Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One injection of estradiol benzoate (EB) (100 micrograms) or vehicle was administered to male rat pups 5 days after birth. Two months later ventilation, ventilatory responses to 7% carbon dioxide, and to 580 mg/kg aspartic acid (an agent used as a marker of sexually dimorphism in the control of ventilation) were evaluated and body weight, testes weight, and nose-anus length were measured in animals in each group. The EB-treated rats had similar tidal volumes, frequency of breathing, and minute ventilation as did control male rats. The ventilatory responses of EB-treated rats to hypercapnia were markedly less than those of control animals. Aspartic acid administration depressed ventilation in control animals, but had no effect on ventilation in EB-treated males. Body and testes weights, as well as nose-anus length, were less in EB-treated compared with control rats. However, when body weight was normalized by nose-anus length and testes weight was normalized by body weight, the values were comparable between the two groups. Thus, perinatal EB treatment of male rat pups results in small, hypogonadal adult animals whose ventilation in response to hypercapnia was diminished and whose response to aspartic acid was female-like relative to those of control rats.
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PMID:Perinatal estradiol benzoate administration affects control of ventilation in adult male rats. 148 68

We have previously shown that subcutaneous administration of aspartic acid (a dicarboxylic acidic amino acid) at a dose of 580 mg/kg causes long lasting depression of ventilation in adult intact and postpubertally castrated male rats, but not in intact female rats. The purpose of the present study was to determine if hypogonadism induced by perinatal administration of testosterone propionate (TP) will alter ventilation, oxygen consumption, and the ventilatory response to aspartic acid and to hypercapnia in adult males. TP treatment resulted in adult males who had lower body, prostate, heart, and testes weights than those of control male rats. Ventilation in air and oxygen consumption were comparable between the two groups as was the ventilatory response to aspartic acid. In contrast, TP-treated rats exhibited a significantly decreased ventilatory response to hypercapnia due predominantly to lower tidal volumes compared to control animals. Aspartic acid treatment did not affect oxygen consumption in either group. Thus, TP treatment results in the development of adult male rats who, although hypogonadal, retain a male-like ventilatory response to aspartic acid, but whose response to hypercapnia is more like that of hypogonadal men and rats.
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PMID:Control of ventilation in androgenized hypogonadal male rats. 152 34

The effects of aspartic acid (aa) on ventilation were evaluated in awake male and female rats prior to and 15, 30, and 45 minutes after saline, 100 mg/kg or 580 mg/kg aa was injected subcutaneously. Subsequently, rats were exposed to hypoxic and hypercapnic gas challenges. In males, 100 mg/kg aa increased ventilation (VE) by increasing inspiratory flow rate (VT/TI), tidal volume (VT), and frequency of breathing (f) by 30 minutes, whereas in females VT was increased above saline levels only at 15 minutes. VE did not decrease over time. A dose of 580 mg/kg aa depressed ventilation in males for 2 hours by decreasing VT, VT/TI and f. In contrast, female rats exhibited a decreased ventilation only at 15 minutes which then began to return to saline levels by 45 minutes. Neither male nor female rats treated with either dose of aa showed a depressed response to hypoxia or hypercapnia. These data indicate that aa at two doses can affect the pattern of ventilation differently in male and female rats. One mechanism responsible for the differences noted between the two groups is the effect aspartic acid may have on testosterone production. An additional study comparing ventilatory responses of sham operated and castrated males to various doses of aa indicated that testosterone was not necessary to show the 'male' pattern of response.
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PMID:Acute effects of aspartic acid on ventilation of male and female rats. 338 87

In this study ventilation was evaluated in 12-mo-old male and female rats who had received large doses of aspartic acid neonatally. Rats of both sexes treated with aspartic acid were obese, stunted, and exhibited hypogonadism. Although metabolic rates of the aspartic acid-treated rats were not different compared with sex-matched controls, ventilatory patterns were different. Aspartic acid-treated females breathed with a smaller tidal volume (VT), higher frequency (f), and similar minute ventilation (VE) compared with control females. This pattern is commonly observed in many patients who are obese. The aspartic acid-treated females responded to hypercapnic and hypoxic challenges by increasing f more than VT. Tissue pocket gases (PCO2 and PO2) of aspartic acid-treated females were normal. In contrast, aspartic acid-treated males hypoventilated compared with control males. Tissue pocket gas values suggested that aspartic acid-treated males were hypoxemic and hypercapnic. Moreover, the response of aspartic acid-treated males to hypercapnia was parallel to but was less than that of control male rats. The ventilatory response of aspartic acid-treated male rats to hypoxia was blunted. This study has shown that neonatal administration of aspartic acid causes a decreased ventilation and blunted response to hypoxia in adult male but not female rats.
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PMID:Aspartic acid administered neonatally affects ventilation of male and female rats differently. 374 70

Ventilation, oxygen consumption, the ventilatory equivalent for oxygen, and ventilatory responses to hypoxia and to hypercapnia were evaluated in conscious male rats who received each of four treatments: (1) microinjection of artificial cerebrospinal fluid (aCSF) into the arcuate nucleus and subcutaneously saline (CS); (2) aspartic acid into the arcuate nucleus and saline subcutaneously (AS); (3) aCSF into the arcuate nucleus and naloxone subcutaneously (CN); and (4) aspartic acid into the arcuate nucleus and naloxone subcutaneously (AN). Rats treated with CN exhibited a depression of ventilation, ventilatory equivalent, ventilatory response to hypercapnia, and tidal volume response to hypoxia and to hypercapnia. AS had no effect on any parameters. Administration of both aspartic acid and naloxone attenuated all the effects of CN except the depression of minute ventilation in response to hypercapnia. Therefore the naloxone (a mu opioid receptor antagonist) induced a depression of ventilation that was attenuated by aspartic acid acting on N-methyl-D-aspartic acid receptors in the arcuate nucleus.
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PMID:Aspartic acid in the arcuate nucleus attenuates the depressive effects of naloxone on ventilation. 986 84

Malnutrition, hypoxia and energy deficit may affect protein metabolism. We wanted to evaluate the cross-sectional association between serum amino acids and fat-free mass in a group of hypoxic patients. We also wanted to explore, in the same group of patients, whether the blood amino-acid pattern could possibly be influenced by differences in lung function and energy intake. Serum amino acids were measured in 71 hypoxic underweight and normal-weight patients with advanced pulmonary disease and related to the fat-free-mass index, arterial oxygen (PaO2) and carbon dioxide tension (PaCO2), forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1) and energy intake. Only one amino acid (aspartic acid) remained significantly correlated to the fat-free-mass index after adjustments for age and sex (beta = -0.30, P=0.011). None of the amino acids were significantly correlated to PaO2 but alanine was significantly negatively correlated to PaCO2 (beta = -0.46, P<0.001), phenylalanine to FVC1 (beta = 0.52, P=0.001) and tyrosine to FVC (beta = 0.36, P=0.008). Citrulline and tryptophan were significantly correlated to energy intake (beta = 0.32, P=0.008; beta=0.37, P=0.009 respectively). In conclusion, there was no convincing association between fat free mass and serum amino acids. The negative effect of hypercapnia and reduced lung function on some serum amino acids was suggested and some amino acids were sensitive to reduced energy intake.
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PMID:Serum amino acids in relation to nutritional status, lung function and energy intake in patients with advanced pulmonary disease. 1100 Oct 78