Mast cells in the rat heart during normal growth and in cardiac hypertrophy.

Rakusan, K; Sarkar, Kiriti; Turek, Z.; Wicker, P.

doi:10.1161/01.res.66.2.511

Cited by 64 publications

(39 citation statements)

References 13 publications

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“…This explains why DSCG applied at the end of hypoxic exposure has no effect on pulmonary vascular resistance and vascular remodeling. In contrast, Rakusan et al [26] reported a persistent increase in the number of mast cells in hearts of rats acclimatized to high altitude for 4 weeks. The interesting finding of their study is that a similar increase in the heart mast cell density was not found in rats with renal hypertension.…”

Section: Discussionmentioning

confidence: 93%

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Baňasová¹,

Maxová

Hampl³

et al. 2008

Respiration

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Background: Chronic hypoxia induces lung vascular remodeling, which results in pulmonary hypertension. Vascular remodeling is associated with collagenolysis and activation of matrix metalloproteinases (MMPs). One of the possible sources of MMPs in hypoxic lung are mast cells. Objective: The role of lung mast cell collagenolytic activity in hypoxic pulmonary hypertension was tested by the inhibitor of mast cell degranulation disodium cromoglycate (DSCG). Methods: Rats were treated with DSCG in an early or later phase of isobaric hypoxia. Control groups were exposed to hypoxia only or to normoxia. Lung hemodynamics, muscularization and collagen metabolism in the walls of peripheral pulmonary vessels in the lungs were measured. Results: DSCG applied at an early phase of exposure to hypoxia reduced the development of pulmonary hypertension, inhibited muscularization in peripheral pulmonary arteries and decreased the amount of collagen cleavage fragments in prealveolar vessels. Conclusions: Mast cell degranulation plays a role in the initiation of hypoxic pulmonary vascular remodeling.

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Section: Discussionmentioning

confidence: 93%

Prevention of Mast Cell Degranulation by Disodium Cromoglycate Attenuates the Development of Hypoxic Pulmonary Hypertension in Rats Exposed to Chronic Hypoxia

Baňasová¹,

Maxová

Hampl³

et al. 2008

Respiration

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“…Mast cells may also play a role in hypertensive heart disease. Although changes in mast cell number were not observed in hearts from a Goldblatt model of hypertension in rats (30), studies in spontaneously hypertensive rats led investigators to suggest that mast cells play a role in the cardiac fibrosis and hypertrophy that occur in hypertension, possibly due to the secretion of cytokines and growth factors (26,32). Experiments also showed that the progression from compensated hypertrophy to decompensated failure in a pressure overload model is largely prevented in mast celldeficient mice or in wild-type mice treated with tranilast, a mast cell stabilizer (15).…”

mentioning

confidence: 78%

“…It has been reported that cardiac mast cell density increases during the first month of life in rats and then declines to a lower adult level (30); however, the role of mast cells in normal cardiac development and function is unknown. The present experiments using a mast cell-deficient rat model were designed to determine whether mast cells affect cardiac function in adults in the absence of insult.…”

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confidence: 99%

Cardiac function in hearts isolated from a rat model deficient in mast cells

Kennedy

Hauer‐Jensen²,

Joseph³

2005

American Journal of Physiology-Heart and Circulatory Physiology

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2004.-Several studies have examined the role of mast cells in the myocardial response to injury such as that caused by hypertension and ischemia-reperfusion. However, little is known about the influence of mast cells on normal myocardial structure and function. The present experiments examined cardiac function in Langendorff-perfused hearts isolated from 6-and 9-mo-old male mast cell-deficient (Ws/Ws) and mast cell-competent rats. A fluid-filled balloon catheter was used to measure left ventricular diastolic and systolic function at increasing preload volumes. At 6 mo of age, mast cell-deficient rats showed a slight cardiac hypertrophy (as monitored by heart weight and heart weight-to-body weight ratio) but no significant change in maximum observed systolic or diastolic function. In contrast, at 9 mo of age, the mast cell-deficient group showed no signs of hypertrophy but displayed a diastolic dysfunction characterized by decreased compliance without a significant decline in maximum observed basal ϪdP/dt max. There were no significant differences in maximum observed values for measures of systolic function (developed pressure and ϩdP/dtmax). In summary, the results of this study in adult rats suggest that mast cells influence cardiac function in the absence of injury and that observed differences between mast cell-competent and -deficient animals vary with age. Thus it is important to consider these "physiological" actions and resulting changes in function when studying effects of insult in mast cell-deficient models.compliance; diastolic dysfunction; Langendorff-perfused hearts MAST CELLS are part of the innate immune system that provides the first line of defense against tissue damage. In addition to their critical role in immunoglobulin E-dependent, histaminemediated hypersensitivity, mast cells release and modulate cytokines, growth factors, chemokines, proteases, and other mediators, which in turn regulate a vast array of important biological processes. Many mast cell mediators (e.g., histamine, heparin, tryptase, chymase, TNF-␣, and interleukin-4) are preformed and stored in large amounts in secretory granules, available for immediate release (21). Studies have demonstrated that mast cells reside in the myocardium even under physiological conditions, with their distribution along the coronary capillaries being more dense in the arteriolar section (30).Several studies have examined the potential role of mast cells in the myocardial response to injury. However, in many cases, the results of these studies have been contradictory. For example, numerous investigators have monitored the contribution of mast cells to preconditioning as well as ischemic injury. Parikh and Singh (27, 28) suggested that ischemia-and norepinephrine-induced preconditioning are mediated in part by degranulation of resident mast cells in the rat heart, whereas Wang et al. (37) reported that mast cell degranulation is not involved in ischemic cardiac preconditioning in rabbits. Similarly, the role of mast cells in the acute tissue damage...

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“…Mast cells are present in most tissues and are often found in close proximity to blood vessels, including capillaries and postcapillary venules (18)(19)(20). Upon Adenosine has potent effects on both the cardiovascular and immune systems.…”

Section: Introductionmentioning

confidence: 99%