Ultrastructural and metabolic alterations in myocardium from altitude-acclimated rats

Wd, Bowers; Burlington, RF; Bk, Whitten; Rc, Daum; Packham, MA

doi:10.1152/ajplegacy.1971.220.6.1885

Cited by 12 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Relaxation was not studied, but morphological examination revealed swelling and disruption of sarcoplasmic reticulum (Maher et al 1972). In other studies hypoxia led to mitochondrial damage (Bowers, Burlington, Whitten, Daum & Posiviata, 1971) in cardiac and skeletal muscles, and increased hypoxic resistance in vitro (McGrath, Bullard & Komives, 1969). Thus parallels may be drawn between the effects of experimental diabetes and hypoxia.…”

Section: Discussionmentioning

confidence: 98%

Polyol pathway‐related skeletal muscle contractile and morphological abnormalities in diabetic rats

Cameron²,

Robertson³

et al. 1993

Experimental Physiology

View full text Add to dashboard Cite

SUMMARYThis study examined the effect of inhibition of aldose reductase, the first enzyme in the polyol pathway, on fast and slow twitch skeletal muscle morphology and function in streptozotocininduced diabetes in rats. There was a preventative investigation with diabetes duration of 4 months, and a reversal investigation where treatment was given for 2 months following an untreated period of 2 months. For slow twitch soleus muscle, contractions were prolonged by diabetes, and this was partially prevented but not reversed by treatment. Relaxation was profoundly slowed, and both prevention and reversal ameliorated the changes. Diabetes had minimal effects on tension production for soleus. However, for fast twitch extensor digitorum longus, although there was little effect on speed-related contractile parameters, tetanic tension production was progressively reduced with diabetes duration. This effect was antagonized by treatment. Soleus fatigue resistance was markedly reduced by diabetes, but restored to normal by treatment. There was a reduction in oxidative enzyme staining (succinic dehydrogenase), and capillary-fibre ratio, both of which were ameliorated by aldose reductase inhibition. Mean soleus fibre area was reduced after 4 months of diabetes, and this was prevented but not reversed by treatment. Fibre area was also reduced in extensor digitorum longus, particularly for fast glycolytic fibres. There was a small amelioration with treatment. It is concluded that enhanced polyol pathway activity makes a contribution to diabetic myopathy, and that aldose reductase inhibitors can prevent this by actions on muscle fibres and their vascular supply.

show abstract

Section: Discussionmentioning

confidence: 98%

Polyol pathway‐related skeletal muscle contractile and morphological abnormalities in diabetic rats

Cameron²,

Robertson³

et al. 1993

Experimental Physiology

View full text Add to dashboard Cite

show abstract

“…Noise‐induced ultrastructural alteration in cardiomyocytes is substantially evident at mitochondrial levels (Paparelli et al, 1995; Soldani et al, 1997a). In effect, mitochondria represent the main target in various stress situations, such as exhaustive exercise (Banister et al, 1971; King and Gollnick, 1970; Laguens and Gomez‐Dumm, 1967; Laguens et al, 1966), cold temperatures (Lopes et al, 1992), and high altitudes (Bischoff et al, 1969; Bowers et al, 1971). In particular, ultrastructural effects of loud noise on rat myocardium were extensively studied by our research group and reviewed in 2002 (Gesi et al, 2002a).…”

Section: Effect Of Noise On Heartmentioning

confidence: 99%

MDMA (ecstasy) enhances loud noise‐induced morphofunctional alterations in heart and adrenal gland

Fulceri¹,

Ferrucci²,

Lenzi³

et al. 2010

Microscopy Res & Technique

View full text Add to dashboard Cite

Noise is an environmental stressor increasingly more present in modern life and, in particular, in a variety of recreational contexts. The aim of this work is to show the effects of noise on the myocardium and adrenal gland, through a careful review of the literature dealing with the peripheral effects of noise exposure in experimental and clinical studies. Noise induces adverse effects in human health, principally involving the cardiovascular and autonomic nervous systems, and the endocrine apparatus. Several factors in recreational environments potentially worsen the effects induced by loud noise. Among these, the intake of 3,4-methylenedioxymethamphetamine (MDMA) is frequently associated with noise exposure in recreational situations, because of its high compliance within social and relaxation settings. For this reason, MDMA is defined as a club drug--as its intake by young people often occurs in association with other factors, such as aggregation, high temperatures, and noise. It is known that self-administration of MDMA by humans causes severe toxicity. In particular, the myocardium is affected early after MDMA intake--resulting in tachycardia, hypertension, and arrhythmia. Furthermore, MDMA alters the activity of the adrenal glands by elevating catecholamines and corticosterone levels. This review shows that combining MDMA and loud noise exposure potentiates the effects that are produced by each single stimulant alone as seen in experimental animal models. The convergence of the effects of prolonged loud noise exposure and the consumption of MDMA on the same system might explain the sudden fatal events that happen in recreational situations.

show abstract

“…For instance, it has been reported that prolonged exercise (Banister et al, 1971;King and Gollnick, 1970;Laguens and Gomez-Dumm, 1967), cold stress (Lopes et al, 1992), and living at high altitude (Bischoff et al, 1969;Bowers et al, 1971) provoke mitochondrial changes in the rat myocardium. In all these conditions, mitochondria represent the subcellular organelles primarily affected.…”

Section: Ultrastructural Modification Ofmentioning

confidence: 99%

Morphological alterations induced by loud noise in the myocardium: The role of benzodiazepine receptors

Gesi

Fornai

Lenzi

et al. 2002

Microscopy Res & Technique

View full text Add to dashboard Cite

Noise represents an environmental stress factor affecting several organs and apparati, including the cardiovascular system. In experimental animals undergoing noise exposure, subcellular myocardial changes have been reported, especially at mitochondrial level; in particular, after 6 hours of exposure only the atrium exhibited significant mitochondrial alterations, whereas after 12 hours as well as subchronic exposure both atrium and ventricle were damaged. The first part of the present article overviews the experimental evidence on effects of noise on the myocardium. In the second part, the review analyzes the role of benzodiazepine receptors and the potential efficacy of benzodiazepine ligands in preventing the mitochondrial damage induced by noise exposure. Drugs acting at both central and peripheral benzodiazepine receptors significantly prevent this damage. Differences in the amount and the duration of the protective effect might depend on variability in the potency and pharmacokinetics of the specific drug. The effects of the combined treatment with selective and non-selective peripheral benzodiazepine ligands on noise stimulation are discussed at biochemical level reviewing studies on the effects of noise exposure on mitochondrial fractions.

show abstract

Ultrastructural and metabolic alterations in myocardium from altitude-acclimated rats

Cited by 12 publications

References 0 publications

Polyol pathway‐related skeletal muscle contractile and morphological abnormalities in diabetic rats

Polyol pathway‐related skeletal muscle contractile and morphological abnormalities in diabetic rats

MDMA (ecstasy) enhances loud noise‐induced morphofunctional alterations in heart and adrenal gland

Morphological alterations induced by loud noise in the myocardium: The role of benzodiazepine receptors

Contact Info

Product

Resources

About