Biomedical subjects

Ken-Ichi Iwasaki

Publications and source records attributed to Ken-Ichi Iwasaki.

6 recordsLinked to original sources

PubMed2006

Cascade model of ventricular-arterial coupling and arterial-cardiac baroreflex function for cardiovascular variability in humans.

Cardiovascular variability reflects autonomic regulation of blood pressure (BP) and heart rate (HR). However, systolic BP (SBP) variability also may be induced by fluctuations in stroke volume through left ventricular end-diastolic pressure (LVEDP) variability via dynamic ventricular-arterial coupling during respiration. We hypothesized that dynamic ventricular-arterial coupling is modulated by changes in left ventricular compliance associated with altered preload and that a cascade control mechanism of ventricular-arterial coupling with arterial-cardiac baroreflex function contributes to the genesis of cardiovascular variability at the respiratory frequency. Seven healthy young subjects underwent 6-min recordings of beat-by-beat LVEDP, SBP, and HR in the supine position with controlled respiration at 0.2 Hz during hyper- and hypovolemia. Spectral and transfer function analysis of these variables was conducted between 0.18 and 0.22 Hz. Dynamic ventricular-arterial coupling gain (Gain LVEDP-SBP) was smaller by 25% (P = 0.009) during hypervolemia than during hypovolemia, whereas arterial-cardiac baroreflex function gain (Gain SBP-HR) was similar. As predicted from a cascade model, a linear relationship between Gain LVEDP-HR and LVEDP-SBP times Gain SBP-HR was identified (R(2) = 0.93, P < 0.001). Gain LVEDP-HR was smaller by 40% (P = 0.04) during hypervolemia than during hypovolemia, leading to a reduction in spectral power of HR variability by 45% (P = 0.08). We conclude that dynamic ventricular-arterial coupling gain is reduced during hypervolemia because of a decrease in left ventricular compliance. A cascade model of ventricular-arterial coupling with the arterial-cardiac baroreflex contributes to the genesis of cardiovascular variability at the respiratory frequency.

Adult↗

PubMed2005

Hypergravity exercise against bed rest induced changes in cardiac autonomic control.

An intermittent exposure to artificial hypergravity with physical exercise by a human centrifuge may provide a countermeasure against various physiological problems after space flight. To test the effects of hypergravity with ergometric exercise on dynamic regulation of heart rate during weightlessness, we quantified autonomic cardiovascular control before and after head-down-tilt bed rest (HDBR) with and without the countermeasure. Twelve male subjects underwent a 14-day period of HDBR. Six of them were exposed to a hypergravity (+1.2 Gz acceleration at heart level) for 30 min with ergometric exercise (60 W, n=4; 40 W, n=2) as a countermeasure on day 1, 2, 3, 5, 7, 9, 11, 12, 13 and 14, during HDBR (CM group). The remaining six were not exposed to a hypergravity exercise during HDBR (control group). Blood pressure and ECG were recorded at a supine position before and after HDBR. The high frequency power of R-R interval (HFRR; 1,008+/-238 to 353+/-56 ms(2) P<0.05) as an index of cardiac parasympathetic activity, and transfer function gain between BP and R-R interval in the high frequency range (GainHF; 21.9+/-5.4 to 14.5+/-4.2 ms/mmHg, P<0.01) as an index of vagally mediated arterial-cardiac baroreflex, decreased significantly after HDBR in the control group. However, these changes were not statistically significant in the CM group (HFRR, 1,150+/-344 to 768+/-385 ms(2); GainHF, 21.5+/-3.3 to 18.6+/-3.4 ms/mmHg). Moreover, baroreflex gain by sequence analysis showed similar results. This observation suggests that the intermittent exposure to hypergravity with ergometric exercise may attenuate the decreases in the parasympathetic activity and the spontaneous arterial-cardiac baroreflex function after weightlessness.

Adult↗

PubMed2005

Effect of a repeated series of intermittent hypoxic exposures on ventilatory response in humans.

The purpose of this study was to elucidate the magnitude and the time course of ventilatory changes resulting from a repeated series of hypoxic exposures. Eight healthy males participated in the present study. The subjects spent 1 h/day in normobaric hypoxia (12% inspired oxygen). Inspired minute ventilation (V(I)), end-tidal partial pressure of carbon dioxide (P(ET(CO2))), and arterial oxygen saturation (SaO2) were measured in a hypoxic tent. These measurements were taken for 10 consecutive days (series 1), and were taken again after the subjects had been away from hypoxic exposure for 1 month (series 2). P(ET(CO2)) decreased and SaO2 increased progressively in the hypoxic tent during the 10 days of intermittent hypoxia in series 1. At the onset of series 2 (days 1 to 3), P(ET(CO2)) was significantly lower and SaO2 was significantly higher than those on day 1 during series 1. These results suggest that humans who have had previous hypoxic exposure adapt sooner to hypoxic condition due to an increase in the magnitude of hyperventilation in the first few days of a series of reexposures to hypoxia.

Acclimatization↗

PubMed2005

Cardiovascular neuroregulation during acute exposure to 40, 70, and 100% oxygen at sea level.

BACKGROUND: Humans encounter increased partial pressures of inspired oxygen in some kinds of diving as well as during use of hyperoxic mixtures to shorten decompression times and hyperbaric oxygen therapy for decompression sickness or other clinical conditions. Although it is known that hyperoxia may affect cardiovascular regulation, such effects are generally obscured by stress and the diving reflex. In this study, we evaluated cardiovascular neuroregulation for various levels of hyperoxia in a laboratory setting. METHODS: There were 10 healthy adults who were exposed to 21, 40, 70, and 100% oxygen administered via mask as a series of stepwise increases. Subjects breathed at a fixed respiratory rate of 15 breaths x min(-1) while their heart rate (HR) and blood pressure (BP) were measured continuously over 5-min intervals. RESULTS: HR decreased with increasing fraction of inspired oxygen (FIO2) (21%: 65 +/- 9, 40%: 63 +/- 9, 70%: 61 +/- 8, 100%: 60 +/- 8 bpm) and the high-frequency power of HR variability (an index of cardiac parasympathetic activity) increased as FIO2 rose (21%: 773 +/- 565, 40%: 880 +/- 590, 70%: 966 +/- 681, 100%: 1114 +/- 715 ms2); both changes were significant at the 70% and 100% oxygen levels. The low-frequency power of systolic BP variability (an index of vasomotor sympathetic activity) did not change. Low- and high-frequency transfer function gains (indices of arterial-cardiac baroreflex function) increased with FIO2. CONCLUSION: Parasympathetic activity and arterial-cardiac baroreflex function increased with hyperoxia in a dose-dependent manner. This increase may help reduce the likelihood of arrhythmias during diving.

Administration, Inhalation↗

PubMed2004

Reduced baroreflex control of heart period after bed rest is normalized by acute plasma volume restoration.

Adaptation to spaceflight or head-down-tilt bed rest leads to hypovolemia and an apparent abnormality of baroreflex regulation of cardiac period. In a previous study, we demonstrated that both chronic (2 wk) head-down-tilt bed rest and acute induced hypovolemia led to similar impairments in spontaneous baroreflex control of cardiac period, suggesting that a reduction in plasma volume may be responsible for this abnormality after bed rest. Therefore we hypothesized that this reduced "baroreflex function" could be restored by intravenous volume infusion equivalent to the reduction in plasma volume after bed rest. Six healthy subjects underwent 2 wk of -6 degrees head-down bed rest. Beat-by-beat arterial blood pressure and ECG were recorded during 6 min of spontaneous respiration and fixed-rate breathing (0.2 Hz), and transfer function analysis between systolic blood pressure and R-R interval was performed. Plasma volume was measured with Evans blue dye, and cardiac filling pressures were directly measured (Swan-Ganz catheter). After bed rest, studies were repeated before and after plasma volume restoration, with which both plasma volume and left ventricular end-diastolic pressure were restored to pre-bed rest levels by intravenous dextran40 infusion (288 +/- 31 ml). Transfer function gain in the high-frequency range, used as an index of vagally mediated arterial-cardiac baroreflex function, decreased significantly (13.4 +/- 3.1 to 8.1 +/- 2.9 ms/mmHg, P < 0.05) after bed rest. However, reduced transfer function gain was normalized to the pre-bed rest level (12.2 +/- 3.6 ms/mmHg) after precise plasma volume restoration. This result confirms that reductions in plasma volume, rather than a unique autonomic nervous system adaptation to bed rest, are largely responsible for the observed changes in spontaneous arterial-cardiac baroreflex function after bed rest.

Adult↗

PubMed2003

Dose-response relationship of the cardiovascular adaptation to endurance training in healthy adults: how much training for what benefit?

Occupational or recreational exercise reduces mortality from cardiovascular disease. The potential mechanisms for this reduction may include changes in blood pressure (BP) and autonomic control of the circulation. Therefore, we conducted the present long-term longitudinal study to quantify the dose-response relationship between the volume and intensity of exercise training, and regulation of heart rate (HR) and BP. We measured steady-state hemodynamics and analyzed dynamic cardiovascular regulation by spectral and transfer function analysis of cardiovascular variability in 11 initially sedentary subjects during 1 yr of progressive endurance training sufficient to allow them to complete a marathon. From this, we found that 1) moderate exercise training for 3 mo decreased BP, HR, and total peripheral resistance, and increased cardiovascular variability and arterial baroreflex sensitivity; 2) more prolonged and intense training did not augment these changes further; and 3) most of these changes returned to control values at 12 mo despite markedly increased training duration and intensity equivalent to that routinely observed in competitive athletes. In conclusion, increases in R-wave-R-wave interval and cardiovascular variability indexes are consistent with an augmentation of vagal modulation of HR after exercise training. It appears that moderate doses of training for 3 mo are sufficient to achieve this response as well as a modest hypotensive effect from decreasing vascular resistance. However, more prolonged and intense training does not necessarily lead to greater enhancement of circulatory control and, therefore, may not provide an added protective benefit via autonomic mechanisms against death by cardiovascular disease.

Adaptation, Physiological↗