Histamine and interstitial Pulmonary Edema in the Dog

Abstract

Histamine, administered to dogs by various routes, produced peribronchial interstitial edema. Using colloidal carbon as an electron-dense tracer, it was shown that bronchial venules had become leaky at the same time that the minute blood vessels of the pulmonary circulation remained unaffected by the histamine. The effect of histamine was rapid and brief in duration: wide interendothelial gaps appeared in the walls of bronchial venules through which blood and tracer escaped into the interstitium. This action of histamine seemed to be related to the presence in the bronchial venular endothelium of abundant cytoplasmic fibrils that presumably have contractile capacity. Water content of the lungs was consistent with morphologic evidence that histamine promoted the accumulation of fluid in the lungs. The same pattern of response was observed after bradykinin or compound 48/80, a mast cell degranulator. In contrast to these three agents, serotonin did not affect bronchial venular permeability to colloidal carbon. Consideration of these observations in the light of the large extent of the bronchial venular plexus, raises the possibility that the bronchial venular system may play an important reabsorptive role under normal circumstances and that it may also be involved in the genesis of certain types of interstitial pulmonary edema. KEY WORDSserotonin bradykinin 48/80 permeability bronchial circulation endothelial contraction electron microscopy colloidal carbon • In the systemic circulation, histamine, serotonin, and other vasoactive substances selectively affect the venular end of the microcirculatory bed (1-4). Whether the consecutive segments of the microcirculation the lung react differently to such agents, is unknown. Also unknown is whether the minute blood vessels of the bronchial and pulmonary circulations differ with respect to ultrastructure and permeability. These uncertainties merit clarification since the lung in many species is rich in histamine and other humoral substances that are capable of altering vascular permeability (5). Attempts by others to determine the effects of a variety of humoral agents on the permeability of small pulmonary blood vessels (6-8) have been inconclusive because the agents were administered in such quantities, and by such routes, that they exerted systemic as well as local effects.

Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability.

“…There was no difference between the steady- Histamine has also been shown to increase microvascular permeability in the lung. Pietra et al demonstrated leakage of carbon particles from bronchial venules caused by histamine in dogs (14). We previously reported large, sustained increases in lung lymph flow and lymph protein clearance caused by histamine I____.____.____ t__ infusion in unanesthetized sheep (1).…”

Criteria for a Risk of Pneumonias in Acute Poisoning by Psychotropic Agents

“…Известно, что высокие концентрации гистамина приводят к повышению проницаемости легочных ка пилляров [25] и бронхиальных венул, увеличивая поры их эндотелия [26]. Он также вызывает сужение перифе лабораторных показателей у больных с осложненным течением заболевания (n=22) рических бронхов [27], способствуя нарушению венти ляционной функции легких и создавая предпосылки для развития в них воспалительных процессов.…”

Intravenously administered oligonucleotides can be delivered to conducting airway epithelium via the bronchial circulation

“…Only 150 mg/kg increased leakage and was therefore chosen as the most effective dose. [14][15][16][17][18][19][20]. None of the doses tested altered leakage in the parenchyma.…”

“…10 Inflammatory mediators have previously been shown to cause the formation of gaps up to 500 nm between bronchial endothelial cells. 18,19 We, therefore, developed a model of bronchial microvascular leakage using the inflammatory mediators PAF, histamine and bradykinin, in an attempt to open the gaps between the bronchial endothelial cells and allow more LPD complexes to escape from the bronchial vasculature. Although the combined optimized doses of PAF and histamine significantly increased leakage in the larynx/trachea and main bronchi, the mediators did not increase LPD escape from the bronchial vasculature.…”

“…[14][15][16][17] Inflammatory mediators have previously been shown to cause the formation of gaps up to 500 nm between bronchial endothelial cells in rat and dog airways. 18,19 Previous studies have shown that inflammatory mediators increase the delivery of gene transfer agents to other tissues. [20][21][22] Here, we evaluated the effects of three inflammatory mediators, platelet-activating factor (PAF), histamine and bradykinin and assessed whether the most effective inflammatory mediator(s) could increase escape of LPD and 'naked' ODNs from the bronchial circulation and consequently, increase transfection of the conducting airway epithelium.…”