Inspiratory flow-volume curve in snoring patients with and without obstructive sleep apnea

We analyzed the flow-volume curves of 50 patients with complaints of snoring and daytime sleepiness in treatment at the Pneumology Unit of the University Hospital of Brasília. The total group was divided into snorers without obstructive sleep apnea (OSA) (N = 19) and snorers with OSA (N = 31); the patients with OSA were subdivided into two groups according to the apnea/hypopnea index (AHI): AHI<20/h (N = 14) and AHI>20/h (N = 17). The control group (N = 10) consisted of nonsmoking subjects without complaints of snoring, daytime sleepiness or pulmonary diseases. The population studied (control and patients) consisted of males of similar age, height and body mass index (BMI); spirometric data were also similar in the four groups. There was no significative difference in the ratio of forced expiratory and inspiratory flows (FEF50%/FIF50%) in any group: control, 0.89; snorers, 1.11; snorers with OSA (AHI<20/h), 1.42, and snorers with OSA (AHI>20/h), 1.64. The FIF at 50% of vital capacity (FIF50%) of snoring patients with or without OSA was lower than the FIF50% of the control group (P<0.05): snorers 4.30 l/s; snorers with OSA (AHI<20/h) 3.69 l/s; snorers with OSA (AHI>20/h) 3.17 l/s and control group 5.48 l/s. The FIF50% of patients with severe OSA (AHI>20/h) was lower than the FIF50% of snorers without OSA (P<0.05): 3.17 l/s and 4.30 l/s, respectively. We conclude that 1) the FEF50%/FIF50% ratio is not useful for predicting OSA, and 2) FIF50% is decreased in snoring patients with and without OSA, suggesting that these patients have increased upper airway resistance (UAR).

Role of bradykinin in postprandial hypotension in humans

A transient significant decrease in mean arterial blood pressure (MAP) from 107 ± 3 to 98 ± 3 mmHg (P<0.05) was observed in elderly (59-69 years of age), healthy volunteers 25-30 min following ingestion of a test meal. In young volunteers (22-34 years of age), a postprandial decrease of MAP from 88 ± 3 to 83 ± 4 mmHg was also noted but it was not statistically significant. A 40% decrease in bradykinin (BK) content of circulatory high molecular weight kininogen had previously been observed in human subjects given the same test meal. We presently demonstrate by specific ELISA that the stable pentapeptide metabolite (1-5 BK) of BK increases from 2.5 ± 1.0 to 11.0 ± 2.5 pg/ml plasma (P<0.05) in elderly volunteers and from 2.0 ± 1.0 to 10.3 ± 3.2 pg/ml plasma (P<0.05) in young volunteers 3 h following food intake. This result suggests that ingestion of food stimulates BK release from kininogen in normal man. Postprandial splanchnic vasodilatation, demonstrated by a decrease of plasma half-life of intravenously administered indocyanine green (ICG), a marker of mesenteric blood flow to the liver, from 4.4 ± 0.4 to 3.0 ± 0.1 min (P<0.05) in young volunteers and from 5.2 ± 1.0 to 4.0 ± 0.5 min (P<0.05) in elderly volunteers, accompanied BK release. The participation of BK in this response was investigated in subjects given the BK-potentiating drug captopril prior to food intake. Postprandial decreases of ICG half-lives were not changed by this treatment in either young or elderly subjects, a result which may indicate that BK released following food intake plays no role in postprandial splanchnic vasodilatation in normal man.

Magnesium chloride alone or in combination with diazepam fails to prevent hippocampal damage following transient forebrain ischemia

In the central nervous system, magnesium ion (Mg2+) acts as an endogenous modulator of N-methyl-D-aspartate (NMDA)-coupled calcium channels, and may play a major role in the pathomechanisms of ischemic brain damage. In the present study, we investigated the effects of magnesium chloride (MgCl2, 2.5, 5.0 or 7.5 mmol/kg), either alone or in combination with diazepam (DZ), on ischemia-induced hippocampal cell death. Male Wistar rats (250-300 g) were subjected to transient forebrain ischemia for 15 min using the 4-vessel occlusion model. MgCl2 was applied systemically (sc) in single (1x, 2 h post-ischemia) or multiple doses (4x, 1, 2, 24 and 48 h post-ischemia). DZ was always given twice, at 1 and 2 h post-ischemia. Thus, ischemia-subjected rats were assigned to one of the following treatments: vehicle (0.1 ml/kg, N = 34), DZ (10 mg/kg, N = 24), MgCl2 (2.5 mmol/kg, N = 10), MgCl2 (5.0 mmol/kg, N = 17), MgCl2 (7.5 mmol/kg, N = 9) or MgCl2 (5 mmol/kg) + DZ (10 mg/kg, N = 14). Seven days after ischemia the brains were analyzed histologically. Fifteen minutes of ischemia caused massive pyramidal cell loss in the subiculum (90.3%) and CA1 (88.4%) sectors of the hippocampus (P<0.0001, vehicle vs sham). Compared to the vehicle-treated group, all pharmacological treatments failed to attenuate the ischemia-induced death of both subiculum (lesion: 86.7-93.4%) and CA1 (lesion: 85.5-91.2%) pyramidal cells (P>0.05). Both DZ alone and DZ + MgCl2 reduced rectal temperature significantly (P<0.05). No animal death was observed after drug treatment. These data indicate that exogenous magnesium, when administered systemically post-ischemia even in different multiple dose schedules, alone or with diazepam, is not useful against the histopathological effects of transient global cerebral ischemia in rats.