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At least 685 records · Page 38Linked to original sources
PubMed1995

Nitric oxide is used as an orthograde cotransmitter at identified histaminergic synapses.

1. Nitric oxide (NO) is produced by the enzyme nitric oxide synthase (NOS) and serves as an interneuronal messenger. Here, an identified histaminergic neuron (C2) in the mollusk Aplysia californica is shown to contain NOS with the use of NADPH diaphorase staining, suggesting that NO and histamine are used as cotransmitters by neuron C2. 2. The NOS containing neuron, C2, evokes a very slow excitatory postsynaptic potential in two of its identified postsynaptic follower neurons that are insensitive to H1 and H2 histamine receptor antagonists. 3. The very slow excitatory postsynaptic potential is blocked by inhibitors of NOS, such as nitroarginine methyl ester, and suppressed by the NO scavenger reduced hemoglobin. 4. Treatments with compounds that release NO, such as nitrosocysteine, mimic the membrane depolarization and the decrease in membrane conductance in the follower that are characteristic of the very slow excitatory postsynaptic potential induced normally by the presynaptic C2 neuron. 5. These results indicate that NO is used as an orthograde synaptic cotransmitter at synapses between histaminergic neuron C2 and its followers that receive the very slow excitatory postsynaptic potential.

Animals↗
PubMed1997

Blood gas transport at high altitude.

As a model of human hypoxia, exposure to high altitude causes a number of ventilatory, circulatory and hemopoietic adaptations. A review of the literature on blood gas transport responses to hypoxia indicates that they are influenced not only by altitude, but also by factors related to acclimatization. In addition, it appears that the need to oxygenate tissues conflicts with the need to maintain H+ homeostasis. Thus, the final situation represents a compromise between the respiratory adjustment aimed at increasing blood alkalosis in order to optimize the oxygen transport system, and the metabolic readjustment aimed at reestablishing normal blood pH. There are factors like red cell 2,3-diphosphoglycerate, a compound that decreases the hemoglobin affinity for oxygen, that can influence that balance by affecting arterial oxygen saturation through mechanisms independent of respiration.

2,3-Diphosphoglycerate↗
PubMed1985

Efficacy of iron therapy: a comparative evaluation of four iron preparations administered to anaemic pregnant women.

The authors conducted a clinical investigation on sixty-nine pregnant women, anaemic and non-anaemic, the purpose being to assess the effect of 50 days treatment with four different medicinal iron preparations, namely, ferrous sulphate, iron chondroitinsulfuric acid complex, and ferritin alone or associated with folinic acid and cobamamide, on various haematological parameters (Hb, RCC, Ht, CV, Iron, and Transferrin IBC). The four products demonstrated a similar efficacy in maintaining anaemic conditions under control; moreover, the results confirmed our hypothesis of the absorption of iron ferritin. While three products were well tolerated, ferrous sulphate induced, in some cases, side-effects.

Adult↗
PubMed1988

Chemical modifiers of cancer treatment.

Chemical modification is a concept in cancer therapy in which the state of tumor cells or normal tissues is modified such that a therapeutic gain can be achieved using conventional therapeutic modalities. Hypoxic zones targeted as cells within them may be radiation resistant, poorly perfused by chemotherapeutic agents, and possibly drug resistant due to hypoxia-related gene amplification. Nitroimidazoles have gained particular attention as chemical modifiers because they can increase the radiation sensitivity of hypoxic cells, are cytotoxic to hypoxic cells, can increase sensitivity to chemotherapeutic agents, and are useful for imaging hypoxic cells. While both radiosensitization and chemosensitization require hypoxia, the mechanism of the enhancement of each of the modalities is different. The 2-nitroimidazole hypoxic sensitizers SR 2508 and Ro-03-8799, which are less toxic than the prototype misonidazole (Miso), are in clinical trials, and dual function molecules that include a hypoxic sensitizer and alkylating function are being developed. The presence of both acutely and chronically hypoxic cells in animal tumors has been demonstrated by new imaging techniques. Oxygen delivery to tumors is being altered by the use of perfluorocarbons, and agents that alter hemoglobin affinity for oxygen. Compounds that are selectively toxic to hypoxic cells are being developed. Nonhypoxic modifiers are also being investigated. Thiol modification, particularly the alteration of glutathione concentration, has complex effects on the cell's biochemistry, in addition to affecting the competition between oxygen and thiol groups for the restoration and fixation of radiation-induced radicals. WR-2721 is being studied as a means of reducing the normal tissue toxicity of radiation and chemotherapy. Increased thiol concentration may be a mechanism of cross-resistance between certain chemotherapeutic agents and radiation.

Antineoplastic Agents↗
PubMed2006

Cocaine increases the intracellular calcium concentration in brain independently of its cerebrovascular effects.

Cocaine abuse increases the risk of life-threatening neurological complications such as strokes and seizures. Although the vasoconstricting properties of cocaine underlie its cerebrovascular effects, the mechanisms underlying its neurotoxicity remain incompletely understood. Here, we use optical techniques to measure cerebral blood volume, hemoglobin oxygenation (S(t)O(2)), and intracellular calcium ([Ca(2+)](i)) to test the hypothesis that cocaine increases [Ca(2+)](i) in the brain. The effects of cocaine were compared with those of methylphenidate, which has similar catecholaminergic effects as cocaine (except for serotonin increases) but no local anesthetic properties, and of lidocaine, which has similar local anesthetic effects as cocaine but is devoid of catecholaminergic actions. To control for the hemodynamic effects of cocaine, we assessed the effects of cocaine in animals in which normal blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of transient hypotension (mimicking that induced by cocaine). We show that cocaine induced significant increases ( approximately 10-15%) in [Ca(2+)](i) that were independent of its hemodynamic effects and of the anesthetic used (isofluorance or alpha-chloralose). Lidocaine but not methylphenidate also induced significant [Ca(2+)](i) increases ( approximately 10-13%). This indicates that cocaine at a dose within the range used by drug users significantly increases the [Ca(2+)](i) in the brain and its local anesthetic, but neither its catecholaminergic nor its hemodynamic actions, underlies this effect. Cocaine-induced [Ca(2+)](i) increases are likely to accentuate the neurotoxic effects from cocaine-induced vasoconstriction and to facilitate the occurrence of seizures from the catecholaminergic effects of cocaine. These findings support the use of calcium channel blockers as a strategy to minimize the neurotoxic effects of cocaine.

Anesthetics, Local↗