Intestinal vasoconstriction after hemorrhage: roles of vasopressin and angiotensin
01 Nov 1970-American Journal of Physiology (American Physiological Society)-Vol. 219, Iss: 5, pp 1342-1347
About: This article is published in American Journal of Physiology.The article was published on 1970-11-01. It has received 150 citations till now. The article focuses on the topics: Angiotensin II & Angiotensin receptor.
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TL;DR: The authors are indebted to Carolyn Brewer and Gaynell Barnes for their excellent clerical assistance.
403 citations
TL;DR: It is concluded that low-pressure baroreceptors, presumably in the cardiopulmonary region, initiate splanchnic and forearm vasoconstriction with more pronounced vasconstriction occurring in the forearm.
Abstract: Regional vascular responses to gradual reductions in right atrial pressure and aortic pressure were investigated in nine men. In each study, lower body negative pressure was applied in a ramp of -1 mm Hg/min for 40-50 minutes. During the range from control to -20 mm Hg, right atrial pressure (4 studies) fell from 4.2 mm Hg to -0.6 mm Hg; heart rate was slightly reduced (2 beats/min), and aortic mean pressure and pulse pressure (6 studies) were unchanged. The maximal rate of rise of aortic pressure showed no consistent trends. Forearm blood flow (30 studies) fell with the onset of lower body negative pressure and reached 67% of the control value by -20 mm Hg. Splanchnic blood flow (14 studies) was significantly reduced by -7 mm Hg and fell to 89% of control by -20 mm Hg. During the range from -20 to -50 mm Hg, right atrial pressure continued to fall. Aortic mean pressure fell slightly or was unchanged in four subjects and fell dramatically at -35 mm Hg in two subjects. Aortic pulse pressure began to fall at about -20 mm Hg and fell linearly thereafter. Heart rate paralleled aortic pulse pressure ( r = -0.86 to -0.93). Forearm blood flow fell to 55% and splanchnic blood flow fell to 65% of control at -50 mm Hg. Thus, significant vasoconstriction occurred without measurable change in arterial blood pressure. We concluded that low-pressure baroreceptors, presumably in the cardiopulmonary region, initiate splanchnic and forearm vasoconstriction with more pronounced vasoconstriction occurring in the forearm.
357 citations
TL;DR: An overview of the current understanding of AMI is presented, based on reported evidence, of the poor understanding of its pathophysiology and its mild and nonspecific symptoms, which often delay its diagnosis.
Abstract: Intestinal ischemia has been classified into three major categories based on its clinical features, namely, acute mesenteric ischemia (AMI), chronic mesenteric ischemia (intestinal angina), and colonic ischemia (ischemic colitis). Acute mesenteric ischemia is not an isolated clinical entity, but a complex of diseases, including acute mesenteric arterial embolus and thrombus, mesenteric venous thrombus, and nonocclusive mesenteric ischemia (NOMI). These diseases have common clinical features caused by impaired blood perfusion to the intestine, bacterial translocation, and systemic inflammatory response syndrome. Reperfusion injury, which exacerbates the ischemic damage of the intestinal microcirculation, is another important feature of AMI. There is substantial evidence that the mortality associated with AMI varies according to its cause. Nonocclusive mesenteric ischemia is the most lethal form of AMI because of the poor understanding of its pathophysiology and its mild and nonspecific symptoms, which often delay its diagnosis. Mesenteric venous thrombosis is much less lethal than acute thromboembolism of the superior mesenteric artery and NOMI. We present an overview of the current understanding of AMI based on reported evidence. Although AMI is still lethal and in-hospital mortality rates have remained high over the last few decades, accumulated knowledge on this condition is expected to improve its prognosis.
268 citations
TL;DR: A newly described, cytokine-like molecule, high-mobility group B1, increases permeability of cultured epithelial monolayers in vitro and murine ileal mucosa in vivo.
Abstract: Purpose of review Tight junctions between adjacent epithelial cells are essential for the maintenance of compositionally distinct fluid compartments in various organs, such as the liver, lungs, kidneys, and intestine. These epithelial organs are commonly affected in the condition known as multiple organ dysfunction syndrome, which can complicate the clinical course of patients with sepsis or other conditions associated with poorly controlled systemic inflammation. The gut serves as a useful model for this problem, and studies using reductionist in vitro models and experiments carried out using laboratory animals are starting to clarify the cellular and biochemical mechanisms that are responsible for intestinal epithelial hyperpermeability secondary to critical illness. Recent findings One key factor that has been identified is excessive production of nitric oxide and related species, although other factors, such as increased expression of the cytokine interleukin 6, appear to be important as well. A newly described, cytokine-like molecule, high-mobility group B1, increases permeability of cultured epithelial monolayers in vitro and murine ileal mucosa in vivo. Summary
208 citations