Effect of chronic ethanol consumption in female rats subjected to experimental sepsis.

The objective of this research was to evaluate the interference of ethanol consumption by female rats with cytokines involved in the sepsis process and its correlation with mortality, the main outcome of sepsis. Female Wistar rats in estrus phase were evaluated in three experiments. Experiment 1 (n=40) was performed to determine survival rates. Experiment 2 (n=69) was designed for biochemical analysis, measurement of cytokine and estrogen levels before and after sepsis, and experiment 3 (n=10) was performed to evaluate bacterial growth by colony counts of peritoneal fluid. In all experiments, treated animals were exposed to a 10% ethanol/water solution (v/v) as the single drinking source, while untreated animals were given tap water. After 4 weeks, sepsis was induced in the rats by ip injection of feces. In experiment 1, mortality in ethanol-exposed animals was delayed compared with those that drank water (48 h; P=0.0001). Experiment 2 showed increased tumor necrosis factor alpha (TNF-α) and decreased interleukin-6 (IL-6) and macrophage migration inhibitory factor in septic animals exposed to ethanol compared to septic animals not exposed. Sepsis also increased TNF-α and IL-6 levels in both ethanol- and water-exposed groups. Biochemical analysis showed higher creatinine, alanine aminotransferase and aspartate aminotransferase and decreased glucose levels in septic animals that were exposed to ethanol. In experiment 3, septic animals exposed to ethanol showed decreased numbers of colony-forming units than septic animals exposed to water. These results suggest that ethanol consumption delays the mortality of female rats in estrus phase after sepsis induction. Female characteristics, most probably sex hormones, may be involved in cytokine expression.

Effect of chronic ethanol consumption in female rats subjected to experimental sepsis

The objective of this research was to evaluate the interference of ethanol consumption by female rats with cytokines involved in the sepsis process and its correlation with mortality, the main outcome of sepsis. Female Wistar rats in estrus phase were evaluated in three experiments. Experiment 1 (n=40) was performed to determine survival rates. Experiment 2 (n=69) was designed for biochemical analysis, measurement of cytokine and estrogen levels before and after sepsis, and experiment 3 (n=10) was performed to evaluate bacterial growth by colony counts of peritoneal fluid. In all experiments, treated animals were exposed to a 10% ethanol/water solution (v/v) as the single drinking source, while untreated animals were given tap water. After 4 weeks, sepsis was induced in the rats by ip injection of feces. In experiment 1, mortality in ethanol-exposed animals was delayed compared with those that drank water (48 h; P=0.0001). Experiment 2 showed increased tumor necrosis factor alpha (TNF-α) and decreased interleukin-6 (IL-6) and macrophage migration inhibitory factor in septic animals exposed to ethanol compared to septic animals not exposed. Sepsis also increased TNF-α and IL-6 levels in both ethanol- and water-exposed groups. Biochemical analysis showed higher creatinine, alanine aminotransferase and aspartate aminotransferase and decreased glucose levels in septic animals that were exposed to ethanol. In experiment 3, septic animals exposed to ethanol showed decreased numbers of colony-forming units than septic animals exposed to water. These results suggest that ethanol consumption delays the mortality of female rats in estrus phase after sepsis induction. Female characteristics, most probably sex hormones, may be involved in cytokine expression.

Heart rate responses to deep breathing and 4-seconds of exercise before and after pharmacological blockade with atropine and propranolol.

Two autonomic tests which evaluate cardiac vagal activity, the respiratory sinus arrhythmia and the newer 4-second exercise test, have been compared. From electrocardiograph tracings, respiratory sinus arrhythmia was quantified by the ratio between the longest R-R interval during expiration and the shortest one during inspiration (E/I ratio), and the 4-second exercise test by the ratio between the last R-R interval before and the shortest one during exercise (B/C ratio). In 29 healthy subjects there was a correlation (R = 0.60, p less than 0.05) between the responses to the two tests. In a group of six healthy subjects the same tests were performed after autonomic blockade with intravenous atropine and/or propranolol. The heart rate rise during the 4-second exercise test was nearly abolished by atropine (mean +/- SD) (B/C: control = 1.53/0.33; after atropine = 1.04/0.03), whereas RSA was diminished to a lesser extent (E/I: control = 1.59/0.24; after atropine = 1.13/0.07). beta-adrenoceptor blockade did not affect the test ratios (after propranolol: B/C = 1.51/0.33 and E/I = 1.45/0.14). Successive tests during the following hour after atropine infusion showed a somewhat faster recovery of the respiratory sinus arrhythmia than the heart rate acceleration induced by the 4-second exercise test (p less than 0.05). We conclude that there may be some difference in the mechanisms which contribute to the heart rate changes in these two autonomic cardiovascular tests; these remain to be clarified. The 4-second exercise test may be an alternative to the respiratory sinus arrhythmia test in the non-invasive evaluation of cardiac parasympathetic activity.

Relative roles of the sympathetic and parasympathetic systems in the 4-s exercise test.

To evaluate the relative influence of the two branches of the autonomic nervous system on the 4-s exercise test which measures heart rate acceleration at the onset of exercise, 6 healthy male subjects performed the 4-s test under sympathetic blockade with propranolol, parasympathetic blockade with atropine and dual blockade. The magnitude of the 4-s test results (means +/- SD) was significantly different only between the conditions with and without atropine (1.04 +/- 0.03 vs 1.53 +/- 0.33, respectively), with no differences between the control (1.60 +/- 0.25) and the test under sympathetic blockade (1.51 +/- 0.33). These results support the conclusion that the 4-s exercise test is a specific method for the evaluation of parasympathetic activity.

Relative roles of the sympathetic and parasympathetic systems in the 4-s exercise test

To evaluate the relative influence of the two branches of the autonomic nervous nervous system on the 4-s exercise test which measures heart rat acceleration at the onset of exercise, 6 healthy male subjects performed the 4-s test under sympathetic blockade with propranolol, parasympathetic blockade with atropine and dual blockade. The magnitude of the 4-s test results (meams ñ SD) was significantly different only between the conditions with and without atropine (1.04 ñ 0.03 vs 1.53 ñ 0.33, respectively), with no differences between the control (1.60 ñ 0.25) and the test under sympathetic blockade (1.51 ñ 0.33). These results support the conclusion that the 4-s exercise test is a specific method for the evaluation of parasympathetic activity

Vagal activity: effect of age, sex and physical activity pattern.

Heart rate response to a short (4 s) bicycle exercise test during maximal inspiratory apnea was used to assess vagal activity (VA). This study aims to evaluate the role of age, sex and physical activity pattern on VA. A total of 148 subjects, divided into athletes (N = 90) and non-athletes (N = 58) were tested. No correlation was found between age (range from 15 to 42 years) and VA in the male and female athletes (P greater than 0.05). No gender effect could be identified. In spite of a slight tendency toward higher VA in athletes, no significant differences could be found between the two groups.

Vagal activity: effect of age, sex and physical activity pattern

Heart rate response to a short (4 s) bicycle exercise test during maximal inspiratory apnea was used to assess vagal activity (VA). This study aims to evaluate the role of age, sex and physical activity pattern on VA. A total of 148 subjects, divided into athletes (N = 90) and non-athletes (N = 58) were tested. No correlation was found between age (range from 15 to 42 years) and VA in the male and female athletes (P>0.05). No gender effect could be identified. In spite of a slight tendency toward higher VA in athletes, no significant differences could be found between the two groups