIVE Apoptosis is implicated in vasospasm and long-term sequelae of subarachnoid hemorrhage (SAH). The authors observed that 17beta-estradiol (E2) can attenuate cerebral vasospasm, lower endothelin-1 production, and preserve normal endothelial nitric oxide synthase expression by reduction of

OBJECTIVE The authors previously demonstrated that 17beta-estradiol benzoate (E2) treatment prevents subarachnoid hemorrhage (SAH)-induced cerebral vasospasm and preserves endothelial nitric oxide synthase (eNOS) in male rats. Changes in the expression of estrogen receptor (ER) subtypes ERalpha and

BACKGROUND Hemorrhagic shock followed by resuscitation stimulates an inflammatory response. This study tests the hypothesis that prefeeding with fish oil rich in ω-3 fatty acids (FAs) will attenuate that response. METHODS Male Sprague-Dawley rats (n = 60; 350 ± 30 g) were randomly but unequally

Adult female chickens were force-fed a corn-soy base diet at 150% of the daily amount consumed by those allowed the same diet ad libitum. Other hens were force-fed diets isocaloric to the 150% group just mentioned, but diet composition was adjusted so that 2/3 of the metabolizable energy (M.E.) came

At 135% of control, Single Comb White Leghorn laying hens were force fed for 3 weeks, diets based on corn or wheat, the latter made isocaloric to the corn-based diet with either corn oil, corn starch, or wheat starch. The hens fed ad libitum received a corn-based diet. Force feeding the corn-based

BACKGROUND Calcium and cholesterol play major roles in the formation of atherosclerosis. Whether severe atherosclerosis induced by co-administration of a mixture containing vitamin D2 (vit D2) and cholesterol can result in gastric hemorrhagic damage is unknown. Gastric oxidative stress and

The intraperitoneal inoculation of pregnant hamsters with vitamin E during the first half of gestation reduced the severity or eliminated the occurrence of grossly observable effects of spontaneous hemorrhagic necrosis (SHN) of the central nervous system in their offspring and improved the

Studies have suggested that the significant suppression of cellular immunity following hemorrhage may be due to an increased release of prostaglandin E2 (PGE2) by macrophages. Since diets high in n-3 polyunsaturated fatty acids decrease PGE2 synthesis, we assessed whether hemorrhage-induced

OBJECTIVE Sex differences in the outcome of aneurysmal subarachnoid hemorrhage (SAH) are controversial, and the potential influence of estradiol on vasodilation is unclear. In the present study the authors evaluate the effect and possible mechanism of 17beta-estradiol (E2) on SAH-induced vasospasm

OBJECTIVE Previously, we showed that 17beta-estradiol (E(2)) treatment prevented the subarachnoid hemorrhage (SAH)-induced cerebral vasospasm in male rats. The aim of this study was designed to further delineate the molecular mechanisms underlying E(2)-induced inhibition of inducible nitric oxide