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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine release adjacent to mesenteric arterioles under conditions of ischemia causes vasodilation and increases regional blood flow. This is presumably a protective mechanism which may be blocked by the use of H1 and H2 antagonists. Mesenteric arterioles of 29 rats were observed with intravital microscopy. Diameter and erythrocyte velocity were measured and arteriolar flow was calculated. Histamine was topically applied to the vessels under view in sequentially increasing concentrations (10(-7) to 10(-4) M). Following systemic injection of an H1 or H2 receptor antagonist or ibuprofen, the application of 10(-4) M histamine was repeated. Topical histamine caused vasodilation (122% of control; P less than 0.05) at 10(-4) M with a corresponding increase in erythrocyte velocity and calculated flow (118 and 177% of control, respectively; P less than 0.05 for each). The vasodilatory effects of histamine were blocked by systemic injection of histamine receptor antagonists (H1 + H2 greater than H1 greater than H2), while ibuprofen had no significant effect. In situations in which the gut is at risk for ischemia, the use of H1 and/or H2 receptor antagonists may seriously compromise the mesenteric microcirculation.
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PMID:Effect of histamine and histamine receptor antagonists on rat mesenteric microcirculation. 288 49

In acute experiments carried out in 27 baboons under general anesthesia, the regional gastric mucosal and muscle layer blood flow and gastric acid secretion were measured during 4 hr. Baboons were allocated to each of the following six groups: control, gastric acid stimulation with histamine 40 micrograms/kg/hr intravenous, inhibition of basal or stimulated acid secretion with either ranitidine 50 mg intravenous or omeprazole 1 microgram/kg/hr. There were no significant cardiovascular alterations during the experiments. Histamine stimulation produced a concomitant rise in acid secretion and increase in blood flow only to the mucosal layer of the parietal-cell-bearing area of the stomach. Neither the underlying muscle layer nor the non-parietal-cell-bearing fundic or antral mucosa took part in this response, suggesting that a mechanism controlling blood flow is present in close proximity to the parietal cells. It was also established that the increase in blood flow occurs in response to parietal cell activity and not as a result of the action of histamine on the vascular system. Suppression of both basal and stimulated acid secretion did not cause a fall of mucosal blood flow below basal levels in any part of the stomach, indicating that drugs that inhibit parietal cell activity can be used in conditions where gastric mucosal ischemia should be avoided.
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PMID:Stimulation of gastric acid secretion increases mucosal blood flow in immediate vicinity of parietal cells in baboons. 335 8

Bilateral ischemia induced by occlusion of the carotid arteries for 5 min causes a selective degeneration of CA 1 neurons of the hippocampus of Mongolian gerbils. The degeneration process is complete in 14 days as assessed by light microscopy. After one week, basal values for radioactive cyclic AMP in [3H]adenine-labeled tissue from the CA 1 region of hippocampus are greatly reduced as are the absolute magnitude of accumulations of cyclic AMP elicited by norepinephrine, 2-chloroadenosine and histamine. At 2 and 4 weeks, basal values for radioactive cyclic AMP have nearly attained control values and the response to 2-chloroadenosine is fully restored. The response of cyclic AMP-generating systems to norepinephrine is now significantly greater than in control, while the response to histamine remains reduced in magnitude. The ischemia has no effect on basal values for radioactive cyclic AMP or on responses in [3H]adenine-labeled slices from cerebral cortex. Histamine levels after ischemia are significantly increased above control in the CA 1 region. Basal and histamine-sensitive adenylate cyclase activity in the membrane preparations are slightly decreased during the first week after ischemia, followed by a recovery. There is an inverse correlation between histamine levels and adenylate cyclase activity in individual animals 4 days after ischemia.
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PMID:Degeneration of CA1 neurons in hippocampus after ischemia in Mongolian gerbils: cyclic AMP-systems. 630 59

Histamine is released from the heart during ischaemia-reperfusion injury. As histamine has cardiac effects, we investigated the role of histamine in ischaemia-reperfusion injury of isolated rat hearts. A Langendorff-model with 30 min global (37 degrees C) ischaemia followed by 60 min reperfusion was employed. The effects of ischaemia alone (n = 10, group 1.1 + n = 10, group 2.1, 2 different series), and ischaemia with H1- and H2-receptor blockade with cimetidine (10 microM, n = 10), chlorpheniramine (10 microM, n = 8), terfenadine (10 microM, n = 8), and promethazin (10 microM, n = 9), or both cimetidine and chlorpheniramine (n = 8), were studied. Histamine was measured in the coronary effluent and cardiac tissue of group 1.1. Release of histamine increased from 6.5 +/- 1 pmol min-1 before ischaemia to 19 +/- 3 pmol min-1 at the start of reperfusion. Ischaemia decreased left ventricular developed pressure to 18 +/- 11% (1.1) and 50 +/- 11% (2.1) of initial value (mean +/- SEM) at the start of reperfusion. Left ventricular end-diastolic pressure increased from 0 to 79 +/- 8 mmHg (1.1) and 39 +/- 9 (2.1) mmHg, while left ventricular systolic pressure was unchanged (101 +/- 12% in 1.1 and 101 +/- 10% in 2.1). Severe arrhythmias were induced in 90 (1.1) and 30 (2.1)% of the hearts, while coronary flow decreased during reperfusion. H2-blockade did not modify the changes in left ventricular pressures, coronary flow, or heart rate induced by ischaemia. Three different H1-blockers increased left ventricular systolic pressure, inhibited the decrease of developed pressure, attenuated the increase of end-diastolic pressure, and totally inhibited reperfusion arrhythmias. The effect of both blockers together was similar to that of H1-blockers alone. Coronary flow was increased during reperfusion in two of the groups with H1-blocker compared with ischaemic controls. Increased release of histamine from ischaemic-reperfused rat hearts concurred with depression of left ventricular function and arrhythmias during early reperfusion. Cardiac dysfunction during reperfusion was attenuated by three different H1-receptor blockers.
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PMID:Histamine release and its effects in ischaemia-reperfusion injury of the isolated rat heart. 751 35

The role of histamine in cardiac physiology and pathophysiology is not clarified, but is dependent on species. The effects of exogenous histamine in Langendorff-perfused rat hearts were investigated. 1 mM, 100, 10, 1 and 0.1 microM of histamine (n = 7 each) as 15 min infusions were employed in a dose-response study, and compared to control perfused hearts (n = 7). In another experimental series, 100 microM histamine (n = 15) was added during reperfusion after 25 min global ischemia, and compared to control ischemia-reperfusion (n = 15). The maximal response to histamine in the dose-response study (100 microM) was an increase of left ventricular developed pressure to 126 +/- 8% of initial value (mean +/- SEM, p < 0.04), and increase of coronary flow to 152+6% (p < 0.02) after 5 min infusion. 100 microM histamine did not significantly influence heart rate or rhythm. The lowest concentration (0.1 microM) did not have effects cardiac performance. Reperfusion with histamine for 2 min after ischemia reduced left ventricular developed pressure to 68 +/- 10% of initial value versus 116+17% in ischemic controls (p < 0.05), and increased left ventricular end-diastolic pressure to 24 +/- 8 mmHg compared to 6 +/- 2 mmHg in controls (p < 0.04). Left ventricular pressures were similar in hearts reperfused with histamine and in ischemic controls for the rest of the observation. Coronary flow increased during reperfusion in hearts given histamine. Histamine had a dose-dependent positive inotropic and vasodilatory effect in isolated rat hearts. Exogenous histamine had only minor effects on post-ischemic cardiac function.
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PMID:The effects of exogenous histamine in isolated rat hearts. 765 78

Effects of histamine receptor ligands on the glibenclamide-sensitive K+ currents induced by K+ channel openers, cromakalim and Y-26763, were examined in follicle-enclosed Xenopus oocytes. Histamine H1 receptor antagonists, promethazine, dimethindene and chlorpheniramine all decreased cromakalim-induced K+ currents with IC50 values of 31.5 microM, 29.5 microM and 138 microM, respectively. These compounds also blocked Y-26763-induced K+ currents with comparable IC50 values. Histamine (1 mM) and histamine H2 receptor antagonists, cimetidine (0.5 mM) and ranitidine (1 mM) had little effect on these K+ currents. These results suggest that histamine H1 receptor antagonists inhibit glibenclamide-sensitive K+ currents by a mechanism other than the histamine H1 receptor antagonism. The inhibitory effects might explain, in part, the reported actions of histamine H1 receptor antagonists in ischemia.
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PMID:Inhibition by histamine H1 receptor antagonists of endogenous glibenclamide-sensitive K+ channels in follicle-enclosed Xenopus oocytes. 790 90

Histamine is synthetized in the heart, and released by ischemia-reperfusion injury in several species. Histamine has arrhythmogenic, chronotropic, inotropic and vasoactive effects. Cardiac histamine release during ischemia-reperfusion may be mediated by toxic oxygen metabolites. We studied the effect of ischemia-reperfusion and toxic oxygen metabolites on release and synthesis of histamine in the isolated rat heart (Langendorff model). The following groups were included: I, (n = 10) control perfusion for 60 min; II, (n = 7) H2O2 (200 microM) was given for 10 min followed by 50 min recovery; III, (n = 7) thiourea (15 mM) was given in addition to H2O2; IV, (n = 7) thiourea given alone; V, (n = 7) catalase (150 U/ml) plus H2O2; VI, (n = 7) 20 min ischemia followed by 40 min reperfusion. The contents of histamine in the coronary effluent and in cardiac tissue were measured repeatedly (radioenzymatic method). Ischemia-reperfusion and toxic oxygen metabolites increased release of histamine in the coronary effluent. Concomitantly the histamine contents in cardiac tissue increased, indicating increased synthesis of histamine.
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PMID:Toxic oxygen metabolites and ischemia-reperfusion increase histamine synthesis and release in the isolated rat heart. 844 Nov 80

Myocardial ischemia-reperfusion injury increases both tissue levels and release of histamine. To study the possible effects of ischemia-reperfusion on histamine metabolism tissue activities of histidine decarboxylase (HDC), histamine N-methyl transferase (HNMT) and diamine oxidase (DAO) were investigated in isolated rat hearts subjected to either 20 min global ischemia and 40 min reperfusion (n = 10) or control perfusion (n = 8). Histamine in the coronary effluent increased from 21 +/- 4 nmol/min (mean +/- SEM) before ischemia to 55 +/- 5 and 50 +/- 7 nmol/min after 4 and 10 min reperfusion (p < 0.004 and p < 0.004). Tissue HDC activity did not change during observation in any group. HNMT activity was unchanged in controls, but increased from 0.37 +/- 0.04 to 0.84 +/- 0.18 and 0.96 +/- 0.22 pmol methylhistamine/mg protein hour after 4 and 10 min reperfusion (p < 0.008 and p < 0.01). DAO decreased similarly in controls and ischemic-reperfused hearts during observation. In conclusion, the previously observed increase of tissue histamine during reperfusion cannot be explained by increased histamine synthesis or decreased histamine catabolism.
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PMID:Activity of histamine metabolizing and catabolizing enzymes during reperfusion of isolated, globally ischemic rat hearts. 868 95

The effects of a clinically used purified micronized flavonoid fraction (S5682) containing 90% diosmin and 10% hesperidin on increased microvascular permeability induced by histamine, bradykinin and leukotriene B4 (LTB4) were investigated by intravital microscopy in the cheek pouch preparation of diabetic hamsters. We also investigated the effects of S 5682 on macro- molecular permeability increase and leukocyte adhesion during ischemia-reperfusion using the same preparation. Diabetes was induced by an intraperitoneal injection of streptozotocin (50 mg/kg). S 5682, suspended in 10% lactose solution, or vehicle (10% lactose) was administered orally for 25 days at 20 mg/kg/day (10 mg/kg twice a day), starting 5 days after the streptozotocin injection. Fluorescein isothiocyanate-labelled dextran (molecular weight 150,000) was given intravenously, 30 min after completion of the cheek pouch preparation. The leukocytes were stained by continuous intravenous infusion of acridine orange (0.5 mg/ kg/min). Histamine (2 microMs), bradykinin (1 microM), and LTB4 (0.01 microM), applied topically for 5 min, increased the number of fluorescent vascular leakage sites in postcapillary venules. A temporary ischemia (duration: 30 min) with total circulatory arrest of the cheek pouch was obtained by clamping the neck of the everted pouch. The maximum number of leaky sites (per cm2 in the prepared area) which occurs either at 5 min after the beginning of each topical application or 10 min after the onset of reperfusion was quantified in UV light microscopy. The results from 60 animals divided into ten groups of 6 animals each are presented as means +/- SEM. In comparison with vehicle, S 5682 significantly inhibited the macromolecular permeability increasing the effect of histamine (343.8 +/- 18.5 vs. 91.0 +/- 8.2 leaks/ cm2; p > 0.001), bradykinin (347.0 +/- 14.6 vs. 110.3 +/- 8.5 leaks/cm2; p < 0.001) and LTB4 (323.0 +/- 15.5 vs. 161.3 +/- 13.8 leaks/cm2; p < 0.001). At reperfusion, after 30 min ischemia, S 5682 significantly decreased the observed macromolecular permeability (168.5 +/- 19.7 vs. 52.7 +/- 6.3 leaks/cm2; p < 0.01). Flavonoid-treated animals also tended to have a lower number of leukocytes adhering to the venular endothelium (104.8 +/- 11.0 vs. 75.8 +/- 9.7/6 mm2; p > 0.05). These results demonstrate that oral administration of S 5682 for 25 days at 20mg/kg body weight/day has a protective effect on leakage of macromolecules after application of permeability-increasing substances and during ischemia-reperfusion in the cheek pouch microvasculature of diabetic hamsters. In conclusion, the present data illustrating the inhibitory effect of a clinically relevant doses of S 5682 on the inflammatory processes induced in this in vivo model of microcirculation may serve as a rational basis to explain its clinical efficacy.
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PMID:Effects of oral administration of purified micronized flavonoid fraction on increased microvascular permeability induced by various agents and on ischemia/reperfusion in diabetic hamsters. 872 38

In the present study, the possible role of mast cells in ischemia/reperfusion-induced myocardial injury was evaluated in the isolated 'mast cell depleted' rat heart. Hearts isolated from sensitized and non-sensitized rats were perfused according to Langendorff. After 30 min of normoxic perfusion, hearts were challenged with antigen, a procedure which is known to result in a massive mast cell degranulation in sensitized hearts. After another 20 min, both 'mast cell depleted' and control hearts were subjected to 30 min of ischemia followed by 30 min of reperfusion. The release of lactate dehydrogenase (LDH) was determined, to quantitate the extent of irreversible injury of cardiomyocytes. Histamine release was measured to establish mast cell degranulation. Coronary flow (CF) and left ventricular developed pressure (LVDP) were monitored to study the consequences of the procedures on hemodynamic recovery. It was found that both CF and LVDP significantly increased during the first min after antigen challenge. These changes were accompanied by an almost complete degranulation of cardiac mast cells. The increase in CF and LVDP values were rapidly followed by a decrease, reaching minimal values of 159 +/- 4% and 85 +/- 4% of those before administration of antigen, respectively, at 2-3 min after antigen challenge. No effect of antigen challenge on LDH release were found indicating that mast cell degranulation did not compromise myocyte integrity. During reperfusion following 30 min of ischemia both the increase in CF and LVDP in 'mast cell-depleted' hearts were not significantly different from those in control (non-sensitized) hearts. Similarly, at the end of the reperfusion-phase, CF and LVDP values in sensitized hearts were comparable to those in control hearts. Reperfusion results in increased LDH release, which at no point in time was significantly different between sensitized and non-sensitized hearts. In non-sensitized hearts histamine release during the reperfusion phase was not detectable. Therefore, the results indicate that in the isolated rat heart, mast cells are most likely not involved in acute ischemia/reperfusion-induced myocardial injury.
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PMID:Antigen-evoked mast cell degranulation in the isolated rat heart: no effect on subsequent ischemia-reperfusion induced damage. 908 42


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