摘要:

Short‐term oscillation of heart rate and blood pressure are mainly regulated by the automatic nervous system. It has been proposed that non‐neural factors, such as changes in intrathoracic pressure, can strongly modulate this rhythmicity. Our aim was to evaluate the effect of changing intrathoracic pressure and central autonomic nervous activity on heart rate and blood pressure variability. Evaluation was performed by using spectral analysis techniques with autoregressive modelling. The variability in heart rate and blood pressure remained in animals with open chest or paralysed respiratory muscles. After vagotomy, the variability in heart rate decreased, but not that of blood pressure. Total spinal anaesthesia elicited a decrease in the variability in blood pressure. The pharmacological blockade ofα‐ andβ‐receptors further decreased both variabilities. It was concluded that in anaesthetized dogs heart rate and blood pressure variability are mainly of central origin and non‐neural factors have only minor effect on these central rhythms. High (>0.15 Hz), medium (0.07–0.15 Hz) and, obviously low (0.00–0.07 Hz) frequency variations in heart rate are mostly mediated vagally. In blood pressure, medium and obviously low frequency variations are modulated by sympathetic nervous system, whereas high frequency variations are secondary to the heart

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09404.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Myocardial capillary exchange capacity was investigated by stereologic and functional techniques in parallel during pressure‐overload cardiac hypertrophy and after long‐term antihypertensive therapy with the vasodilator felodipine. In 26‐week‐old female spontaneously hypertensive rats (SHR) blood pressure increased by 25 % and left ventricular weight (LVW/BW) increased by 18% compared to Wistar‐Kyoto rats (WKY). Myocardial capillary surface and volume densities normalized for organ weight were similar in both ventricles for both strains. Moreover, capillary surface density was higher sub‐epicardially (EPI) than in the subendocardium (ENDO) in the left ventricle of SHR. Thirteen weeks of felodipine‐therapy (SHR‐Felo) normalized blood pressure without affecting LVW/BW although a transition from concentric to eccentric hypertrophy is known to occur. Myocardial capillary surface and volume densities and the left ventricular ENDO‐EPI‐gradient in surface density were similar to untreated SHR. However, felodipine‐treatment increased right ventricular weight and capillary volume density.Functional capillary exchange was estimated in terms of permeability surface area products (PS) for Cr‐EDTA and vitamin B12and normalized for organ weight. PScr‐EDTA, PSB12and the ratio PScr‐EDTA/PSB12(an index of capillary permeability) were similar in SHR and WKY. Furthermore, the relation between functional and stereological indices of exchange capacity was investigated in a multiple linear regression analysis. However, no significant correlation between PS and neither capillary surface nor volume density was found.In conclusion, myocardial capillary exchange capacity was well adapted to the pressure overload cardiac hypertrophy present in female SHR. Despite induction of right ventricular hypertrophy, felodipine‐treatment did not affect capillary exchange capacity. Furthermore, when functional and stereologic estimates were performed in parallel, the importance of dynamic factors for myocardial capillary exchange capacity (e.g. h

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09405.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The endurance‐training programme in Experiment 1 (Exp. 1) consisted of a total swimming time of 149–159 h per male Han Wistar rat and in Experiment 2 (Exp. 2) the male NMRI‐mice run on a treadmill at a speed of 25 m min‐11 h per day, 5 days a week for 3 weeks. One group of the rat hearts was perfused with 0.3 mm cumene hydroperoxide (CumOOH) while the others were fractioned (mitochondria, sarcolemma and sarcoplasmic reticulum) and these cell fractions and homogenates were used to determine the total concentration of peroxidative lipids and the susceptibility to lipid peroxidation. The perfusion with CumOOH caused the release of thiobarbituric acid reactive substances (TBARS) into the perfusate. The release of TBARS from the trained hearts was smaller than that of the control hearts (P<0.01). The concentration of TBARS was also smaller in the myocardium of the right ventricle of the trained rats (P<0.01). The concentration of reduced GSH remained at a higher level after the CumOOH perfusion suggesting a better redox state in the hearts of trained animals. The concentration of the lipids susceptible to lipid peroxidation was lower in the homogenates of the trained rat hearts (P<0.05). However, this decrease could not be explained by any of the tissue fractions used when studied in rat hearts. In Exp. 2 the total concentration of lipids susceptible to peroxidation remained unchanged in the mice hearts. However, endurance training by running decreased (P<0.01) the lipid peroxidation rate in mouse hearts and also decreased (P<0.05) the sensitivity of myocardium toin vitrostimulated lipid peroxidation. The results suggest that endurance training by swimming or by running reduces the susceptibility of myocardium of rats and mice to chemically induced lipid peroxidation injuriesi

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09406.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The reactions of resistance vessels in SHR and WKY hindquarters were compared during saline or blood perfusion. During saline constant‐flow perfusion at all initial pressures (80–200 mmHg) sympathetic vasoconstrictor effects were greater in SHR than those in WKY. During perfusion at constant and equal pressure vasoconstrictor responses were greater in SHR vs. WKY only at high pressure ‐ 200 mmHg. On the other hand, under constant pressure conditions at lower pressures (80 and 120 mmHg) sympathetic stimulation induced weaker responses in SHR than in WKY, which at, for example, 80 mmHg was the case at every frequency of sympathetic stimulation used (2–20 Hz). Also, the responses to exogenous noradrenaline and vasopressin occurred during perfusion at low (80 mmHg) and for both equal constant‐pressure conditions lower in SHR than in WKY. Comparison of sympathetic effects in SHR and WKY during blood hindquarter perfusion revealed similar results. Also, when SHR and WKY responses were compared at their ordinary levels of constant‐pressure, sympathetic vasoconstrictor effects in SHR were lower than t

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09407.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

Cardiovascular and renal responses to a step‐up infusion of endothelin‐1 (ET‐1) (1, 5, and 15 ng kg‐1min‐1) were investigated in conscious dogs. In addition, the disappearance of ET‐l in arterial and central venous plasma after an infusion of 10 ng kg‐1min‐1was quantified, and the effects of vasopressin (AVP, 10 ng kg‐1min‐1) and angiotensin II (AII, 2, 5, and 10 ng kg‐1min‐1) on plasma ET‐1 were investigated. The step‐up infusion of ET‐1 increased the plasma level from 3.6 ± 0.3 to 243 ± 23 pg ml‐1. Concomitantly, arterial blood pressure increased and heart rate (HR) decreased dose‐dependently. Diuresis, sodium, and potassium excretion did not change significantly. However, free water clearance increased during the infusion. Clearance of creatinine and excretion of urea decreased (39 ± 4 to 29 ± 3 ml min‐1and 87 ± 16 to 71 ± 14 μmol min‐1, respectively). Decay curves for ET‐1 in venous and arterial plasma were identical, and initial t½was 1.1 ± 0.1 min. Vasopressin increased arterial blood pressure (107 ± 4 to 136 ± 3 mmHg) beyond the infusion period and increased plasma ET‐1 (85%). An equipressor dose of AII tended to decrease plasma ET‐1.It is concluded that the lung is apparently not important in the removal of ET‐1, that the disappearance of ET‐1 follows a complex pattern, and vasopressin – in contrast to angiotensin II – is able to increase the plasma concentration of ET‐1. The latter may suggest that

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09408.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The effects of somatostatin (SS‐14) on glycogenolysis and gluconeogenesis in rat hepatocytes culturedin vitroin a serum‐free medium were investigated. Somatostatin (122 nmol 1‐1) did not significantly change the basal glucose production with or without pyruvate (10 mmol 1‐1). Glucagon strongly (over 100%) increased the glucose production in hepatocytes incubated in a medium supplemented with 10 mmol 1‐1pyruvate. This increase in glucose production is the result of increased rates of gluconeogenesis and glycogenolysis. Somatostatin partially inhibited the glucagon stimulated increase in glucose production. Glucagon also significantly increased the glucose production in a glucose‐free medium without pyruvate, which resulted from an increase of glycogenolysis. Somatostatin did not inhibit the increase in glucose production in these conditions. After a 4 h ‘fast’, glycogen in hepatocytes fell to a very low level. Glucose production was minimal. After the addition of pyruvate, there was a increase in gluconeogenesis and glucose production. Glucagon stimulated the rate of gluconeogenesis. Somatostatin completely inhibited this glucagon‐stimulated increase i

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09409.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

X‐ray micro‐analysis was carried out on cultured respiratory cells from polyps removed from individuals with and without cystic fibrosis (CF). In a first set of experiments, proper experimental conditions were established. Washing the cells with 300 mmol 1‐1mannitol in distilled water was found to give the best removal of the culture medium. The elemental concentrations stabilized in about 10 min after the start of the preincubation. Intracellular [Na] and [Cl]increased slightly with increasing passage number, whereas intracellular [K] decreased. Under resting conditions there were no significant differences in elemental content between CF and control cells, and there were no indications for abnormally high total [Ca]in CF cells. In normal cells, stimulation with a cAMP‐analogue resulted in a decrease of cellular [CI], whereas in CF cells an increase was measured. Exposure of both normal and CF cells to ouabain resulted in decreased [K]and increased [Na] and [CI]level. The calcium ionophore A23187 had a similar effect on normal cells but did not affect CF cells markedly. Application of amiloride to the apical side of the cells resulted in a decrease of cellular [Na] in CF cells, whereas [Na]in control cells was not affected. The results correspond with what is known about the defective cAMP‐regulated transepithelial Cl‐transport in CF cells. The effect of the calcium ionophore on cellular electrolyte content is more complicated and may be the result of two separate effects: efflux of Cl‐via a Ca2+‐dependent mechanism and inhibition of the Na+‐K+‐ATPase by intracellular Ca2+ions causing an influ

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09410.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

The functional effects of a hyperpolarization‐activated membrane current (IQ) in the slowly adapting lobster stretch receptor neurone were investigated. From comparisons between changes in membrane excitability due to blockage of IQby Cs+, in normally impaled and native unimpaled (Edmanet al. 1987 b) cells, it could be concluded that the resting voltage of native cells is distinctly more negative than –65 mV (average membrane voltage of impaled cells) and, therefore, under the control of an activated IQ. Starting from this conclusion, impaled cells were polarized to holding (resting) voltages around –75 mV and their polarization and excitability properties studied after tetanic impulse activity and variation of various external influences (K+, pH, temperature), both in control conditions and after blockage of IQ by 2 mm Cs+. It was found that an unblocked IQ(a) greatly accelerates the initial (90%) decay of post‐tetanic hyperpolarization, and (b) depresses distinctly any polarization and excitability alterations due to increases in extracellular K+concentration (from 2.5 to 10 mM), variations in extracellular pH (between 6.4 and 8.6), and changes in temperature (between 14 and 24 °C). It was inferred that in well polarized cells, IQplays a role as a stabilizer of membrane polarization and excitability in conditions of varying external influences. From a model study of IQit could be concluded that, with its slow dynamic responses, the current is well adapted to its functional purposes and to the rather slow homeostatic effects of the cell's N

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09411.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

In isolated nerve terminals from ox neurohypophyses the following concentrations of polyamines [pmol (μg protein)‐1(mean ± SEM)] were found: spermine: 2.07 ± 0.14 (n = 3), spermidine: 0.22 ± 0.01 (n = 4), putrescine: 0.20 ± 0.01 (n = 4).In secretory granules isolated from the same tissue, the concentrations were: spermine: 0.57 ± 0.02 (n = 3), spermidine: 0.07 ± 0.04 (n = 3), putrescine: 0.13 ± 0.04 (n = 3).After incubation of isolated nerve terminals with the polyamines, they were taken up as a function of time and concentration, approaching saturation at high concentrations.The kinetic parameters of their synthesizing enzyme, ornithine decarboxylase, in ox neurohypophyseal nerve terminals (apparent Km0.75 mm and Vmax22.5 pmol mg protein‐1h‐1) were comparable to those previously found in cerebral cortex of rats.When isolated, hemilobes from rat neurohypophyses were incubated in a medium which contained spermidine (5 mM), and were stimulated by 56 mrs K+, release of vasopressin was smaller than in control experiments. However, after removal of spermidine and after restimulation, 50 min after initial stimulation, the release was significantly elevated.It is suggested that polyamines may take part in modulation of vasopr

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09412.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY

摘要:

In order to determine the major routes of insulin degradation in the body, insulin was labelled with a ‘trapped’ or ‘residualizing’ label: [125I]tyramine‐cellobiose ([125I]TC) and injected intravenously in dogs. In contrast to conventional iodine‐labelled insulin (131I‐insulin), the [125I]TC‐insulin allows measurements of total uptake in specific organsin vivobecause the radioactive degradation products do not leave the cells. One h after the injection of trace doses, the amount of radioactivity recovered in the kidney from [125I]TC‐insulin was nine times higher than when conventional [131I]insulin was used. In the blood, the amount of acid‐precipitable radioactivity was the same for both labelled preparations, indicating similar clearance rates.A comparison of the uptake of insulin in filtering vs. non‐filtering (ureter‐occluded) kidneys indicated that the uptake of insulin is twice as high through the luminal than through the basolateral cell membrane; after 60 min, 8.9 ± 0.8% of the injected [125I]TC‐insulin dose remained in the filtering kidney and 3.2 ± 0.2% of the dose was accumulated in the contralateral kidney, with occluded ureter but normal blood perfusion.In both filtering and non‐filtering (ureter‐occluded) kidneys, the subcellular distributions of [125I]TC‐insulin were studied after various times by isopycnic sedimentation in sucrose gradients. No difference between peritubular and tubular uptake was discernible. The intracellular transport was rapid, leading to accumulation of radioactive label

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1992.tb09413.x

出版商:Blackwell Publishing Ltd    

年代:1992

数据来源: WILEY