Spectral analysis of heart rate variability provides a probe to assess the function of the sympathetic and parasympathetic nervous systems. Time-frequency analysis of heart rate variability is useful for investigating autonomic nervous function in patients with syncope or non-sustained ventricular tachycardia, or in anaesthesia, etc. In this paper, we developed an algorithm for continuous and online analysis of heart rate variability. The algorithm was simulated and evaluated in MATLAB, and implemented on the digital signal processor. The electrocardiogram signals from MIT/BIH arrhythmia database and one patient with syncope demonstrate the capability of the proposed method in the continuous and online analysis of heart rate variability.

Algorithms↗

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Effect of pulmonary edema on tracheal diameter.

BACKGROUND: Though it is well known that cardiogenic and noncardiogenic pulmonary edema can cause changes in lung mechanics, actual alterations in tracheal diameter have not been described. OBJECTIVE: To evaluate the effects of pulmonary edema induced by increased left atrial pressure (cardiogenic) and Perilla ketone (PK; noncardiogenic) on tracheal diameter in chronically instrumented awake sheep. METHODS: We investigated the effects of two mechanistically distinct types of pulmonary edema on tracheal diameter in chronically instrumented awake sheep. Cardiogenic pulmonary edema (analogous to congestive heart failure in humans) was induced by increasing left atrial pressure ( upward arrowP(LA)) by inflating the balloon on a Foley catheter positioned in the mitral valve annulus to cause partial obstruction to flow across the valve (n = 18). Noncardiogenic pulmonary edema (increased pulmonary microvascular permeability pulmonary edema analogous to the acute respiratory distress syndrome in humans) was produced by the intravenous administration of PK (n = 11). Lateral chest radiographs (CXRs) were scored by a standardized 5-point scoring system for the severity of pulmonary edema, and tracheal diameter was measured at a fixed location in the carina. Three radiologists, blinded to sheep identification number and experimental protocol, evaluated the radiographs independently at different points in time for edema severity and tracheal diameter. The sheep were sacrificed immediately after the final CXR, and wet/dry lung weight ratio (W/D ratio) was determined. RESULTS: Both upward arrowP(LA) and PK were associated with statistically significant tracheal narrowing ( upward arrowP(LA): 20.3 +/- 0.6 to 15.1 +/- 0.9 mm; PK: 20.2 +/- 0.6 to 14.1 +/- 1.4 mm). Tracheal narrowing correlated with the severity of the pulmonary edema determined radiographically ( upward arrowP(LA): r = -0.69, p < 0.01; PK: r = -0.62, p < 0.01) and by W/D ratio ( upward arrowP(LA): r = -0.64, p < 0.05; PK: r = -0.54, p < 0. 05). CONCLUSIONS: We conclude that tracheal narrowing occurs in sheep models of both cardiogenic and noncardiogenic pulmonary edema and that the degree of narrowing correlates with the severity of the edema.

Animals↗

PubMedDate not supplied

Nifedipine retard in the treatment of hypertension. A study using ambulatory blood pressure recordings.

The subjects were 24 patients, aged 37 to 66 years, with mild to moderate hypertension, treated with nifedipine retard (mean dose, 47 mg daily) for 7 to 16 weeks. The mean 24-hour ambulatory blood pressure (BP) declined significantly from 158/101 before treatment to 136/87 mmHg after treatment. Daytime BP declined from 160/101 to 133/86 mmHg and nighttime BP from 152/98 to 132/85 mmHg; the diurnal variation in diastolic BP was lost during treatment with nifedipine. The consecutive hourly BPs were all significantly lower after treatment. BPs in response to physiologic tests were significantly reduced after treatment. Heart rate increased significantly during treatment. Side effects (palpitations, pedal edema, and flushing of the face) were reported by four patients. It is concluded that nifedipine retard is safe and effective in the treatment of mild to moderate hypertension.

Adult↗

PubMedDate not supplied

Monoclonal antibodies that recognize specific antigens of Mycoplasma gallisepticum and M. synoviae.

The polypeptide profiles of the type strains of Mycoplasma gallisepticum (PG 31) and M. synoviae (WVU 1853) resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis were compared. Except for a few discrete peptides that were similar, the species varied considerably in peptide profiles. Congruence was observed between the type strains of each species and homologous cloned serotypes. Protein blots of each species were probed with 2 mouse monoclonal antibodies. Monoclonal antibody G 46 was specific for the antigen p 110 (G) in M. gallisepticum, and S 221 was specific for an antigen complex p 45-50 (S) in M. synoviae. The 2 monoclonal antibodies clearly distinguished between all serotypes of M. gallisepticum and M. synoviae that were examined by Western blot transfer. Autoradiographs of 125I-labeled M. gallisepticum and M. synoviae indicated that p 110 (G) and p 45-50 (S) were surface membrane peptides. Indirect immunofluorescence of M. gallisepticum and M. synoviae in Vero cell cultures supported the autoradiographic findings. The p 110 (G) antigen of M. gallisepticum was heat-stable, pronase-sensitive, and resistant to periodate oxidation, suggesting that its chemical composition is protein. In contrast, the p 45-50 antigen complex of M. synoviae appeared as a broad band in protein blots treated with monoclonal antibody S 221, was sensitive to pronase, and responded to Schiff's reagent but was not completely inhibited by periodate oxidation, suggesting that it is a complex of repeating sequences probably composed of glycosylated peptides.

Animals↗

PubMedDate not supplied

Efficacy of mexiletine in ventricular arrhythmias among patients in Taiwan: assessment by 24-hour Holter electrocardiography.

The effects of mexiletine in 30 patients with symptomatic recurrent ventricular arrhythmias were assessed by 24-hour Holter electrocardiography and M-mode echocardiography. The mean daily dose of mexiletine was 534 mg (range, 300 to 900 mg) and the interval of Holter follow-up was 16.9 days (range, 10 to 25 days). Total ventricular premature beats were reduced by 85% or more in 21 patients; in 19 of these patients there was a reduction of one or more modified Lown grades of ventricular arrhythmias. The overall reduction in Lown grades in the 30 patients was from 3.3 +/- 0.8 to 1.5 +/- 1.4 (P less than 0.0001). No significant changes in heart rate before or after mexiletine therapy were noted. Left ventricular echocardiography showed no significant changes in percentage fractional shortening after treatment. Adverse effects included gastrointestinal intolerance in seven patients and neurogenic symptoms in three. During the follow-up period of 1 to 11 (mean, 3.2) months, ventricular arrhythmias recurred in three patients. It is concluded that oral mexiletine is moderately effective and safe in controlling symptomatic recurrent ventricular arrhythmias.

Adult↗