Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

E. coli endotoxin (0.03 mg/ml) added to blood perfusing a heart-lung preparation with a venous return of 600 ml/min produced a significant depression in ventricular function within 4 hours. Fragmented sarcoplasmic reticulum isolated from the myocardium of the endotoxin-perfused heart-lung preparations showed depressed calcium uptake rates and ATPase activity. When venous return was increased to 1,200 ml/min, gram-negative endotoxin had no effect on ventricular function, isolated fragmented sarcoplasmic reticulum calcium uptake, or ATPase activity. These observations suggest that gram-negative endotoxin or a product thereof acts in synergism with low venous return in order to depress myocardial function.
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PMID:The influence of venous return on cardiac mechanical and sarcoplasmic reticulum function during endotoxemia. 14 71

The regulatory mechanism in the aortic actomyosin system was studied. Superprecipitation of desensitized aortic myosin B was not exhibited even in the presence of Ca2+, but was observable only in the presence of native tropomyosin and Ca2+. Reconstituted actomyosin composed of pure aortic myosin and pure skeletal actin did not show superprecipitation. Addition of aortic native tropomyosin and Ca2+ caused a marked superprecipitation. The ATPase of reconstituted actomyosin was enhanced three- or fourfold by aortic native tropomyosin and Ca2+. The extent of superprecipitation of aortic myosin B did not show a biphasic type of response to Mg-ATP concentration. Thus, aortic native tropomyosin induces a real activation of the myosin, actin, and ATP system in the presence of Ca2+, in contrast with the case of skeletal native tropomyosin, which induces the depression of skeletal myosin-actin-ATP interaction in the absence of Ca2+.
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PMID:Regulatory mechanism in arterial smooth muscle contraction. 14 28

The influence of endotoxin shock and of experimentally increased venous return during endotoxin shock on myocardial vesicular calcium uptake and calcium stimulated ATPase activity was investigated. Vesicular calcium uptake was depressed (p less than 0.01) from 0.9 mumoles/mg protein/min to 0.3 mumoles/mg/min after 5 hr of endotoxin shock. Control ATPase did not differ between endocardial surface and epicardial surface. This was accompanied by a depressed (p less than 0.01) ATPase activity from 1.2 mumoles Pi/mg/min at the endocardial surface, and to 0.9 mumoles Pi/mg/min at the epicardial surface. A femoral arteriovenous shunt was used to increase venous return by 313 +/- 71 ml/min (approximately 17 ml/kg) during the shock period. Vesicles from AV shunted animals after endotoxin were capable of normal calcium uptake and normal ATPase activity. Results suggest that myocardial depression during endotoxin shock is more severe on the endocardial surface and is caused by depressed vesicular calcium uptake secondary to depressed ATPase activity. Furthermore, this depression may be avoided by maintenance of an adequate venous return.
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PMID:Influence of endotoxin on myocardial calcium transport and the effect of augmented venous return. 14 34

Myosin and subfragment-1 were prepared from rabbit hearts hypertrophied secondary to pulmonary artery constriction. The Ca2+ -stimulated ATPase activity was reduced while the potassium/EDTA-stimulated ATPase activity was unchanged in both the myosin and subfragment 1 (S-1) from hypertrophied hearts. When hypertrophy myosin was mixed with an equal quantity of control myosin, the ATPase activity of the mixed protein fell halfway between control and hypertrophy values. Similar results were obtained with control and hypertrophy S-1. The actin-stimulated ATPase activity of hypertrophy S-1 was slightly depressed but unlike hypertrophy myosin this depression was not significant when compared to normal S-1. This suggests that papain cleavage may have removed part of the conformational difference that exists between control and hypertrophy myosins.
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PMID:The ATPase activity of subfragment-1 from the hypertrophied heart. 14 12

The effect of halothane on maximal and submaximal Ca2+-activated tension in mechanically disrupted right ventricular papillary muscle from rabbits was studied. Steady-state isometric tension generation was measured in the muscle bundle. The relaxing solution contained (in mM) [Mg2+] = 1, [K+] = 70, [MgATP2-] = 2, [creatine phosphate2-] = 15, [EGTA total] = 7 and imidazole proprionate. The contracting solution contained in addition Ca2+ in various concentrations. In all solutions ionic strength was maintained at 0.15 and pH at 7.00 +/- 0.02 at 20 degrees C. Each fiber bundle was immersed in control solutions equilibrated with 100% N2 and test solutions equilibrated with various concentrations of halothane-N2 mixture. Increasing doses of halothane (1--4%) significantly shifted the relationship between Ca2+ and tension towards higher [Ca2+] and depressed the maximum Ca2+-activated tension. The maximum tension generated at pCa = 3.8 was depressed 5% per 1% increase in halothane concentration. The percentage of maximum tension at submaximum Ca2+ concentrations (pCa = 5.6--5.0) was not significantly decreased until halothane concentration was greater than 2%. It is concluded that halothane slightly but significantly depressed the interactions of contractile proteins and to a lesser degree Ca2+-activation of the regulatory proteins. The halothane-induced depression was completely reversible.
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PMID:Effects of halothane on Ca2+-activated tension development in mechanically disrupted rabbit myocardial fibers. 15 Dec 61

The effects of ether, chloroform, and halothane on calcium accumulation and ATPase activity of rat heart microsomes and mitochondria as well as on myofibrillar ATPase activity were investigated. Chloroform and halothane depressed microsomal and mitochondrial calcium uptake and binding in a parallel fashion. Ether decreased microsomal calcium binding and mitochondrial calcium uptake to varying degrees, while mitochondrial calcium binding was slightly enhanced. Whereas ether had no effect, chloroform depressed microsomal and mitochondrial total APTase activities and halothane decreased microsomsl ATPase and slightly stimulated mitochondrial total ATPase activities. Halothane was found to depress myofibrillar Mg2+-ATPase and ether was capable of decreasing myofibrillar Ca2+-ATPase. Chloroform was seen to inhibit both myofibrillar enzymes. These results suggest that the cardiodepressant actions of volatile anesthetic agents may be due to alterations in the calcium accumulating abilities of microsomal and mitochondrial membranes while direct myofibrillar effects may contribute to the depression seen with relatively higher concentrations of anesthetics.
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PMID:Subcellular effects of some anesthetic agents on rat myocardium. 15 65

1. The process of synaptic depression and recovery were studied in the squid (Loligo pealii) giant synapse with intracellular recording and stimulating electrodes in the prescence of tetrodotoxin (10-minus 7 M). 2. When the synapse was stimulated at 50 Hz, depression occurred rapidly. Recovery after the tetanus was a first-order process with an average recovery time constant of 4-9 sec. The rate of recovery was independent of the amplitude of the post-synaptic potential (p.s.p.) or the degree of depression. 3. For the first five to seven p.s.p.s in the train there was a linear relationship between depression and the total amount of transmitter previously released. This may indicate that depression in this preparation was caused by the depletion of the presynaptic store of transmitter (S). 4. Assuming that this interpretation was correct, we could show that recovery from depression during the tetanus (i.e. 'mobilization') proceeded about 10 times faster than after the end of the tetanus. 5. When the amplitude of the p.s.p. was varied by changing the bathing calcium concentration, [Ca], the degree of depression was correlated to the amplitude of the p.s.p. 6. When the amplitude of the p.s.p. was increased by increasing pre-synaptic depolarization, synaptic depression was found to increase as well. However, synaptic depression increased less than the amplitude of the p.s.p., the relationship between these two measures being non-linear. 7. This finding is interpreted to indicate that the transmitter stores, S, are closely related to the area of the presynaptic membrane which is sufficiently depolarized to release transmitter.
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PMID:Depression and recovery of transmission at the squid giant synapse. 16 84

Major inhalational anesthetics cause inhibition in the electron transport chain in the region of Complex I resulting in decreased oxygen utilization, inhibition of metabolism of NAD-linked substrates, but not of succinate, inhibition of mitochondrial calcium uptake, and depression of synaptic transmission because of postulated changes in ACh sensitivity or GABA inhibition. Many cellular metabolic effects in CNS and other tissues are secondary to the above. Many metabolic changes noted with anesthetics occur subsequent to activation of the sympathetic nervous system either directly by the anesthetic or by surgical stimulation in the presence of light anesthesia. Many important studies remain to be done.
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PMID:Effects of anesthesia on intermediary metabolism. 16 50

Dopamine, serotonin and related compounds (referred to collectively as biogenic amines) were found to modify transmission at the presumably cholinergic synapse made by an axon in the right visceropleural connective onto cell R15 of the abdominal ganglion of Aplysia californica. (1) With chronic application, dopamine hyperpolarizes R15, and serotonin depolarizes R15. Both actions upon the membrane potential desensitize in 10 min. All the actions described below were studied with chronic perfusion of the biogenic amines after desensitization of this postsynaptic action. (2) The biogenic amines drastically reduce the size of the EPSP evoked at the synapse under investigation; but they do not alter the ACh potential evoked in the soma of R15. (3) The biogenic amines reduce the amplitude of synaptic depression. The relationship between the effects of the amines on the size of an isolated EPSP and on synaptic depression differed from this relationship as affected by post-tetanic potentiation (PTP) or by changes in the Ca2+-Mg2+ balance. (4) The biogenic amines increase frequency facilitation, when the latter is defined as the ratio of the facilitated to the isolated EPSP. However, the absolute magnitude of the facilitated EPSP is always reduced at long times after introduction of the agent; shortly after introduction of the biogenic amines the absolute magnitude of the facilitated EPSP is unaffected in most preparations.
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PMID:Dopamine, serotonin and related compounds: presynaptic effects on synaptic depression, frequency facilitation, and post-tetanic potentiation at a synapse in Aplysia californica. 17 67

The monosynaptic and unitary excitatory postsynpatic potential (EPSP) observed in cell R15 of the abdominal ganglion of Aplysia californica upon minimal stimulation of the right visceropleural connective exhibits several presynaptic plasticities (synaptic depression, frequency facilitation, post-tetanic potentiation). We studiied effects of branchial nerve stimulation (heterosynaptic stimulation) on these plasticities of the homosynaptic (right connective) path. A burst of heterosynaptic stimulation (20 pulses at 4/sec) decreased the amplitude of an isolated homosynaptic EPSP. The rate of recovery from heterosynaptic inhibition (HSI) was a function of the rate of stimulation of the homosynaptic path so that at a stimulus frequency of 1 pulse/sec to the right connective (RC) the HSI lasted less than 20 sec while at a RC stimulus frequency of 1/10 sec the HSI persisted for more than 60 sec. While the frequency facilitated EPSP (during homosynaptic stimulation at 1/sec) was only transiently affected by heterosynaptic stimulation the effect on the subsequent post-tetanic potentiation was much more pronounced and longer lasting (more than 30 min). This suggests a specific effect of HSI on the rate constant of decay of elevated fractional release, as observed upon bath applications of biogenic amines. Heterosynaptic stimulation also reduces synaptic depression but the reduction in the depression is more than would be caused by comparable reduction of the first EPSP of a pair of high Mg2+, low Ca2+ or the addition of carbachol to the perfusion medium. The duration of the effect on synaptic depression was the same as the effect on EPSP1.
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PMID:Heterosynaptic inhibition modifies the presynaptic plasticities of the transmission process at the synapse in Aplysia californica. 17 68


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