T. Kuriyama

Effects of acetazolamide in patients with the sleep apnoea syndrome.

There is as yet no convincing evidence that acetazolamide, a carbonic anhydrase inhibitor, is effective in obstructive sleep apnoea. A study was therefore designed to examine the effect of acetazolamide (250 mg/day) on sleep events and ventilatory control during wakefulness in nine patients with the sleep apnoea syndrome. In eight of the nine patients the apnoea index and the total duration of apnoea were reduced by acetazolamide, and the mean (SEM) apnoea index of all patients changed from 25.0 (6.7) to 18.1 (5.8) episodes an hour. Furthermore, the total time of arterial oxygen desaturation (SaO2)--more than 4% depression in SaO2 from the baseline sleeping level--divided by total sleep time was also significantly decreased and its mean (SEM) value improved from 24.1 (7.9) to 13.6 (4.8)% of total sleep time. Five of the seven patients with varying degrees of daytime hypersomnolence had their symptoms obviously improved. There was no patient whose predominant type of apnoea was converted from the obstructive to the central type, or vice versa. In the studies of wakefulness, metabolic acidosis, an increase of arterial oxygen tension (PaO2) and a decrease of arterial carbon dioxide tension (PaCO2) were observed. The slopes of the occlusion pressure response and the ventilatory response to carbon dioxide increased, and the carbon dioxide ventilatory response line shifted to the left. It is suggested that acetazolamide cannot remove apnoea completely but has a beneficial effect in mild cases of obstructive sleep apnoea through an augmentation of central (CO2, H+) drive and a stabilising effect on ventilatory control.

Controlling malignant pericardial effusion by intrapericardial carboplatin administration in patients with primary non-small-cell lung cancer

Malignant pericarditis, when associated with massive pericardial effusion, presents a critical condition in lung cancer patients. Because this condition often arises in terminally ill patients, intensive therapy such as multi-drug combination chemotherapy is rarely appropriate. This study evaluated the clinical relevance of intrapericardial administration of carboplatin for controlling malignant pericardial effusions associated with non-small-cell lung carcinoma (NSCLC). The method used for 10 eligible patients consisted of draining the pericardial effusion and infusing 300 mg/body of carboplatin in 50 ml of saline through an in-place catheter into the pericardial space and clamping the catheter for 40 min. Nine of the 10 patients showed satisfactory results, and 8 experienced complete regression of the effusion. No major or minor adverse effects were observed. Pharmacokinetics analysis revealed that the concentration of free platinum in the pericardial fluid was very high while that of total platinum in the circulating plasma was very low, assuring the usefulness of the intrapericardial instillation of carboplatin in terminally ill patients for controlling malignant pericardial effusion when the systemic delivery of cytotoxic agents is inappropriate.

Stable pulmonary capillary haemangiomatosis without symptomatic pulmonary hypertension

Pulmonary capillary haemangiomatosis is a rare disorder characterised by multiple angiomatous lesions composed of proliferating capillary vessels in the lung parenchyma that usually progress rapidly to establish fatal pulmonary hypertension. The 29 year old man presented here, however, has been stable for 3.5 years since the diagnosis without symptoms of pulmonary hypertension. High resolution computed tomographic findings of the pulmonary lesions seemed specific to the disease.

Individual differences in ventilatory and HR responses to progressive hypoxia following 100% O2 exposure in humans.

Ventilatory response to sustained hypoxia is known to exhibit a biphasic profile: an initial rapid augmentation followed by a gradual decline. The former is induced by an excitation of the peripheral chemoreceptor. Interestingly, regarding the latter secondary depression (defined as hypoxic ventilatory depression, HVD), it has been suggested by several investigators that its magnitude is in some way also determined by a centrally mediated discharge from the peripheral chemoreceptor (4).

Augmented ventilatory response to sustained normocapnic hypoxia following 100% O2 breathing in humans.

The presence of hyperoxic hyperventilation seems to have been well confirmed in humans by Becker et al (1995) when the PETco2 is maintained at a normocapnic level. They also observed that augmented ventilation at higher than the control level still continued even 15 min after termination of hyperoxia, suggesting that a humoral agent might be involved to stimulate ventilation.

Possible presence of hypoxic ventilatory depression while breathing ambient air at sea level in humans

Abstract The ventilatory response to progressive isocapnic hypoxia (HVR) was examined in 14 healthy subjects, following 10 min hyperoxic or control normoxic exposure (defined +O 2 and −O 2 runs, respectively). During HVR test, it was tried to keep end-tidal P CO 2 constant at the level of room air breathing in both +O 2 (39.1±4.2 mmHg) and −O 2 (39.2±4.8 mmHg) runs. Six of the 14 subjects had a consistent and definitely higher slope of HVR (VE/Sa O 2 ) in +O 2 runs than −O 2 runs (−0.45±0.07 vs. −0.19±0.04 l/min per %Sa O 2 , P 2 exposure and were defined the negative responders. It was also noted that the slope of HVR in the positive responders while breathing ambient air (0.19±0.04 l/min per %Sa O 2 ) was significantly lower than the negative responders (0.36±0.07 l/min per %Sa O 2 ) ( P

Effect of Prior O2 Breathing on Hypoxic Hypercapnic Ventilatory Responses in Humans

In the previous communication(11), we reported that prior O2 breathing lasted for 10 min effectively augmented the subsequent ventilatory level in isocapnic sustained hypoxia. In addition, we found that involvement of a humoral agent, excitatory amino acid glutamate, may be responsible for inducing this phenomenon.