摘要:

The relationship between food intake and oxygen consumption was studied in a group of 60 rats acclimated at environmental temperatures of either 30 or 10 °C. Three separate experiments were performed. In the first, 28 rats were divided into two groups: control, which received 20 and 32 g of food/day at 30 and 10 °C, respectively, from 0800 to 1700 and experimental, which received 10 and 25 g of food/day at 30, and 10 °C, respectively. The experimental period lasted 6 weeks. Oxygen consumption was measured weekly at environmental temperatures of 5, 15, 25, 30, and 35 °C. In the second experiment, 16 rats were subjected to the same food intake as the animals in the first experiment. After 1 week, their oxygen consumption was measured at 25 °C over a period of 24 h. The third experiment was carried out with 16 other rats in which the control groups received the same amount of food as in the first experiment, and the experimental groups were fed 6 and 11 g/day at 30 and 10 °C, respectively, during 1 week. In the first experiment, no changes in oxygen consumption (per kilogram0.67) were apparent in the experimental rats during 6 weeks. However, after 1 week on severe food restriction a significant decrease in oxygen consumption (per kilogram0.67) was observed. A long-lasting thermic effect of food was observed in control rats from the second experiment and a rapid effect was apparent in restricted rats. The results seem to indicate that in the rat, although the oxygen consumption does depend on the level of food intake, it is necessary to have a higher level of restriction to make it apparent when compared with larger species of animals. It is also suggested that energy conservation mechanisms did not interfere with cold acclimation.

ISSN:0008-4212    

DOI:10.1139/y87-001

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

To try to compare receptor compartment kinetics, receptor binding, and binding–response coupling for two smooth muscle typesin vivo, pressor and uterine responses to oxypressin, an equipotent analog of oxytocin and vasopressin, were studied simultaneously in urethane-anesthetized, pentolinium–indomethacin treated rats. Access of peptide to the pressor and uterine receptor compartments and peptide–receptor dissociation rate had a negligible effect on the two responses. During both injections and infusions, the blood pressure response seemed to be determined largely by plasma levels of oxypressin. The uterine response to oxypressin, however, was paradoxical. The heights of individual uterine contractions seemed to be determined throughout by plasma oxypressin concentrations. The interval between contractions also seemed to be determined by plasma peptide concentrations during injections. However, as plasma peptide increased and reached steady state during infusion, contraction interval behaved as if plasma peptide concentrations were decreasing. This effect was more marked at the beginning of infusion. The implication of these results is that binding determines the pressor response to oxypressin and binding–response coupling does not change. In contrast, although binding determines the uterine response to oxypressin during injection and binding–response coupling appears constant, some factor in addition to binding affects the contraction interval portion of the uterine response and modifies the apparent binding–response coupling of this parameter during infusion.

ISSN:0008-4212    

DOI:10.1139/y87-002

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

A short latency projection of group I afferent fibers from ankle dorsiflexors to knee extensor muscles has been categorized as species specific to humans. However, the effects of the pathway have only been inferred from conditioning homonymous reflexes in relaxed muscle. This study focused directly on the responses evoked in the electromyogram of the heteronymous muscles when active, in two experiments. In the first, preferential activation of group I afferents of ankle dorsiflexors, by electrical stimulation of the common peroneal nerve, excited both vastus medialis (mean latency, 26.3 ms) and rectus femoris (mean latency, 33.5 ms). No excitation or inhibition in either muscle was associated with stimulation of the tibial nerve. The second experiment compared vastus medialis responses with common peroneal nerve stimulation during three different movement conditions in which the muscle was equally contracted: (i) rhythmic isotonic (pedalling), (ii) episodic isotonic, (iii) isometric contraction. Responses were identified in all three active states, with no significant differences in amplitude or latency. No responses were seen in the relaxed muscle.

ISSN:0008-4212    

DOI:10.1139/y87-003

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

Interactions of derivatives of befunolol (BFE-37, BFE-55, and BFE-61), carteolol, and pindolol with β-adrenoceptors were tested in guinea pig isolated taenia caecum. All the drugs used acted as partial agonists on the β-adrenoceptors when compared with isoprenaline, a full agonist. The pA2values of BFE-61, carteolol, and pindolol were significantly larger than their pD2values, while there was no significant difference between the pA2and pD2values for BFE-37 and BFE-55. The specific binding of [3H]befunolol to microsomal fractions from the guinea pig taenia caecum distinguished two binding sites, high affinity and low affinity sites. Both sites are considered to be bound by 50 nMof [3H]befunolol. Specific3H binding was displaced by BFE-61, carteolol, and pindolol in a biphasic manner but in a monophasic manner by BFE-37 and BFE-55. Furthermore, [3H]befunolol binding was only partially displaced by BFE-55 but completely displaced by the other drugs used. These results, together with our previous findings, suggest that BFE-61, carteolol, and pindolol discriminate between the two affinity binding sites in the β-adrenoceptors, which are not discriminated between by BFE-37, and further that BFE-55 may bind with only the high affinity site.

ISSN:0008-4212    

DOI:10.1139/y87-004

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

Tetrodotoxin-resistant relaxations produced by electrical field stimulation, 5-hydroxytryptamine (5-HT), and A23187 (calimycin) were investigated in the rat isolated oesophageal tunica muscularis mucosae subjected to cold storage of varied duration. Cold storage for 2 days abolished cholinergic nerve mediated contractions to field stimulation; however, field stimulation evoked relaxations and muscarinic agonist evoked contractions persisted undiminished. After 5 days of cold storage, field-stimulated relaxations, as well as tension generating capacity of the tissue, were significantly reduced. Proximodistal differences were observed in tunica muscularis mucosae sensitivity to the relaxant effects of serotonin and A23187 and these were exaggerated after cold storage. In the distal segment, cold storage for 2 days unmasked ketanserin-sensitive 5-HT receptors mediating contractions. Similarly, A23187 induced contractions rather than relaxation in cold-stored distal tunica muscularis mucosae; however, this effect was resistant to ketanserin. Immunohistochemical staining by means of the peroxidase–antiperoxidase technique revealed 5-HT-like immunoreactive "mast cells" within the tunica muscularis mucosae. These cells appeared to be associated with the smooth muscle rather than the vasculature. It is concluded that (i) field-stimulated relaxation is not dependent on intramural nerves, and (ii) it is unlikely that the release of 5-HT from mast cells or other cells mediates field-stimulated relaxation. However, confirmation awaits the provision of an antagonist against the novel 5-HT receptor that mediates 5-HT-induced relaxations.

ISSN:0008-4212    

DOI:10.1139/y87-005

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

Arginine vasopresin is hypothesized to act as a neurotransmitter or neuromodulator in the ventral septal area of the rat brain. To examine this role of vasopressin further, it was applied by microiontophoresis or micropressure from multiple-barrelled micropipettes onto spontaneously active or glutamate-activated neurons. Applied in this manner, vasopressin reduced glutamate-evoked excitation in 32 of the 47 cells studied. Further, micropressure application of the vasopressin antagonist d(CH2)5Tyr(Me)AVP reversed the vasopressin effects. In contrast, administration of vasopressin had no effect on excitations evoked by acetylcholine iontophoresis or on the spontaneous activity of the majority of the ventral septal neurons studied. These observations suggest that vasopressin may be acting on aV1-like receptor on specific neurons in the ventral septal area as a modulator of glutamate actions. Evoked responses were also obtained in the same population of ventral septal cells following stimulation of a variety of limbic areas. Inhibitory input onto most of the vasopressin responsive neurons studied was obtained following electrical stimulation of the paraventricular nucleus and bed nucleus of the stria terminalis, two cell groupings that are potential sources of vasopressin to the ventral septal area. Thus, the similarity in action of exogenously applied vasopressin and the evoked responses following paraventricular nucleus and bed nucleus stimulation suggests that vasopressin may be a neurotransmitter in this pathway.

ISSN:0008-4212    

DOI:10.1139/y87-006

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

The effects of sodium pentobarbital were studied using intracellular recordings from CA1and CA3pyramidal cells in slices of guinea pig hippocampus. Drugs were applied either by perfusion or by pressure ejection at concentrations of 10−6, 10−5, and 10−4 M. Pentobarbital at all concentrations caused neuronal hyperpolarization, decreased spontaneous activity, and sometimes decreased input resistance. Hyperpolarization also occurred in zero calcium perfusate or with tetrodotoxin in the perfusate. The postspike train long-lasting afterhyperpolarization, which is an intrinsic calcium-mediated potassium conductance, was increased at all doses. γ-Aminobutyric acid induced depolarizing dendritic responses were augmented only at 10−4 Mpentobarbital. It is proposed that one of the important mechanisms of pentobarbital neuronal inhibition, particularly at lower doses, is an increase in potassium conductance.

ISSN:0008-4212    

DOI:10.1139/y87-007

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

We have reported previously that aminophylline has an ameliorating effect on the course and severity of glycerol-induced myoglobinuric acute renal failure in rats. Since aminophylline dissociates into theophylline in biological fluids and since theophylline is an adenosine receptor antagonist, we attributed the ameliorating effects to antagonism of the hemodynamic effects of endogenous adenosine. However, theophylline blocks tubuloglomerular feedback and produces natriuresis, and either of these effects might have accounted for the beneficial effects in acute renal failure. Therefore, this study was designed to further characterize the effects of theophylline in glycerol-induced acute renal failure in rats. Aminophylline had dose-dependent beneficial effects, as judged by the peak serum creatinine during the 3 days following induction of acute renal failure, by the number of animals with peak serum creatinine >1 mg/dL, and by the mortality rate. Both furosemide and theophylline block tubuloglomerular feedback and produce natriuresis, but aminophylline had protective effects, whereas furosemide actually increased mortality, compared with aminophylline, following induction of myoglobinuric acute renal failure. Therefore, aminophylline's protective effects are independent of tubuloglomerular feedback and natriuresis. These results offer further support for the hypothesis that adenosine-induced hemodynamic changes play a pathogenic role in glycerol-induced acute renal failure in rats.

ISSN:0008-4212    

DOI:10.1139/y87-008

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

The effects of an acute increase in preload, afterload, and inotropic state on several indices of left ventricular contractility were studied in 20 anesthetized intact dogs. The behaviour of the exponential rate of fiber shortening (ERFS), a newly described index, which is based on the instantaneous fiber length – time relationship through ejection, was compared with other classical ejection and isovolumic indices of left ventricular contractility. Acute volume overload by dextran 40 infusion produced a significant increase in preload as reflected by a 103% (p < 0.01) increase in left ventricular end-diastolic pressure and a 121% (p < 0.001) increase in end-diastolic circumferential wall stress. There was also a smaller but significant increase (p < 0.05) of heart rate (30%) and of peak systolic circumferential wall stress (24%). None of the left ventricular contractility indices showed any significant change. Acute pressure overload, produced mechanically by an aortic balloon, increased the afterload significantly as reflected by a 33% (p < 0.05) rise of end-systolic circumferential wall stress and a 43% (p < 0.001) increase in systemic resistance. Stroke volume decreased significantly by 23% (p < 0.05). All ejection indices, including ERFS, were significantly diminished by 30 – 37%; all isovolumic indices showed no significant changes. Positive inotropic intervention was induced by dopamine infusion, which caused a significant 28% (p < 0.05) increase in cardiac output. End-diastolic and end-systolic circumferential wall stress were significantly diminished. All indices of left ventricular contractility increased significantly and ERFS showed the quantitatively greatest change. This study suggests that ERFS is an ejection index of myocardial contractility, which is quite sensitive to inotropic intervention, independent of preload but sensitive to afterload.

ISSN:0008-4212    

DOI:10.1139/y87-009

出版商:NRC Research Press    

年代:1987

数据来源: NRC

摘要:

The purpose of this study was to compare the specific cortisol-binding protein found associated with human amnion with specific cortisol binding in human amniotic fluid and plasma. The electrophoretic mobility on polyacrylamide gels of the specific cortisol binding in amnion, amniotic fluid, and maternal plasma was identical. The influence of pH on cortisol binding activity was similar in all tissues and the cortisol binding was immunoprecipitable by a polyclonal antibody raised against human corticosteroid-binding globulin. The interaction of the cortisol binding protein with concanavalin A was studied in preterm amniotic fluid, term amniotic fluid, term amnion, and plasma from pregnant women at term and women under oral contraceptive treatment. Binding to concanavalin A was similar in term amnion and term amniotic fluid but was less than that found with both preterm amniotic fluid and term plasma. These results indicate that the cortisol binding portein associated with human amnion has similar characteristics to plasma corticosteroid-binding globulin, but that its state of glycosylation appears to be more like that of the cortisol binding protein in term amniotic fluid rather than in plasma.

ISSN:0008-4212    

DOI:10.1139/y87-010

出版商:NRC Research Press    

年代:1987

数据来源: NRC