Analysis Of Arterial Pressure Variability Research Articles

Analysis of arterial pressure variability in patients with acute cerebral stroke depending on the time of occurrence.

Analysis of arterial pressure variability in patients with acute cerebral stroke depending on the time of occurrence.

Abstract 061: Prevention Of Oxidative Stress In The Paraventricular Nucleus (PVN) Does Not Attenuate Hypertension During High Fat Diet (HFD), Despite Blunting Weight Gain.

We recently reported that PVN-specific deletion of the NADPH oxidase subunit p22 phox attenuates oxidative stress in this brain region and prevents diet-induced obesity (DIO) in mice. In addition to its importance in the regulation of energy homeostasis, the PVN is a well-described cardiovascular regulatory center. Since increased oxidative stress in the central nervous system is causally linked to both hypertension and obesity, we hypothesized that attenuating oxidative stress in the PVN would reduce sympathetic nerve activity (SNA) and improve hypertension during HFD. In mice harboring loxP-sites flanking the p22 phox gene (p22 phox/flox ), we tested if p22 phox deletion in the PVN reduces arterial pressure (AP) and heart rate (HR) during HFD. For these experiments, p22 phox/flox mice underwent bilateral PVN-targeted injection of adenoviral vectors encoding Cre recombinase (AdCre) or control LacZ (AdLacZ). Following 1-week recovery, mice were started on a 42% HFD or normal chow (NC). After 7 weeks of HFD, radiotelemeters were implanted and 3 weeks later (after 10 weeks HFD) we recorded AP and HR. HFD caused a significant elevation in AP (AdLacZ NC: 104 ± 2.8 mmHg vs. AdLacZ HFD 113 ± 0.6 mmHg n = 3-5, P < 0.05) and HR (AdLacZ NC: 487 ± 7 bpm vs. AdLacZ HFD 537 ± 12 bpm; n = 3-5, P < 0.05). Importantly, despite a significant reduction in body weight after deletion of p22 phox in the PVN (AdLacZ HFD: 32 ± 1.2 g, vs. AdCre HFD 27 ± 0.6 g, P < 0.05), removal of oxidative stress in the PVN did not blunt AP (AdLacZ HFD 113 ± 0.6 mmHg vs. AdCre HFD: 112 ± 2.0 mmHg, n = 5, P > 0.05) or HR (AdLacZ HFD 537 ± 12.3 bpm vs. AdCre HFD: 540 ± 6.3 bpm, n = 5, P > 0.05). We utilized power spectral analysis of AP variability to assess SNA in mice during NC and HFD. We found that HFD elevated SNA similarly in AdLacZ and AdCre mice (1.7-fold and 1.5-fold, respectively vs. NC mice, P > 0.05). Thus, while our data demonstrate that oxidative stress in the PVN is a major player in the regulation of metabolism and adiposity, these results suggest that PVN oxidative stress does not contribute to increased SNA, AP or HR during HFD. While the underlying mechanism(s) of this divergence is currently being investigated, these data emphasize that there is differential central neural regulation of cardiovascular and metabolic responses to HFD.

Time course of cardiovascular neural regulation during programmed 20-sec apnea in rats

Long-term hypoxia results in hemodynamic breakdown in patients in the intensive care unit; however, intermittent hypoxia causes hypertension in individuals with sleep apnea. The objective of this study was to explore the sequential cardiovascular neural alterations in response to acute hypoxic apnea. The authors conducted a prospective, randomized animal study. The study was conducted in a university animal laboratory. A programmable apnea model was developed in anesthetized rats, in which a 20-sec period of apnea was produced and subsequently divided into the early (2.0 to 7.9 secs), middle (8.0 to 13.9 secs), and late apneic phases (14.0 to 19.9 secs) and immediate reventilatory phase (20.0 to 25.9 secs). Evident hypoxia developed during 20-sec apnea. Arterial pressure increased in the early apneic phase and returned to control level in the middle phase. Significant hypotension developed in the late apneic phase and deteriorated in the reventilatory phase. Interbeat interval increased mildly along the apneic event. The increase of pressure in the early and middle phases was inhibited by propranolol (1.0 mg/kg intravenously [iv]) but was provoked by phentolamine (2.5 mg/kg iv). The decrease of pressure in the late and reventilatory phases was reversed, at least in part, by phentolamine. Atropine (0.5 mg/kg iv) did not produce discernible effects in the arterial pressure. The increase of interbeat interval was suppressed by propranolol. Power spectral analysis of arterial pressure variability demonstrated significant increases of the low-frequency (sympathetic vasomotor activity) and normalized high-frequency (cardiac sympathetic modulation) power after reventilation. Although the sympathetic activity is excited during and after a hypoxic apnea, the immediate pressor effect is related to an inotropic response of cardiac sympathetic regulation, whereas the negative chronotropic and subsequent depressor effect is associated with a failure in the cardiovascular response to sympathetic excitation.

Spectral Analysis of Arterial Pressure Variability During Induction of Propofol Anesthesia

Spectral Analysis of Arterial Pressure Variability During Induction of Propofol Anesthesia