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排序方式: 共有1581条查询结果,搜索用时 15 毫秒
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O. V. Karachentseva V. N. Yartsev D. P. Dvoretsky I. V. Zhdanova 《Acta physiologica (Oxford, England)》2005,185(2):99-107
Aim: Dependence of the melatonin‐evoked potentiation of the rat tail artery neurogenic reactivity on degree of the change in the reactivity was studied. Method: Electrical field stimulation‐evoked contractile response of the juvenile rat tail artery segment under isometric conditions was recorded. 0.1 μm melatonin was administered after the change in the response produced both spontaneously and by acidification (pH 6.6) or alkalinization (pH 7.8) of the solution. Results: During the course of experiment, the contraction force continuously declined, being reduced by 12 ± 5, 24 ± 7 and 32 ± 6% at 20, 70, and 170 min after beginning of experiment, respectively. Melatonin applied at these time points increased the contraction by 20 ± 5, 41 ± 10, and 48 ± 8%, respectively, relative to control. This increase in potentiating effect of melatonin during the course of experiment was not because of sensitization of the segment to the hormone. Acidosis‐induced considerable decline in neurogenic contraction was counteracted by melatonin, while after alkalosis‐induced augmentation in the contraction the hormone was not effective. Melatonin increased the artery response to 0.1 μm noradrenaline. Conclusion: These data suggest that melatonin can restore an attenuated neurogenic reactivity of the juvenile rat tail artery. The effect is more pronounced with further decrease in reactivity and might be due to a change in sensitivity of the post‐junctional membrane to noradrenaline. 相似文献
3.
Shelley A. Klemm Richard D. Gordon Terry J. Tunny Wendy L. Finn 《Clinical and experimental pharmacology & physiology》1990,17(3):191-195
1. Plasma potassium and chloride concentrations were raised and plasma renin activity, aldosterone, bicarbonate and arterial pH were reduced in two brothers with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome), on unrestricted or moderately restricted sodium diets. 2. These abnormalities were corrected in both patients within 10 days of severe sodium restriction. 3. Pressor sensitivity to cold and angiotensin II decreased on low sodium diet, associated with a fall in blood pressure. 4. Increasing distal tubular sodium delivery by infusion of normal saline increased fractional excretion of potassium when aldosterone had been stimulated by severely restricted sodium diet, but not when aldosterone levels were low on unrestricted sodium diet. 5. These findings are consistent with excessive sodium reabsorption as the primary renal lesion in Gordon's syndrome, leading to volume expansion and suppression of renin and aldosterone. Severe dietary sodium restriction leading to volume contraction, by stimulating renin and aldosterone and promoting kaliuresis, corrects the abnormalities. 相似文献
4.
Summary In a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes [MELAS] who had normal mitochondrial enzyme activity, high doses of coenzyme Q10 (CoQ) were administered. Clinical improvement with decreased serum lactate and pyruvate levels was observed. Though the mechanism of action of CoQ is not known, a trial is worthwhile in patients with MELAS. 相似文献
5.
6.
ALBERTO Q FARIAS LUCIANA L GONÇALVES EDUARDO LR CANÇADO ANTONIO C SEGURO SILVIA B CAMPOS CLARICE P ABRANTES-LEMOS FLAIR J CARRILHO 《Journal of gastroenterology and hepatology》2006,20(1):147-152
Background and Aims: Primary biliary cirrhosis (PBC) might be complicated by osteoporosis, whose etiology remains unknown but seems to be multifactorial. Prevalence rates of 30% to 60% for distal renal tubular acidosis (DRTA) have been reported in PBC patients, generally as incomplete DRTA. Although it is undisputed that a reduced bone mineral density (BMD) is the expected outcome among patients who have been suffering from longstanding chronic metabolic acidosis, it is unclear if incomplete DRTA is also associated with metabolic bone disease in PBC patients. The present study was undertaken to compare the BMD of PBC patients with and without DRTA.
Methods: The BMD of 23 PBC patients (11 with DRTA and 12 without), all with normal clearance of creatinine, was assessed by dual energy radiograph absorptiometry. The diagnosis of DRTA was made if the urine pH was above 5.4 in all samples after the oral acid overload, showing tubular inability to acidify urine in the presence of test-induced systemic metabolic acidosis.
Results: Densitometric signs of osteoporosis were found in 82% of DRTA cases and in 83% of patients without DRTA (difference not significant). There were no significant differences in BMD measurement, T and Z scores of patients with and without DRTA.
Conclusions: The present study could not support a correlation between the presence of DRTA and the bone loss observed in PBC patients. 相似文献
Methods: The BMD of 23 PBC patients (11 with DRTA and 12 without), all with normal clearance of creatinine, was assessed by dual energy radiograph absorptiometry. The diagnosis of DRTA was made if the urine pH was above 5.4 in all samples after the oral acid overload, showing tubular inability to acidify urine in the presence of test-induced systemic metabolic acidosis.
Results: Densitometric signs of osteoporosis were found in 82% of DRTA cases and in 83% of patients without DRTA (difference not significant). There were no significant differences in BMD measurement, T and Z scores of patients with and without DRTA.
Conclusions: The present study could not support a correlation between the presence of DRTA and the bone loss observed in PBC patients. 相似文献
7.
Anesthetized, paralyzed and mechanically ventilated pigs were exposed to extreme hypercapnia (Paco2-20 kPa) at Fio2 0.4 for 480 min, with (n = 6) or without (n = 6) continuous infusion of isotonic buffers (bicarbonate and trometamol). Arterial pH was higher in buffered animals than controls, 7.21 ±0.01 vs 7.01±0.01 (mean ± s.e.mean, P < 0.01). Serum osmolality and Paco2 did not differ between groups throughout the experiment. The hemodynamic response to hypercapnia was attenuated in the buffered group, who had lower heart rate, 133 ± 6 vs 189±12 min-1 (P < 0.01), mean arterial pressure (MAP) 109 ± 4 vs 124 ± 4 mmHg (14.5 ± 0.5 vs 16.5 ± 0.5 kPa) (P < 0.05), mean pulmonary arterial pressure 16±1 vs 23 ± 1 mmHg (2.1 ±0.1 vs 3.1 ±0.1 kPa) (P < 0.01), and pulmonary vascular resistance (PVR) 249 ± 21 vs 343 ± 20 dyn s-cm-5 (2490±210 vs 3430±200 μN-s-cm-5) (P < 0.01), compared with the control group. Subsequently, both groups were exposed to hypercapnic hypoxemia by stepwise increases in Fio2 (0.15, 0.10, 0.05) at 30-min intervals, while Fico2 was kept at 0.2. PVR increased in both groups (P < 0.05) but, except for heart rate, all hemodynamic differences between the groups disappeared during hypoxia. At Fio2 0.15, buffered animals had higher arterial oxygen saturation (73 ± 5%) than the controls (55 ± 5%), (P < 0.05). The control animals died after 1–29 min (mean 14 min) at Fio2 0.10, while all buffered animals survived Fio2 0.10 with stable MAP (122 ± 14 mmHg (16.3 ± 1.9 kPa). The buffered animals died after 4–22 min (mean 15 min) at Fio2 0.05. We conclude that buffering to a pH of 7.21 attenuates the observed hemodynamic response in extreme hypercapnia and improves survival in hypercapnic hypoxemia. 相似文献
8.
Reversible low-molecular-weight proteinuria in patients with distal renal tubular acidosis 总被引:2,自引:0,他引:2
Takashi Igarashi Hidehiko Kawato Shigehiko Kamoshita 《Pediatric nephrology (Berlin, Germany)》1990,4(6):593-596
Four patients with untreated renal tubular acidosis had a urinary excretion of low-molecular-weight (LMW) proteins which was restored to normal by alkali therapy. Hypokalaemic proximal tubular damage in untreated patients with distal renal tubular acidosis is believed to be the cause of LMW proteinuria. An examination of urinary excretion of LMW proteins is useful for determining hypokalaemic proximal tubular dysfunction, as well as the efficiency of alkali therapy. 相似文献
9.
G. J. Kemp C. H. Thompson A. L. Sanderson G. K. Radda 《Magnetic resonance in medicine》1994,31(2):103-109
We used 31P magnetic resonance spectroscopy to compare the response of rat skeletal muscle to three kinds of proton load. During exercise (tetanic sciatic nerve stimulation), protons from lactic acid were buffered passively and consumed by net hydrolysis of phosphocreatine (PCr). During recovery from exercise, the pH-dependent efflux of protons produced by PCr resynthesis could be partially inhibited by amiloride or 4,4′-diisothiocyanostilbene-2,2′-disulphonate (DIDS), implicating both sodiudproton and bicarbonatelchloride exchange, but was not inhibited by simultaneous respiratory acidosis. In early recovery, up to 30% of proton efflux was mediated by lactatelproton cotransport. During acute respiratory acidosis at rest, the eventual change in muscle pH was consistent with passive buffering and was unaffected by amiloride or DIDS, implying no significant contribution of proton fluxes. 相似文献
10.
G. J. van Ekeren A. M. Stadhouders J. A. M. Smeitink R. C. A. Sengers 《European journal of pediatrics》1993,152(3):255-259
The objectives of this study were to describe the course of two forms of an hereditary syndrome characterised by congenital cataract, mitochondrial myopathy of heart and skeletal muscle and lactic acidosis. We also sought to determine clinical, physicochemical and histopathological data which might allow early distinction between the two forms. We compared the ages at which clinical and physicochemical signs appeared in 16 patients. In 5 patients, enzyme-histochemical and ultrastructural data of skeletal muscle were available and muscle fibre composition analysed morphometrically. In any particular family only one form of the syndrome occurred. Amongst the patients who did not survive (range 14–34 years) 4 patients died in the neonatal period and 7 died at a median age of 23 years. The median age of the survivors was 19 years (range 15–42 years). Outflow obstruction of the left ventricle was noted in four deceased patients at variable times prior to death. The other deceased patients were not examined, but the cause of death was invariably heart failure. In none of the surviving patients was outflow obstruction noted. Enzyme-histochemical and ultrastructural findings were not specific for the course of the disease. In one biopsy, taken at the age of 3.5 months from a patient who survived, strong lipid accumulation was noted. Morphometric analysis showed proliferation of the mitochondria in muscle fibres, which increased during the course of the disease. 相似文献