Comparative age-related acute and chronic pulmonary oxygen tolerance in rats

1994 ◽  
Vol 77 (6) ◽  
pp. 2709-2719 ◽  
Author(s):  
S. Laudert ◽  
D. W. Thibeault ◽  
M. M. Rezaiekhaligh ◽  
S. M. Mabry ◽  
M. Huntrakoon
Keyword(s):  
Enzyme Activity ◽  
Heart Weight ◽  
Pulmonary Insufficiency ◽  
Initial Increase ◽  
Lung Water ◽  
Oxygen Tolerance ◽  
Young Rats ◽  
Arterial Blood ◽  
Age Related ◽  
Old Rats

Young rats are thought to be more tolerant to hyperoxia. We propose that this may not be proven and depends on how tolerance is defined. We assessed oxygen tolerance in Sprague-Dawley rats from birth to maturity by comparing survival, lung water, antioxidant enzyme activity, lung morphometrics, heart weight, and arterial blood gases in newborn and 27-, 44-, 48-, and 96-day-old rats exposed to 100% O2 or room air for 22 days. Some 96-day-old rats (rest group) received only 50% O2 between 48 and 72 h. Mortality after 5 days of O2 was 0% in newborn and 27-day-old rats and 27% in 44-day-old rats but was > 80% in 48- and 96-day-old rats. Between 5 and 22 days, the death rate was 100% in newborns, 25% in 27-day-old rats, and 0% in 44- to 96-day-old rats. Death occurred when lung water was > 84% except in newborns, which tolerated high lung water for the first 7 days. In chronically exposed 44- and 96-day-old rats, lung water returned to normal. Enzyme activity increased with O2 at all ages but did not relate to survival. In 96-day-old rats, the initial increase was suppressed on day 3. All chronically O2-exposed rats had minimal nonvascular parenchymal changes but developed right ventricular hypertrophy and increased alveolar ductal artery muscularization and lost alveolar capillaries. The most mature rats were least affected. In O2, there was pulmonary insufficiency the first 3 days, followed by recovery, and later hypercarbia and decreased arterial PO2. We conclude that young rats, 0–44 days old, are more O2 tolerant for 5 days. More mature animals, surviving 5 days, are more tolerant to chronic exposure.

scholarly journals Effects of β-adrenergic receptor agonists on drinking and arterial blood pressure in young and old rats

2011 ◽  
Vol 300 (4) ◽  
pp. R1001-R1008 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Connie L. Grobe ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Aged Rats ◽  
Middle Aged ◽  
Young Rats ◽  
Arterial Blood ◽  
Age Related ◽  
Old Rats

These experiments examined water-drinking and arterial blood pressure responses to β-adrenergic receptor activation in young (4 mo), “middle-aged” adult (12 mo), and old (29 mo) male rats of the Brown-Norway strain. We used isoproterenol to simultaneously activate β1- and β2-adrenergic receptors, salbutamol to selectively activate β2-adrenergic receptors, and the combination of isoproterenol and the β2-adrenergic receptor antagonist ICI 118,551 to stimulate only β1-adrenergic receptors. Animals received one of the drug treatments, and water drinking was measured for 90 min. About 1 wk later, animals received the same drug treatment for measurement of arterial blood pressure responses for 90 min. In some rats, levels of renin and aldosterone secretion in response to isoproterenol or salbutamol were measured in additional tests. Old and middle-aged rats drank significantly less after isoproterenol than did young rats and also had greater reductions in arterial blood pressure. Old and middle-aged rats drank significantly less after salbutamol than did young rats, although reductions in arterial blood pressure were equivalent across the ages. The β2-adrenergic antagonist ICI 118,551 abolished drinking after isoproterenol and prevented most of the observed hypotension. Renin secretion after isoproterenol and salbutamol was greater in young rats than in middle-aged rats, and wholly absent in old rats. Aldosterone secretion was reduced in old rats compared with young and middle-aged rats after treatment with isoproterenol, but not after treatment with salbutamol. In conclusion, there are age-related differences in β-adrenergic receptor-mediated drinking that can be explained only in part by age-related differences in renin secretion after β-adrenergic receptor stimulation.

scholarly journals Gut Microbiota Is Involved in Alcohol-Induced Osteoporosis in Young and Old Rats Through Immune Regulation

2021 ◽  
Vol 11 ◽  
Author(s):  
Ming Cheng ◽  
Bo Tan ◽  
Xiaojing Wu ◽  
Feng Liao ◽  
Fei Wang ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Gut Microbiota ◽  
Bone Metabolism ◽  
Alcohol Metabolism ◽  
Excessive Alcohol Consumption ◽  
Young Rats ◽  
Age Related ◽  
Different Ages ◽  
Old Rats

Long-term and excessive alcohol consumption are risk factors for osteoporosis. Excessive drinking can reduce bone density and also cause imbalance of gut microbiota. And gut microbiota can affect bone metabolism through various mechanisms, and the regulation of gut microbiota is closely related to age. However, the effects of gut microbiota on alcohol-induced osteoporosis at different ages are unclear. In this study, young and old rats were used to induce osteoporosis by long-term alcohol consumption, and alcohol metabolism, bone morphology, bone absorption and immune activity of rats were analyzed to determine the effects of alcohol on rats of different ages. In addition, changes of gut microbiota in rats were analyzed to explore the role of gut microbiota in alcohol-induced osteoporosis in rats of different ages. The results showed the ability of alcohol metabolism was only associated with age, but not with alcohol consumption. Long-term alcohol consumption resulted in the changes of bone metabolism regulating hormones, bone loss, activation of receptor activator of NF-κB ligand (RANKL) signaling and inflammatory response. And osteoporosis was more severe in old rats than young rats, suggesting that alcohol-induced osteoporosis is age-related. In addition, long-term drinking also affected the composition of gut microbiota in rats, with a significant increase in the proportion of pro-inflammatory microorganisms. Overall, this study found that long-term alcohol consumption induced osteoporosis and affected the composition of gut microbiota. And alcohol can activate T lymphocytes directly or indirectly by regulating the changes of gut microbiota to produce cytokines, and further activate osteoclasts. In addition, the osteoporosis was more severe in the old rats than young rats, which may be due to the higher diversity and stronger regulation ability of gut microbiota in young rats compared with old rats.

Dysregulation of hepatic iron with aging: implications for heat stress-induced oxidative liver injury

2008 ◽  
Vol 294 (4) ◽  
pp. R1165-R1174 ◽  
Author(s):  
Steven A. Bloomer ◽  
Kyle E. Brown ◽  
Garry R. Buettner ◽  
Kevin C. Kregel
Keyword(s):  
Lipid Peroxidation ◽  
Heat Stress ◽  
Liver Injury ◽  
Iron Content ◽  
Nonheme Iron ◽  
Hepatic Iron ◽  
Young Rats ◽  
Age Related ◽  
Old Rats ◽  
Labile Iron

Environmental heat stress is associated with an age-related increase in hepatic oxidative damage and an exaggerated state of oxidative stress. The purpose of this investigation was to evaluate the regulation of hepatic iron after heat stress. A secondary aim was to determine a potential role for iron in heat stress-induced liver injury. Hyperthermia-induced alterations in hepatic iron were evaluated in young (6 mo) and old (24 mo) Fischer 344 rats by exposing them to a two-heat stress protocol. Livers were harvested at several time points after the second heating and assayed for labile and nonheme iron. In the control condition, there was no difference in labile iron between age groups. Both labile iron and storage iron were not altered by hyperthermia in young rats, but both were increased immediately after heating in old rats. To evaluate a role for iron in liver injury, hepatic iron content was manipulated in young and old rats, and then both groups were exposed to heat stress. Iron administration to young rats significantly increased hepatic iron content and ferritin but did not affect markers of lipid peroxidation under control conditions or after heat stress. In old rats, iron chelation with deferoxamine prevented the increase in nonheme iron, labile iron, ferritin, and lipid peroxidation after heat stress. These results suggest that iron may play a role in hepatic injury after hyperthermia. Thus, dysregulation of iron may contribute to the gradual decline in cellular and physiological function that occurs with aging.

scholarly journals Hypotension- and osmotically induced thirst in old Brown Norway rats

2009 ◽  
Vol 297 (1) ◽  
pp. R149-R157 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Arterial Pressure ◽  
Brown Norway ◽  
Aged Rats ◽  
Middle Aged ◽  
Young Rats ◽  
Age Related ◽  
Cellular Dehydration ◽  
Old Rats ◽  
Middle Aged Adult ◽  
Norway Rats

Compared to young cohorts, old rats drink less water in response to several thirst-inducing stimuli. In these experiments, we characterized water drinking in response to hypotension and cellular dehydration in young (4 mo), middle-aged adult (12 mo) and old (29–30 mo) male Brown Norway rats. We injected the vasodilator, minoxidil as an intravenous bolus in a range of doses (0–20 mg/kg), so that drinking responses could be compared at equivalent reductions of arterial pressure. Old rats had greatly diminished reflex tachycardia and became significantly more hypotensive after minoxidil compared with young and middle-aged rats. When compared at equivalent reductions of arterial pressure, old rats drank one-third as much as middle-aged rats, and one-fifth as much as young rats. In addition, there were age-related deficits in drinking in response to a range of administered loads of sodium (0.15–2 M NaCl, 2 ml/100 g body wt). Urinary excretion of water and sodium in response to the loads was equivalent across ages. Both middle-aged and old rats were less able than young rats to repair their water deficits after sodium loading, attributable almost entirely to their reduced drinking responses compared with young rats. Lastly, age-related declines in drinking appeared to be more severe in response to hypotension than in response to cellular dehydration.

scholarly journals Drinking and arterial blood pressure responses to ANG II in young and old rats

2010 ◽  
Vol 299 (5) ◽  
pp. R1135-R1141 ◽  
Author(s):  
Robert L. Thunhorst ◽  
Terry G. Beltz ◽  
Alan Kim Johnson
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Ang Ii ◽  
Middle Aged ◽  
Reduced Pressure ◽  
Water Drinking ◽  
Young Rats ◽  
Arterial Blood ◽  
Old Rats ◽  
Blood Pressure Responses

We investigated water drinking and arterial blood pressure responses to intravenous infusions of ANG II in young (4 mo), middle-aged adult (12 mo), and old (29 mo) male Brown Norway rats. Infusions of ANG II began with arterial blood pressure either at control levels or at reduced levels following injection of the vasodilator minoxidil. Under control conditions, mean arterial pressure (MAP) in response to ANG II rose to the same level for all groups, and middle-aged and old rats drank as much or more water in response to ANG II compared with young rats, depending on whether intakes were analyzed using absolute or body weight-adjusted values. When arterial blood pressure first was reduced with minoxidil, MAP in response to ANG II stabilized at significantly lower levels compared with control conditions for all groups. Young rats drank significantly more water under reduced pressure conditions compared with control conditions, while middle-aged and old rats did not. Urine volume in response to ANG II was lower, while water balance was higher, under conditions of reduced pressure compared with control conditions. Baroreflex control of heart rate was substantially reduced in old rats compared with young and middle-aged animals. In summary, young rats appear to be more sensitive to the inhibitory effects of increased arterial blood pressure on water drinking than are older animals.

Pharmacological effects of the continuous administration of an LHRH agonist in the ageing male rat: comparison with orchidectomy

1990 ◽  
Vol 124 (2) ◽  
pp. 261-NP ◽  
Author(s):  
Y. Amir-Zaltsman ◽  
Y. Ausher ◽  
B. Gayer ◽  
S. Lichter ◽  
F. Serour ◽  
...  
Keyword(s):  
Tissue Response ◽  
Continuous Treatment ◽  
Male Rat ◽  
Moderate Increase ◽  
Lhrh Agonist ◽  
Pharmacological Effects ◽  
Young Rats ◽  
Age Related ◽  
Ageing Male ◽  
Old Rats

ABSTRACT The age-related changes in tissue response to chronic treatment for 1 month with a potent LHRH agonist were investigated in the ageing male rat, and the observed pharmacological effects were compared with orchidectomy. In both young (4 months) and old (22 months) rats, treatment resulted in a significant decrease in the weights of prostates and testes, a decrease in plasma LH and testosterone levels, a loss of LH receptors in the testes and in a complete depletion of prostatic nuclear androgen receptors, reaching levels observed after castration. In young rats, treatment with an LHRH agonist or orchidectomy induced a three- or sixfold increase in prostatic creatine kinase (CK) activity which may have been induced by the local stimulatory effect of oestradiol arising from the conversion of precursor steroids secreted by the adrenal. On the other hand, in old rats, 7 days after orchidectomy or after treatment with an LHRH agonist a twofold increase or no change was induced in prostatic CK activity respectively. SDS gel electrophoresis patterns of cytosolic prostatic proteins of young rats treated with an LHRH agonist or young rats orchidectomized 7 days previously revealed the presence of several intensified proteins, two of them having apparent molecular weight of 67 kDa and 43 kDa, whereas in the old rats treated with LHRH agonist or old rats castrated 7 days previously, these two proteins were not intensified. The results of this study confirmed that continuous treatment with an LHRH agonist to young and old rats induces medical castration since the pharmacological effects observed were the same as those induced with surgical castration. However, in the old rats, the lack of an increase in prostatic CK activity upon treatment with LHRH agonist, and the moderate increase in CK activity upon orchidectomy, suggest that prostatic cells in older rats have decreased sensitivity to hormonal manipulation. Journal of Endocrinology (1990) 124, 261–268

Age-related alterations in prolactin binding sites in the female rat

1991 ◽  
Vol 124 (3) ◽  
pp. 314-321 ◽  
Author(s):  
Philippe Schneiter ◽  
Marianne J. Reymond ◽  
Thérèse Lemarchand-Béraud
Keyword(s):  
Binding Sites ◽  
Mammary Glands ◽  
Female Rats ◽  
Affinity Constant ◽  
Female Rat ◽  
Binding Studies ◽  
Young Rats ◽  
Age Related ◽  
Old Rats ◽  
Nulliparous Female

Abstract. Aging is associated with various neuroendocrine alterations, including in the rat a hypersecretion of PRL with maintained ovulations (repetitive pseudopregnancy) and a reduced activity of the hypothalamic dopaminergic neurons with loss of the neuron responsiveness to PRL, suggestive of age-related alterations in PRL receptors. In this study we have investigated PRL binding sites in the hypothalamus as well as in the mammary glands, the ovaries and the liver of young and old nulliparous female rats. The old rats (26-28 months) displayed spontaneous repetitive pseudopregnancies and they were compared with young (4-6 months) pseudopregnant rats; the binding studies were performed by saturation analysis using 125I-oPRL as ligand and particulate membrane preparations. In the hypothalamus, a negligible binding of PRL was observed in all fragments studied, mediobasal hypothalamus, median eminence, in both young and old rats and no characterization of the binding sites could be achieved. In the mammary glands, the number of PRL binding sites was appreciable in spite of the nulliparity of the rats, but it was smaller in the old than in the young rats (9.0±1.4 vs 14.9±1.2 fmol/mg protein; mean ± sem; p<0.02). In the ovaries, the density of PRL binding sites was similar in the old and young rats (112.6±9.7 vs 115.0±8.9 fmol/mg protein), illustrative of a maintained luteotropic effect of PRL with age in the rat. In contrast, in the liver a greater number of binding sites was found in the old than in the young rats (261.9±36.6 vs 63.6±5.8 fmol/mg protein; p<0.001), supportive of the ability of PRL to induce its own receptors in that tissue. The affinity constant of PRL binding was not altered with age in the tissues studied. These results are illustrative of tissue-specific modifications in the number of PRL binding sites with age and they are suggestive of a sustained biological activity of PRL in the old rats.

scholarly journals Age impairs Flk-1 signaling and NO-mediated vasodilation in coronary arterioles

2008 ◽  
Vol 295 (6) ◽  
pp. H2280-H2288 ◽  
Author(s):  
Amanda J. LeBlanc ◽  
Robert D. Shipley ◽  
Lori S. Kang ◽  
Judy M. Muller-Delp
Keyword(s):  
Nitric Oxide ◽  
Vascular Endothelial Growth Factor ◽  
Growth Factor ◽  
Vascular Endothelial ◽  
Coronary Resistance ◽  
Young Rats ◽  
Age Related ◽  
Old Rats ◽  
Endothelial Growth Factor ◽  
Coronary Arterioles

Impairment of flow-induced vasodilation in coronary resistance arterioles may contribute to the decline in coronary vasodilatory reserve that occurs with advancing age. This study investigated the effects of age on flow-induced signaling and activation of nitric oxide (NO)-mediated vasodilation in coronary resistance arterioles. Coronary arterioles were isolated from young (∼6 mo) and old (∼24 mo) male Fischer-344 rats to assess vasodilation to flow, vascular endothelial growth factor (VEGF), and ACh. Flow- and VEGF-induced vasodilation of coronary arterioles was impaired with age ( P ≤ 0.05); however, ACh-induced vasodilation was preserved with age. NG-nitro-l-arginine methyl ester (l-NAME) (1 × 10−5 M) eliminated vasodilation to flow, VEGF, and ACh, indicating dependence of these responses on NO. SU-1498, an inhibitor of vascular endothelial growth factor receptor 2 (VEGFR, also known as Flk-1), abolished age-related differences in flow-induced vasodilation. Flow-stimulated phosphorylation of Flk-1 in coronary arterioles from young but not old rats and Flk-1 protein was reduced in coronary arterioles from old rats compared with those from young rats. Flow stimulated phosphorylation of endothelial nitric oxide synthase (eNOS) in coronary arterioles from both young and old rats. VEGF induced phosphorylation of both protein kinase B (Akt) and eNOS in coronary arterioles. VEGF-induced phosphorylation of Akt, but not eNOS, was significantly reduced in arterioles from old rats compared with arterioles from young rats. Wortmannin, an inhibitor of phosphatidylinositol (PI) 3-kinase, eliminated age-related differences in both flow- and VEGF-induced vasodilation. These results indicate that impairment of Flk-1/PI3-kinase signaling contributes to the reduction of flow-induced vasodilation in coronary arterioles with advancing age.

scholarly journals INFLUENCE OF ATP-LONG AND MOLSIDOMINE COMBINATION ON THE BIOELECTRIC ACTIVITY OF THE MYOCARDIAL OF YOUNG AND OLD RATS IN CHRONIC SOFT STRESS

2021 ◽  
pp. 5-11
Author(s):  
Liana Kuprash ◽  
Ludmila Sharabura ◽  
Tetyana Panteleymonova ◽  
Svitlana Hudarenko ◽  
Nina Sykalo ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Negative Impact ◽  
Circulatory System ◽  
Stress Factors ◽  
Bioelectrical Activity ◽  
Young Rats ◽  
Adaptive Capabilities ◽  
Age Related ◽  
Male Wistar Rats ◽  
Old Rats

Introduction. Age-related changes in the cardiovascular system lead to a decrease in its reserve adaptive capabilities and an increase in the likelihood of developing diseases under stress and overstrain. A number of experiments have proven the significant role of emotional overstrain and stress in the development of cardiovascular diseases. The high incidence of the circulatory system, the long course and severity of diseases in elderly and old people determine the relevance of the search for treatment using effective and safe drugs. Aim: iinvestigate the effect of a combination of ATP-LONG and molsidomine on the functional state of the myocardium of young and old rats under chronic soft stress. Materials and methods. In experiments on young (10 months) and old (24 months) male Wistar rats, the cardiotropic and cardioprotective activity of the combination of the metabolic cardioprotector ATP-LONG and the vasodilator molsidomine was studied under conditions of chronic soft stress. Results. The negative impact of chronic soft stress on the bioelectrical activity of the myocardium – a violation of the processes of repolarization, conduction and contractility of the heart was found in young rats. The combination of ATP-LONG and molsidomine normalized the bioelectrical activity of the myocardium and increased its resistance to stress factors. In old rats under the influence of chronic stress, signs of impaired repolarization and electrical instability of the heart were more significant than in young animals. The combination ATP-LONG and molsidomine prevented the damaging effect of chronic stress and contributed to the normalization of the electrophysiological parameters of the myocardium of old rats. Conclusions. The results of experiments indicate the pharmacological cardiotropic activity of the combination of ATPLONG and molsidomine in young and old rats with chronic soft stress. Keywords: young rats, old rats, chronic soft stress, myocardium, electrocardiogram, bioelectrical activity of the heart, ATP-LONG, molsidomine, cardioprotective effect.

scholarly journals Age-Related Decrease in the Schaffer Collateral-Evoked EPSP in Awake, Freely, Behaving Rats

2000 ◽  
Vol 7 (3) ◽  
pp. 167-178 ◽  
Author(s):  
C. A. Barnes ◽  
G. Rao ◽  
G. Orr
Keyword(s):  
Spatial Behavior ◽  
Synaptic Response ◽  
Cognitive Changes ◽  
Schaffer Collateral ◽  
Young Rats ◽  
Ca1 Region ◽  
Age Related ◽  
Old Rats ◽  
Freely Behaving

Synaptic response size in the CA1 region of the hippocampus in aged rats is reduced for a given stimulus intensity, compared with that elicited in young rats. Consistent with the in vitro findings of reduced Schaffer collateral-evoked CA1 EPSPs in old rats, the population currents evoked to iontophoretically applied AMPA are also smaller relative to the presynaptic fiber potential amplitude. On the other hand, the size of the presynaptic fiber potential and amplitude of unitary intra-cellularly recorded EPSP responses do not change across age in the CA1 region. These electrophysiological findings are consistent with the hypothesis that old rats have fewer functional synaptic contacts per Schaffer collateral axon than do young rats. The possibility that this age change arises as a result of a differential tissue recovery response to in vitro preparation was examined in the present study. CA1 presynaptic fiber potential and EPSP amplitudes evoked by the stimulation of Schaffer collateral afferents were studied in intact, freely behaving young and old rats. We confirmed in vivo the pattern of electrophysiophysiological results previously reported in vitro and found significant correlations between the synaptic response amplitudes and the accuracy of spatial behavior in the Morris swim task. The data suggest that changes in functional connectivity of old rats may be a significant contributor to cognitive changes during aging.

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