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Biomedical subjects

A Haji

Publications and source records attributed to A Haji.

49 records · Page 3Linked to original sources
PubMed1990

Effects of glycine and GABA on bulbar respiratory neurons of cat.

1. Bulbar respiratory neurons of unanesthetized, decerebrate cats were impaled with the center pipette of a compound, coaxial microelectrode. This electrode allowed intracellular recording of membrane potential (MP) through the central pipette and extracellular iontophoresis of glycine or gamma-aminobutyric acid (GABA) from micropipettes encircling the center pipette with their tips recessed 20-40 microns from the tip of the center pipette. 2. Seventy-seven studies were carried out on 32 inspiratory and 28 postinspiratory neurons with the use of brief pulses (0.3-0.5 s) or long pulses (3-10 s) spanning one or more respiratory cycles. In both neuronal types, GABA and glycine decreased spike frequency, synaptic "noise," respiratory fluctuations of MP, and "input" resistance in a dose-related fashion. 3. In most cases, the membrane was hyperpolarized by the amino acid. The reverse response (depolarization) was observed when the membrane had been hyperpolarized by current clamp. This reversal from hyperpolarization to depolarization occurred at a MP of -81 +/- 2.3 mV (mean +/- SE, n = 7) for glycine and -81 +/- 1.6 (n = 6) for GABA. 4. After intracellular iontophoresis of chloride ions, application of GABA and glycine depolarized the membrane. 5. During relatively long (3-10 s) periods of iontophoresis of glycine or GABA, the effects on MP and input resistance waned. In some cases (23%), the amino acid depolarized the membrane at the most hyperpolarizated portion of the MP trajectory. This was never observed with brief iontophoretic pulses. Such effects of long duration iontophoresis may reflect changes in membrane properties secondary to the primary action of the amino acid on the membrane of the impaled neuron or indirect synaptic actions via changes in discharge of neighboring neurons. 6. Extracellular iontophoresis of a GABA uptake inhibitor, nipecotic acid, potentiated the effects of GABA. 7. Extracellular application of tetrodotoxin appeared to act pre- and postsynaptically to reduce respiratory fluctuations in membrane potential and to increase input resistance without altering the effects of iontophoresed glycine and GABA, suggesting that the amino acids act on postsynaptic membrane receptors not linked to fast sodium channels.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1989

Microiontophoresis of flurazepam on inspiratory and postinspiratory neurons in the ventrolateral medulla of cats: an intracellular study in vivo.

Effects of flurazepam on the periodic inhibitory postsynaptic potentials (IPSPs) and on the action of locally applied gamma-aminobutyric acid (GABA) were studied in bulbar respiratory neurons of decerebrate cats using concentric multibarrelled electrodes for intracellular recording and extracellular iontophoresis. Iontophoresis of flurazepam augmented spontaneous IPSPs and increased the hyperpolarization induced by GABA. Iontophoretic application of bicuculline suppressed the action of flurazepam. The reversal potential for spontaneous IPSPs was similar to that for the GABA-response. Intracellular Cl- injection shifted both the IPSP wave and the GABA response in a depolarizing direction. Flurazepam enhanced these depolarizing responses. These results suggest that GABA mediates the postsynaptic inhibition in bulbar respiratory neurons.

Animals↗
PubMed1989

Diazepam potentiates postsynaptic inhibition in bulbar respiratory neurons of cats.

The purpose of this study was to assess the effect of benzodiazepine on inhibitory postsynaptic potentials (IPSPs) of medullary respiratory neurons in decerebrate, paralyzed cats. Diazepam (0.05 and 0.1 mg/kg i.v.) reversibly increased the IPSP waves occurring during the inactive phase of the respiratory cycle in all inspiratory and postinspiratory neurons examined. Input resistances of these neurons were reduced at that phase. The reversal potential for the IPSP wave was unaltered. Intracellular injection of chloride ions reversed the IPSP to depolarization, and diazepam produced a purely depolarizing effect. The drug effects observed during the active phase of each neuron include a decrease in the firing rate and a shortening of the burst activity. The firing threshold and shape of these spikes, however, remained unaltered. These results suggest that diazepam depresses the bulbar respiratory neuronal activities specifically by potentiating the periodic postsynaptic inhibition.

Animals↗
PubMed1989

The influence of halothane and thiopental on respiratory-related nerve activities in decerebrate cats.

The effects of halothane and thiopental on the respiratory efferent activities in the phrenic, recurrent laryngeal and hypoglossal nerves were studied in decerebrate, paralyzed and artificially ventilated cats. Inhalation of halothane (2%, 90 s) and intravenous injection of thiopental (2-3 mg/kg) produced a similar change in the breathing pattern, characterized by an increase in respiratory frequency and a decrease in the respiratory burst discharge in the three nerves studied. Depression of the respiratory activity was greatest in the hypoglossal nerve, intermediate in the recurrent laryngeal nerve, and least in the phrenic nerve. Both drugs diminished the whole power spectral densities of the three nerves. Thiopental selectively attenuated the high frequency peaks of these spectra and shifted the peak frequencies to lower values. Bilateral section of the vagus and carotid sinus nerves had no effect on the action of thiopental on the respiratory neural activities, whereas it decreased, but did not eliminate, the action of halothane. The present results demonstrate that both halothane and thiopental produce a selective depression of the upper airway motor activities, with stronger effects on the hypoglossal nerve. Effects on the peripheral receptors and the central respiratory drives differ between the two drugs.

Administration, Inhalation↗
PubMed1989

Rapid shallow breathing caused by pulmonary vascular congestion in cats.

The vasculature of one lung of unanesthetized spontaneously breathing decerebrate cats was isolated and congested with blood. Such pulmonary vascular congestion (PVC) consistently resulted in a shallow tachypnea associated with expiratory activation of the diaphragm and thyroarytenoid muscles, signifying augmented expiratory braking. With progressive increases in pulmonary vascular pressure, tachypnea and expiratory braking increased progressively and ultimately obscured phasic activity in the diaphragm and thyroarytenoid. Thus the apnea caused by PVC constitutes not an arrest of neural respiratory activity but rather a continuous activation of thoracic inspiratory and laryngeal adductor muscles. When capsaicin, a neurotoxin that activates nonmyelinated afferents, was injected into the pulmonary artery of the isolated lung, it produced changes in timing and distribution of respiratory motor output that resembled those with PVC but were more abrupt in onset. Capsaicin, applied perineurally to the cervical vagi, preferentially blocked the conduction of nonmyelinated afferent fibers. This procedure, which produced little degradation in Hering-Breuer reflexes, eliminated tachypnea and expiratory braking caused by PVC or capsaicin injection. The results indicate that activation of pulmonary vagal afferent fibers of C or A-delta category in unanesthetized cats reflexly modifies the respiratory motor output in a way that resembles the human response to PVC or pulmonary embolism. This is a brain stem reflex.

Animals↗
PubMed1988

Electrophysiological properties of respiratory laryngeal motoneurons and effects of thiopental.

Transmembrane potentials of the respiratory laryngeal motoneurons were recorded in decerebrate, vagotomized and paralyzed cats. Twenty inspiratory and thirteen postinspiratory neurons were identified. Periodic membrane potential (MP) fluctuations as well as patterns of postsynaptic potentials (PSPs) were characterized in each type of neurons by measuring the input resistance and injecting Cl- to reverse inhibitory PSPs. On the basis of PSP patterns, two subtypes of inspiratory neurons could be distinguished. Thiopental (2-3 mg/kg, i.v.) produced depolarization together with reduction of firing in most laryngeal neurons. Excitatory and inhibitory PSPs were both depressed and MP fluctuations became smaller in each phase of the respiratory cycle. Elevation of the firing threshold and separation of IS-SD spikes often occurred after thiopental. These results suggest that thiopental depresses the laryngeal motoneuron through inhibition of synaptic transmission and of spike generation.

Animals↗
PubMed1987

Effects of acetaldehyde on the monosynaptic reflex pathway in the cat spinal cord.

The effects of acetaldehyde on monosynaptic reflexes were investigated in the cat spinal cord. Intravenous injection of lower doses of acetaldehyde (0.1-0.5 mg/kg) increased the amplitude of the ventral root monosynaptic reflex potentials elicited by the dorsal root stimulation; the amplitude was decreased at higher doses (1.0-10.0 mg/kg). Acetaldehyde hyperpolarized the motoneuron at lower and depolarized it at higher doses. In some cells, however, acetaldehyde induced an initial, brief depolarization and subsequent hyperpolarization. Depolarization increased with increasing the dose of acetaldehyde. Hyperpolarization was always associated with an increased amplitude of the monosynaptically-induced action potentials. Depolarization was accompanied by a decreased amplitude or block of the action potentials. During aldehyde-induced depolarization, antidromic action potentials were more severely depressed than orthodromic ones. The present results suggest that acetaldehyde acts predominantly on the motoneuron membrane resulting in hyperpolarization at relatively lower doses and in depolarization at higher doses.

Acetaldehyde↗
PubMed1986

[Antitumor effects of a podophyllotoxin derivative, VP 16-213].

Single and combination chemotherapies of VP 16-213, a new antitumor agent were evaluated for its antitumor effect against several murine tumors. Dose-dependent antitumor effects were observed when VP 16-213 was administered via any of the three routes, i.p., i.v. and orally, on days 1 and 5 after i.p. or s.c. inoculation of Ehrlich carcinoma and sarcoma 180. The drug also proved effective against i.v. inoculated EL-LP-12 (subline of Ehrlich carcinoma), i.p. or s.c. inoculated P388 and B16 melanoma, i.p. inoculated colon 26, and s.c. inoculated colon 38 and Lewis lung carcinoma. However, oral administration of the drug was not effective against B16 melanoma, colon 26 and Lewis lung carcinoma despite the fact that the doses employed for this route was higher than those employed for i.v. and i.p. routes. The optimum dosing schedule was also investigated with oral administration of the drug against s.c. inoculated Ehrlich carcinoma. A single dose (day 1) or two doses (days 1 and 5) were more effective than three doses (days 1, 3 and 5) or five consecutive daily doses. VP 16-213 showed additive and more than additive effects in combination with the antitumor agents, cyclophosphamide, BCNU, mitomycin C or cisplatin against s.c. inoculated Ehrlich carcinoma and i.v. inoculated EL-LP-12.

Administration, Oral↗
PubMed1986

[General pharmacological studies of VP 16-213. Effect on the peripheral system].

The general pharmacological studies of VP 16-213, an antitumor agent, in the peripheral system were carried out by oral and i.v. administration with laboratory animals. VP 16-213 had no effect on the resting tone and spontaneous motility of all the isolated smooth muscle organs tested at concentrations of up to 10(-5) g/ml. VP 16-213 showed no significant influences on the neuromuscular transmission in the sciatic nerve-tibial muscle preparation of rabbits, on renal function in dogs and rats, on blood sugar level in rabbits, and on charcoal meal transport in mice. At a dose of 20 mg/kg, i.v., VP 16-213 reduced gastric secretion in rats. Antiinflammatory, local irritation and hemolytic effects were not observed after the administration of the drug. Single administration of VP 16-213 had orally no effect on the excretion of serum BSP in rats. However, successive administration of the drug (20 mg/kg/day) once daily for 10 days significantly depressed it. VP 16-213 decreased the number of hemolytic plaque forming cells in the spleens of immunized mice.

Animals↗
PubMed1985

Dual effects of acetaldehyde on electrical activity in the isolated frog spinal cord.

Acetaldehyde (1.4 X 10(-7)-1.4 X 10(-5) M) produced a transient depolarization followed by a distinct hyperpolarization of the ventral and dorsal roots as recorded by sucrose-gap in the isolated spinal cord. This effect occurred more frequently at lower concentrations than at higher concentrations of acetaldehyde, and the depolarization increased with doses increasing. The ventral root reflex potentials evoked by the dorsal root stimulation had decreased amplitudes during depolarization and increased during hyperpolarization. In the presence of Mg2+ or tetrodotoxin, acetaldehyde produced only hyperpolarization. Acetaldehyde slightly prolonged glutamate-induced depolarization of both roots. These results suggest that acetaldehyde acts not only on the spinal motoneuron resulting in membrane hyperpolarization but also on the presynaptic sites, which causes postsynaptic membrane depolarization probably through an increased release and decreased uptake or inactivation of the excitatory transmitter.

Acetaldehyde↗
PubMed1983

Electrical activities of the frog spinal cord are resistant to perfusion with hypoxic medium.

Synaptic functions of the isolated and intra-arterially perfused frog spinal cord were investigated in terms of dorsal root-dorsal root potential (DR-DRP) and dorsal root-ventral root reflexes (DR-VRR), and under the influences of hypoxic Ringer solution, replacement of medium glucose with 2-deoxyglucose ('hypoglycemic Ringer'), and suspension of perfusion. The synaptic functions were markedly degraded during the suspension of perfusion, but they were remarkably resistant to hypoxic or hypoglycemic Ringer for more than 6 h, if the preparation was continuously perfused. The presynaptic inhibition of the first spike potential of the DR-VRR induced by a conditioning antidromic stimulation, however, was markedly reduced during prolonged exposure to hypoxic conditions. In contrast to earlier concepts that the spinal cord is vulnerable to hypoxia, the present results demonstrate that the frog spinal cord is resistant to prolonged perfusion with hypoxic and hypoglycemic media, although they suggest a latent deterioration of some processes which are believed to be more energy dependent.

Animals↗