Histamine in stress ulcer prophylaxis in rats.

BACKGROUND: Gastrin and its analogues increase the gastric acid secretion, but also enhance mucosal defense mechanisms. On the other hand, increased formation of histamine leading to an increase in gastric acid secretion is accompanied with gastroprotection and acceleration of gastric ulcer healing. AIM: Of this study was to examine the effect of histamine on stress induced gastric ulcers in rats. METHODS: Male Wistar rats were exposed to water immersion and restrain stress (WRS) for 3.5 h at 23 degrees C. Before WRS rats were pretreated with saline, histamine, ranitidine or omeprazole. RESULTS: WRS produces gastric lesions which were strongly reduced by ranitidine or omeprazole. Also treatment with histamine markedly reduced ulcer area evoked by WRS. Addition of histamine to ranitidine or omeprazole caused an additional reduction in ulcer area. Gastroprotective effect of histamine was accompanied with the increase in gastric blood flow (GBF). Administration of omeprazole or ranitidine alone was without significant effect on GBF. Histamine caused an slight decrease in gastric luminal pH, whereas ranitidine or omeprazole significantly increased gastric luminal pH. Plasma interleukin-1beta was significantly reduced after administration of omeprazole, ranitidine, or histamine, however, the effect of histamine was less pronounced. DNA synthesis was increased after administration of omeprazole, ranitidine or histamine when compared with WRS alone. Administration of histamine in combination with ranitidine or omeprazole caused an additional increase in DNA synthesis. CONCLUSIONS: Histamine exhibits protective effect and increases gastroprotective effect of ranitidine and omeprazole against stress-induced gastric lesions. This effect of histamine seems to be independent on gastric acid secretion but related to the increase in gastric blood flow and the reduction in activation of cytokine cascade.     

Acute postembolic pulmonary edema in vagotomized rats

1. In the rat, pulmonary embolism induced by intravenous administration of gaseous carbon dioxide increases intrapulmonary water content. When the rat is vagotomized before emboli are produced, an important lung edema is found. 2. Strong respiratory stimulation with lung hyperinflation seems to be the cause of this facilitated alveolar transudation. 3. Mechanical factors operating after pulmonary embolism are those which explain transudation after inhalation of hypercapnic gas mixtures in vagotomized rats.     

Histamine dependence of pentagastrin-stimulated gastric acid secretion in rats.

Does gastrin stimulate gastric acid secretion by direct action on oxyntic cells, by releasing histamine, or by being potentiated by histamine? Previous studies in the mouse pointed to gastrin-regulated histamine release. Guinea pig and rat are well known to vary in their sensitivity to histamine. Therefore, the effects of histamine and pentagastrin were compared quantitatively on isolated, lumen-perfused, stomach preparations from these species in the absence and presence of histamine H2-receptor blockade. The loss of potency of histamine in the rat was mirrored by a loss of potency of pentagastrin consistent with the idea that pentagastrin acts by releasing histamine. In the rat, a well-defined pentagastrin curve was obtained in the presence of histamine H2-receptor block as though pentagastrin acts both directly on the oxyntic cell and indirectly by releasing histamine. It was not necessary to invoke a potentiating interaction between histamine and pentagastrin at the oxyntic cell; the two effects appeared simply to add. Potentiation was observed, however, between other combinations of stimuli, for example, between vagal nerve and pentagastrin stimulation. The physiological consequences of these results are discussed.     

Histamine content of peritoneal and tissue mast cells of growing rats

Summary p-Phenylenediamine/pyrocatechol mixture (PPD-PC) was evaluated as a reagent for the ultracytochemical demonstration of retrograde axonal transport of horseradish peroxidase (HRP). HRP crystals were applied to the proximal stumps of the severed infraorbital nerves in rats. After 48 h the rats were sacrificed by perfusion, and the trigeminal ganglia ipsilateral to the severed nerves were processed for HRP cytochemistry and then prepared for electron microscopy. PPD-PC was rapidly oxidized in HRP-labeled neurons to form a dark brown-black osmiophilic reaction product which was more readily visible than the DAB product in the sections. This facilitated selection by light microscopy of areas in the epoxy wafers for ultrathin sectioning. In thin sections viewed under the electron microscope, the osmicated electron opaque PPD-PC reaction product was present in membrane-bound structures including smooth endoplasmic reticulum and granules of various sizes. The PPD-PC reaction product formed after 10-min incubation appeared to be more electron opaque than the DAB reaction product formed after 20 min. PPD-PC was found to be much less readily oxidized than DAB by endogenous hemoproteins. This methodology facilitated the ultracytochemical localization of HRP in neurons following retrograde axonal transport.Supported by NIH Grants DE 04730, DE 02668 and DE 00288 from the National Institute for Dental Research, NIH Grant RR 0533 from the Division of Research Facilities and Resources, and a grant to the Neurobiology Program from the Alfred P. Sloan Foundation     

Pulmonary blood volume and edema in postpneumonectomy lung growth in rats

After pneumonectomy in young animals, the contralateral lung undergoes compensatory growth and generally attains the same weight and air space volume as both lungs in age-matched controls. In this study, we determined the contribution of lung edema and increased blood volume to the weight gain in rats. Three weeks after pneumonectomy (n = 18) or sham pneumonectomy (n = 17), the pulmonary blood volume and the extravascular water and albumin were evaluated by use of 51Cr-labeled erythrocytes and 125I-labeled albumin. The air space volume, blood-free lung weights, and DNA and protein content were also compared. The data show that the total pulmonary blood volumes and the blood volume per gram of blood-free dry lung were similar in pneumonectomized and age-matched sham controls. The total extravascular albumin and the extravascular albumin per gram of blood-free dry lung were also similar as well as the extravascular lung water, wet-to-dry weight ratios, DNA and protein content, and air space volumes. These data indicate that the increased weight of the postpneumonectomy lung was due to cellular and stromal proliferation. The blood volume and interstitial fluid increased in proportion to the increase in lung parenchyma. Neither vascular congestion nor increased extravascular protein and water contributed to the observed weight gain.     

MRI detection of hyperoxia-induced lung edema in Zn-deficient rats

In a pioneering application of proton Magnetic Resonance Imaging (MRI), lung edema has been monitored in vivo in Zn-deficient rats exposed to 85% oxygen. Dietary Zn appears to play a role in protecting against hyperoxia-induced lung damage.     

Acute pulmonary edema induced by CO2 in rats

High concentrations (FiCO2 0.3) of carbon dioxide in the inspired air provoke acute pulmonary oedema in the vagotomized rats only, the animals dying of acute asphyxia in a few minutes. Vagotomy accelerates the production of pulmonary transudates mainly by increasing capillary-alveolar transmural pressure: tidal volume and pleural depression are largely augmented after stimulation of the respiratory centers by CO2.     

Histamine mediates the pro-inflammatory effect of latex of Calotropis procera in rats

INTRODUCTiON: Calotropis procera is known to produce contact dermatitis and the latex of this plant produces intense inflammation when injected locally. However, the precise mode of its pro-inflammatory effect is not known. In present study we have pharmacologically characterized the inflammation induced by latex of C. procera in a rat paw edema model and determined the role of histamine in latex-induced inflammation. METHODS: Inflammation was induced in the hind paw of rats by injecting different doses of dried latex (DL) of C. procera. The inhibitory effect of phenylbutazone, dexamethasone, celecoxib, cyproheptadine, chlorpheniramine and compound 48/80 on edema volume was evaluated and compared with that against carrageenan. The histamine content of DL was measured fluorometrically. RESULTS: DL produced dose-dependent inflammation of the rat paw. Cyproheptadine and chlorpheniramine effectively inhibited DL-induced inflammation (90%; p < 0.01), while anti-inflammatory drugs phenylbutazone, dexamethasone and celecoxib were more effective against carrageenan-induced inflammation. Depletion of mast cell histamine by compound 48/80 produced a significant decrease in DL-induced inflammation as compared with carrageenan (500% versus 25%). DL was also found to contain about 6 microg/g of histamine. CONCLUSIONS: Thus, our study shows that the biogenic amines play a significant role in C. procera latex-induced inflammation and antihistaminic drugs could be effectively used to inhibit inflammatory response elicited by exposure to latex.     

Histamine paw edema of mice was increased and became H2-antagonist sensitive by co-injection of nitric oxide forming agents,but serotonin paw edema was decreased

Nitric oxide (NO) suprisingly caused the opposite effect on histamine and serotonin edema. The local injection of acidified nitrite (0.3–30 μg /paw which correspond to 10 μg−1mg/kg) increased histamine edema of mice up to 45±4% and suppressed serotonin edema to 90±3%. Other NO-generators (nitroprusside sodium and hydroxylamine) showed similar effects. These results were in accordance with our previous data on endogenous NO. Methylene blue (MB, 30ng/paw which corresponds to 1 μg/kg) suppressed histamine edema (62±3%) and increased serotonin edema (43±3%) in normal mice, being reversed by acidified nitrite. This suggests the involvement o of guanosine 3′, 5′ -cyclic monophosphate (cGMP) formation for the action of NO. Histamine edema became sensitive to H₂-antagonist, cimetidine, by co-injection of 30 μg/paw (which corresponds to 1mg/kg) acidified nitrite (ED₅₀=30 μg/kg versus ⪢ 1mg/kg). NO seemed to modify the histamine receptor(s) or tautomeric form of histamine. NO, O₂⁻ and other oxyradicals might finely control the vascular permeability together with inflammatory mediators.     

Histamine agonist and antagonist drugs: interference with CNS control of GH release in rats

The effects of the administration into the brain ventricle of histamine, selective H1- and H2-receptor agonists and antagonists and chemically similar substances with nonspecific activity on basal and morphine-stimulated growth hormone (GH) secretion in normal male rats were studied. None of the drugs had any significant effect on baseline rat GH levels, but histamine and H1 agonists were able to decrease the rat GH release evoked by morphine. Mepyramine (H1 antagonist) had no consistent effect by itself but was effective in preventing the inhibitory action of 2-methylhistamine (H1 agonist). H2 agonists and antagonists and their chemical analogues were all inhibitory, but by a mechanism which is nonspecific and must be interpreted cautiously. These results confirm the inhibitory effect of histamine on rat GH release and indicate that H1 receptors in the CNS are responsible for this effect.     

Histamine and microcirculation

Recent research of histamine metabolism suggests that microvascular smooth muscle and endothelial cells are under the continuous dilator influence of minute quantities of intrinsically formed histamine, produced by action of an inducible form of histidine decarboxylase. Various autonomous dilator activities of the microcirculation, e.g., vasomotion, reactive and post- exercise hyperemia and autoregulation, may all involve interplay of this intrinsic dilator with an intrinsic constictor mechanism. Drastic stimuli which cause a marked increase in histamine output locally or systemically, may lead to the early, slowly-developing microvascular changes in inflammation and shock, respectively.