Biochemical and physiological effects of compound 48/80 on canine trachea in vivo

1983 ◽  
Vol 54 (3) ◽  
pp. 720-729 ◽  
Author(s):  
A. R. Leff ◽  
J. K. Brown ◽  
M. Frey ◽  
B. Reed ◽  
W. M. Gold
Keyword(s):  
Mast Cells ◽  
Muscle Tension ◽  
Arterial Blood ◽  
Marked Variability ◽  
H2 Antagonist ◽  
Anesthetized Dogs ◽  
Threshold Doses ◽  
Tracheal Tissue ◽  
H1 Antagonist

We studied changes in tracheal histamine content and tracheal muscle tension after degranulation of tracheal mast cells by compound 48/80 in 32 anesthetized dogs. In four dogs compound 48/80 caused an increase in tracheal tension [13 +/- 5 (SD) g/cm], while femoral arterial blood pressure decreased only 14 +/- 11%. Tracheal tissue histamine decreased 17 +/- 6% in five dogs receiving intra-arterial compound 48/80 (5 X 10(-3) to 10(-1) mg/kg). Chlorpheniramine, an H1-antagonist, selectively inhibited tracheal contraction to compound 48/80 and histamine. Cimetidine, an H2-antagonist, did not alter the response to intra-arterial histamine. In 11 dogs, the doses of both intra-arterial histamine and acetylcholine required to produce a threshold increase in tracheal tension of 8 g/cm were compared. Threshold doses for acetylcholine varied 10-fold, compared with 100-fold variation for histamine among these dogs. There was a significant correlation between increased tracheal tension produced by compound 48/80 and histamine (r = 0.62). We conclude that compound 48/80 causes a variable increase in tracheal tension in vivo because of marked variability in the H1-receptor response of tracheal smooth muscle to histamine and because of variability in the release of mediator from respiratory mast cells by compound 48/80.

In vivo characterization of vasocontractile activities in erythrocytes

1983 ◽  
Vol 58 (3) ◽  
pp. 356-361 ◽  
Author(s):  
Michael P. McIlhany ◽  
Lydia M. Johns ◽  
Thomas Leipzig ◽  
Nicholas J. Patronas ◽  
Frederick D. Brown ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Content Type ◽  
Control Value ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Chronic Cerebral Vasospasm ◽  
In Vivo Characterization

✓ Partially purified protein from washed and artificially hemolyzed erythrocytes, known to cause significant contractions of isolated canine cerebral vessels in vitro, was injected into the cisterna magna of intact anesthetized dogs. Cerebral blood flow, measured by the xenon-133 washout technique, decreased from a control value of 49.5 ± 1.17 ml/100 gm/min to an experimental value of 34.1 ± 1.65 ml/100 gm/min at 2 hours. Cerebral vascular resistance rose from a control value of 2.05 ± 0.17 PRU (peripheral resistance units) to an experimental value of 2.91 ± 0.25 PRU at 2 hours. Mean arterial blood pressure, heart rate, intracranial pressure, and cerebral perfusion pressure remained stable. Cardiac output also fell significantly (in 2-hour control animals it was 2.89 ± 0.37 liter/min, and in 2-hour experimental animals 1.43 ± 0.13 liter/min) and peripheral vascular resistance rose. These changes were evident by 10 minutes after the cisternal injection of the hemolysate protein, and remained for the duration of the 2-hour monitoring period. Serial vertebrobasilar angiograms demonstrated marked narrowing of the intracranial basilar artery when compared to control values. The narrowing persisted for several days in most animals, and tended to increase with time. Relaxation occurred by the 10th through the 14th day. The authors conclude that this experimental preparation may be a useful model for both in vitro and in vivo investigation of chronic cerebral vasospasm.

Distribution oand pharmacological release of histamine in canine lung in vivo

1978 ◽  
Vol 44 (3) ◽  
pp. 455-463 ◽  
Author(s):  
M. R. Nisam ◽  
A. Zbinden ◽  
S. Chesrown ◽  
D. Barnett ◽  
W. M. Gold
Keyword(s):  
Lung Parenchyma ◽  
Smooth Muscle Contraction ◽  
Lung Compliance ◽  
Internal Diameter ◽  
Cellular Interactions ◽  
Arterial Blood ◽  
Beta Adrenergic Agonists ◽  
Anesthetized Dogs ◽  
Tissue Histamine

We have examined the physiological effects of stored mediators released from airways by compound 48/80 aerosols in anesthetized dogs. In 13 dogs, both mast cell numbers and tissue histamine were related inversely to bronchial internal diameter (P less than 0.0001). Compound 48/80 aerosols degranulated mast cells and decreased histamine content (-29.0 +/- 10.0%; mean +/- SE) in 5–10 mm bronchi, but not in 3–4 mm bronchi or lung parenchyma. This was associated with increased plasma histamine (31.8 +/- 18.4 ng/ml), increased airflow resistance (Rrs: + 452 +/- 257%), decreased lung compliance (-28 +/- 10%), and decreased arterial blood pressure (-41 +/- 6.5%) at 2 min. The increased Rrs was reversed by beta-adrenergic agonists, indicating it was caused by bronchial smooth muscle contraction; prevented by chlorpheniramine, indicating it was caused by histamine action on H1-receptors; and augmented and prolonged by propranolol, suggesting that histamine triggered sympathetic mechanisms which modulated the effect of 48/80. This experimental approach permits the study of mechanisms in vivo which may be involved in the sequence of reactions initiated by antigen-IgE interaction. However, the latter involve not only stored mediators, but also unstored mediators, neural reflexes, and complex cellular interactions.

Effect of histamine on microvascular permeability in the rat stomach

1983 ◽  
Vol 245 (2) ◽  
pp. G201-G207
Author(s):  
H. Nagata ◽  
P. H. Guth
Keyword(s):  
Histamine Receptors ◽  
Microvascular Permeability ◽  
In Vivo Microscopy ◽  
Rat Stomach ◽  
Serosal Surface ◽  
H2 Antagonist ◽  
H1 Antagonist ◽  
Dose Dependent ◽  
Muscularis Externa

The effect of histamine on gastric microvascular permeability to macromolecules in the rat was studied using fluorescent in vivo microscopy. Histamine was applied topically to the serosal surface for study of the muscularis externa, to the submucosa, and to the superficial mucosa, and the area of leaks of a fluorescein-albumin conjugate from microvessels was quantitated. In the muscularis externa both histamine and an H1-agonist, but not an H2-agonist, caused dose-dependent leak of conjugate from venules. An H1-antagonist, but not an H2-antagonist, decreased the histamine-induced leak. In the submucosa histamine caused dose-dependent dilatation of arterioles but not leak of conjugate. In contrast, bradykinin caused both dose-dependent dilatation of arterioles and leak of conjugate from venules. In the superficial mucosa histamine did not cause any leak. In conclusion, topical histamine 1) increased microvascular permeability to macromolecules from venules in the muscularis externa via H1-receptors, 2) did not affect microvascular permeability in the submucosa (this may be due to lack of histamine receptors on the venules as bradykinin increased venular permeability), and 3) did not affect microvascular permeability in the superficial mucosa, but there might not have been adequate histamine backdiffusion.

Effects of histamine receptor stimulation on regional myocardial blood flow

1983 ◽  
Vol 245 (3) ◽  
pp. H461-H467 ◽  
Author(s):  
C. W. Christensen ◽  
G. J. Gross ◽  
H. F. Hardman ◽  
H. L. Brooks ◽  
D. C. Warltier
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Histamine Receptor ◽  
Regional Myocardial Blood Flow ◽  
Intracoronary Infusion ◽  
H2 Antagonist ◽  
Tracer Microspheres ◽  
Anesthetized Dogs ◽  
H1 Antagonist ◽  
Regional Myocardial Blood

The effect of histamine (H) and specific H1 and H2 agonists and antagonists on regional myocardial blood flow was studied in anesthetized dogs by use of tracer microspheres. Intracoronary infusion of histamine (15 and 34 micrograms/min) produced a dose-related increase in transmural myocardial blood flow (from 0.82 to 1.36 and 2.25 ml X min-1 X g-1) without alteration of heart rate or blood pressure. Infusion of the H1 agonist 2-(2-thiazolyl)ethylamine (135 and 442 micrograms/min) produced an increase in transmural perfusion (from 0.69 to 1.22 and 1.65 ml X min-1 X g-1) and a significant (P less than 0.05) increase in the ratio of flow between subendocardium and subepicardium (endo/epi from 0.97 to 1.31 and 1.54). Infusion of the H2 agonist dimaprit (195 and 390 micrograms/min) produced an increase in transmural myocardial blood flow (from 0.97 to 1.49 and 2.00 ml X min-1 X g-1) without a change in endo/epi. The H1-mediated increase in regional myocardial perfusion and endo/epi was blocked by the H1 antagonist diphenhydramine but not by the H2 antagonist cimetidine. These results suggest that stimulation of H1 coronary receptors preferentially distributes flow to the subendocardium, whereas H2 receptors mediate vasodilation in subepicardium as well as subendocardium.

Characterization of H1- and H2-receptor function in pulmonary and systemic circulations of sheep

1982 ◽  
Vol 53 (1) ◽  
pp. 175-184 ◽  
Author(s):  
T. Ahmed ◽  
K. B. Mirbahar ◽  
W. Oliver ◽  
P. Eyre ◽  
A. Wanner
Keyword(s):  
Vascular Tone ◽  
Base Line ◽  
H2 Receptor ◽  
Receptor Response ◽  
H2 Antagonist ◽  
H2 Receptors ◽  
H1 Antagonist ◽  
Vasodepressor Response

We investigated the histamine H1- and H2-receptor function in the pulmonary and systemic circulations of sheep by in vivo and in vitro techniques. Combined H1 and H2 stimulation (by intravenous histamine) in vivo increased pulmonary vascular resistance (PVR) to 435% of base line and decreased systemic vascular resistance (SVR) to 49% of base line. Selective H2 stimulation (histamine after chlorpheniramine pretreatment) decreased PVR and SVR to 86 and 82% at base line, respectively, while selective H1 stimulation (histamine after metiamide pretreatment) increased PVR to 424% of base line and decreased SVR to 64% of base line. Combined H1- and H2-antagonist pretreatment completely blocked the effects of histamine on SVR, while PVR still decreased to 85% of base line, suggesting a mild “atypical” H2-receptor response in the pulmonary circulation under conditions of resting vascular tone. With increased pulmonary vascular tone (hypoxia), histamine decreased PVR to 55% (H1-antagonist pretreatment) and to 58% (combined H1- and H2-antagonist pretreatment) of posthypoxia values, respectively, demonstrating a marked atypical H2-receptor response. In vitro, both pulmonary arterial and venous strips showed a contractile dose-response to histamine, which was blocked by the H1-antagonist pyrilamine (mepyramine). In precontracted strips, both histamine and the H2-agonists (dimaprit and impromidine) elicited a relaxant response, which was neither blocked by H1-antagonist alone nor by combined H1- and H2-antagonists. We conclude that in sheep the histamine-induced pulmonary vasoconstrictor response is mediated by H1-receptors, while the pulmonary vasodepressor response is mediated by atypical H2-receptors. The systemic vasodepressor response is mediated by both H1- and typical H2-receptors.

A method for continuous recording in vivo of blood oxygen tension

1960 ◽  
Vol 15 (1) ◽  
pp. 77-82 ◽  
Author(s):  
F. Kreuzer ◽  
E. D. Harris ◽  
C. G. Nessler
Keyword(s):  
Oxygen Tension ◽  
Pressure Change ◽  
Continuous Recording ◽  
Blood Oxygen ◽  
Arterial Blood ◽  
Pulsatile Pressure ◽  
Cardiac Catheters ◽  
Anesthetized Dogs

A catheter-type Po2 electrode has been developed which permits the polarographic continuous recording of the blood oxygen tension in vivo. The electrodes have the size of ordinary cardiac catheters and yield continuous Po2 tracings in the animal over several hours, with a standard deviation of less than 3%. Model experiments assessed the dependency of the polarographic readings on temperature and showed that static pressure was without effect, but pulsatile pressure caused mechanical deflections depending on the rate of pressure change, and the readings became constant with linear velocities of more than 8–10 cm/sec. In experiments with anesthetized dogs, the readings were calibrated on arterial blood samples analyzed in an in vitro polarograph. With changing inspiratory o2 concentrations, the time for reaching a new equilibrium was found to be 3–4 minutes. The course of the alveolar-arterial o2 gradient was studied over the whole range of inspiratory o2 concentrations. The value of this gradient in the higher o2 ranges permitted the estimation of venous admixture in the anesthetized dog; the average was 5.5% of the cardiac output. Submitted on February 20, 1959

Stimulation of brain mast cells by compound 48/80, a histamine liberator, evokes renin and vasopressin release in dogs

2008 ◽  
Vol 294 (3) ◽  
pp. R689-R698 ◽  
Author(s):  
Itsuro Matsumoto ◽  
Yasuhisa Inoue ◽  
Toshio Shimada ◽  
Tomoe Matsunaga ◽  
Tadaomi Aikawa
Keyword(s):  
Mast Cells ◽  
Receptor Antagonist ◽  
Third Ventricle ◽  
Plasma Osmolality ◽  
Plasma Renin ◽  
Vasopressin Release ◽  
Arterial Blood ◽  
Endogenous Histamine ◽  
Before And After ◽  
Anesthetized Dogs

Because degranulation of brain mast cells activates adrenocortical secretion ( 41 , 42 ), we examined whether activation of such cells increases renin and vasopressin (antidiuretic hormone: ADH) secretion. For this, we administered compound 48/80 (C48/80), which liberates histamine from mast cells, to pentobarbital-anesthetized dogs. An infusion of 37.5 μg/kg C48/80 into the cerebral third ventricle evoked increases in plasma renin activity (PRA), and in plasma epinephrine (Epi) and ADH concentrations. Ketotifen (mast cell-stabilizing drug; given orally for 1 wk before the experiment) significantly reduced the C48/80-induced increases in PRA, Epi, and ADH. Resection of the bilateral splanchnic nerves (SPX) below the diaphragm completely prevented the C48/80-induced increases in PRA and Epi, but potentiated the C48/80-induced increase in ADH and elevated the plasma Epi level before and after C48/80 challenge. No significant changes in mean arterial blood pressure, heart rate, concentrations of plasma electrolytes (Na+, K+, and Cl−), or plasma osmolality were observed after C48/80 challenge in dogs with or without SPX. Pyrilamine maleate (H1histaminergic-receptor antagonist) significantly reduced the C48/80-induced increase in PRA when given intracerebroventricularly, but not when given intravenously. In contrast, metiamide (H2histaminergic-receptor antagonist) given intracerebroventricularly significantly potentiated the C48/80-induced PRA increase. A small dose of histamine (5 μg/kg) administered intracerebroventricularly increased PRA twofold and ADH fourfold (vs. their basal level). These results suggest that in dogs, endogenous histamine liberated from brain mast cells may increase renin and Epi secretion (via the sympathetic outflow) and ADH secretion (via the central nervous system).

Pulmonary gas exchange during induction of pulmonary edema in anesthetized dogs

1964 ◽  
Vol 19 (3) ◽  
pp. 403-407 ◽  
Author(s):  
Sami I. Said ◽  
Joseph W. Longacher ◽  
Ronald K. Davis ◽  
Chandra M. Banerjee ◽  
William M. Davis ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Pulmonary Edema ◽  
Left Atrial ◽  
Pulmonary Gas Exchange ◽  
Venous Admixture ◽  
Shunt Flow ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Arterial Blood Oxygen

We examined pulmonary gas exchange in 19 anesthetized dogs during the induction of acute pulmonary edema by intravenous infusion of dextran in saline. We monitored pulmonary capillary pressure by a left atrial catheter, and arterial blood Po2 by an indwelling electrode. PaOO2 remained near normal until just before pulmonary edema was grossly apparent, when it fell precipitously; left atrial pressure mounted to a peak and then declined. The apparent “steady-state” DlCO was reduced as much as 61%, but the dominant cause of hypoxemia was an increased venous admixture (shunt flow) on O2 breathing. Since the shunt was reversible by forcible inflation of the lungs, induced pulmonary edema was probably associated with closure of alveolar units. pulmonary venous admixture (shunt flow) and diffusing capacity; alveolar closure; arterial blood oxygen; tension in vivo; hypoxemia Submitted on August 14, 1963

Measurement of the Platelet Response to Laser- induced Microvascular Injury

1974 ◽  
Vol 32 (02/03) ◽  
pp. 704-713 ◽  
Author(s):  
F. N McKenzie ◽  
K.-E Arfors ◽  
N. A Matheson
Keyword(s):  
Inhibitory Effect ◽  
Microvascular Blood Flow ◽  
Platelet Response ◽  
High Concentration ◽  
Platelet Activity ◽  
Microvascular Injury ◽  
Arterial Blood ◽  
Proximal Site ◽  
Adenosine Phosphates

SummaryA study has been made of the biochemical factors underlying the platelet response to laser-induced microvascular injury. A platelet aggregating substance is produced at sites of laser-induced injury which markedly stimulates platelet activity at a site of injury inflicted a short distance downstream. Distal sites of injury are not similarly influenced if the distance between the injuries is increased or if the proximal site no longer shows platelet-stimulating activity. The stimulating effect of an adjacent proximal injury on platelet activity at a distal site is inhibited by local intra-arterial infusion of adenosine. Measurements of arterial blood pressure and microvascular blood flow velocity during adenosine infusion showed that its inhibitory effect on platelet activity is largely independent of its vasodilator properties. The effect of infusion of different adenosine phosphates (AMP, ADP, ATP) was also studied. Very small amounts of ADP markedly stimulated platelet activity and the emboli formed were similar to those normally produced at sites of laser injury. At high concentration AMP inhibited while ATP stimulated platelet activity in vivo. The results emphasise the fundamental role of ADP as a mediator of the platelet response at sites of laser- induced microvascular injury.

Cardiovascular Effects of Micromeria graeca (L.) Benth. ex Rchb in Normotensive and Hypertensive Rats

2020 ◽  
Vol 20 (8) ◽  
pp. 1253-1261
Author(s):  
Mourad Akdad ◽  
Mohamed Eddouks
Keyword(s):  
Blood Pressure ◽  
Cardiovascular System ◽  
Arterial Blood Pressure ◽  
Antihypertensive Activity ◽  
Computer Assisted ◽  
Hypertensive Rats ◽  
Vasorelaxant Effect ◽  
Arterial Blood

Aims: The present study was performed in order to analyze the antihypertensive activity of Micromeria graeca (L.) Benth. ex Rchb. Background: Micromeria graeca (L.) Benth. ex Rchb is an aromatic and medicinal plant belonging to the Lamiaceae family. This herb is used to treat various pathologies such as cardiovascular disorders. Meanwhile, its pharmacological effects on the cardiovascular system have not been studied. Objective: The present study aimed to evaluate the effect of aqueous extract of aerial parts of Micromeria graeca (AEMG) on the cardiovascular system in normotensive and hypertensive rats. Methods: In this study, the cardiovascular effect of AEMG was evaluated using in vivo and in vitro investigations. In order to assess the acute effect of AEMG on the cardiovascular system, anesthetized L-NAME-hypertensive and normotensive rats received AEMG (100 mg/kg) orally and arterial blood pressure parameters were monitored during six hours. In the sub-chronic study, rats were orally treated for one week, followed by blood pressure assessment during one week of treatment. Blood pressure was measured using a tail-cuff and a computer-assisted monitoring device. In the second experiment, isolated rat aortic ring pre-contracted with Epinephrine (EP) or KCl was used to assess the vasorelaxant effect of AEMG. Results: Oral administration of AEMG (100 mg/kg) provoked a decrease of arterial blood pressure parameters in hypertensive rats. In addition, AEMG induced a vasorelaxant effect in thoracic aortic rings pre-contracted with EP (10 μM) or KCl (80 mM). This effect was attenuated in the presence of propranolol and methylene blue. While in the presence of glibenclamide, L-NAME, nifedipine or Indomethacin, the vasorelaxant effect was not affected. Conclusion: This study showed that Micromeria graeca possesses a potent antihypertensive effect and relaxes the vascular smooth muscle through β-adrenergic and cGMP pathways.

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