aminophylline/hypoxia

OBJECTIVE To investigate the effect of Shen-Mai injection (SMI) and aminophylline on diaphragmatic muscle cell apoptosis and the Fas/FasL expression in chronic hypoxic rats. METHODS Seventy-five male Wistar rats were randomly divided into three equal groups, control group (A group), SMI group (B

Peripheral chemoreceptors may be immature in neonatal animals, exhibiting maturational changes in the perinatal period. Even though methylxanthines are respiratory stimulants, many premature neonates do not respond to them. Thus, we hypothesized that carotid body activity is necessary for

To clarify the mechanism of action of aminophylline on the hypoxic ventilatory response in humans, we analyzed the effects of aminophylline on respiratory neural output. To evaluate the respiratory neural output, we analyzed the electromyogram (EMG) of the parasternal intercostal muscle, one of the

Male Hooded Wistar rats were exposed to three five-minute periods of hypoxia in which they breathed a gas mixture comprising 7% O2 and 93% N2. Before the second and third hypoxic exposures rats were injected (i.m.) with aminophylline (an adenosine antagonist) at a dose of 15 mg.kg-1. In control

In newborns and adults of a number of species, exposure to acute hypoxemia produces a "regulated" decrease in core temperature, the mechanism of which is unknown. The present experiments were carried out on chronically instrumented newborn (5-10 days of age; n = 27) and older (25-30 days of age; n =

In 10 normal young adults, ventilation was evaluated with and without pretreatment with aminophylline, an adenosine blocker, while they breathed pure O2 1) after breathing room air and 2) after 25 min of isocapnic hypoxia (arterial O2 saturation 80%). With and without aminophylline, 5 min of

1. In previous studies adenosine has been postulated to be the mediator in coronary blood flow regulation and aminophylline was found to inhibit the coronary vasodilator action of adenosine. The present study was performed to determine whether aminophylline inhibits coronary vasodilatation induced

In humans and cats, the ventilatory response to 30 min of moderate hypoxia is biphasic, an initial increase being followed by a decrease in ventilation to levels that are often less than halfway between the initial response and the air-breathing control level. The decrease, or hypoxic depression, is

We designed experiments to evaluate changes in ventral medullary (VM) extracellular fluid (ECF) PCO2 and pH during hypoxemia-induced ventilatory depression (VD). Our aim was to investigate effects of aminophylline on VD and VM ECF acid-base variables. We used aminophylline because it inhibits

In hypoxia, endurance exercise performance is diminished; pharmacotherapy may abrogate this performance deficit. Based on positive outcomes in preclinical trials, we hypothesized that oral administration of methazolamide, a carbonic anhydrase inhibitor, aminophylline, a nonselective adenosine

During sustained hypoxia the decline in ventilation that occurs in normal adult humans may be related to central accumulation of a neurochemical with net inhibitory effect. Recent investigations have shown that the putative neurotransmitter adenosine can effect a prolonged respiratory inhibition.

We hypothesized that concomitant pharmacological inhibition of the endothelin and adenosine pathway is safe and improves exercise performance in hypoxic humans, via a mechanism that does not involve augmentation of blood oxygenation. To test this hypothesis, we established safety and drug

OBJECTIVE To investigate the anti-hypoxia and anti-oxidation effects of aminophylline on human with acute high-altitude exposure. METHODS Totally 100 young male army members newly recruited from Sichuan province (400 meters above sea level) were enrolled. They were randomly divided into two groups:

The progression of pulmonary hypertension secondary to chronic airflow obstruction is thought to be related to the degree of nocturnal oxygen desaturation. We have studied 11 patients with severe smoking-related hypoxic chronic airflow obstruction (mean FEV1 0.67 L, mean arterial PO2 6.83 kPa) who

A 17-year old boy presented with severe, predominantly central sleep apnoeas secondary to structural damage in the medulla. At low O2 saturation, the electroencephalogram showed the sudden onset of slow waves. Hypercapnic ventilatory response was low and hypoxic ventilatory response was absent. Low