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Biomedical subjects

P B Persson

Publications and source records attributed to P B Persson.

At least 37 records · Page 2Linked to original sources
PubMed2000

High-frequency oscillations of the heart rate during ramp load reflect the human anaerobic threshold.

The aim of this study was to analyze the dynamic behavior of the high-frequency component (HF > 0.15 Hz) of heart rate variability (HRV) and the respiratory frequency in relation to the anaerobic threshold (AT). Twenty-two healthy subjects [mean (SD) age: 24 (6) years, height: 175 (10) cm, body mass: 65 (11) kg] completed a ramp load, with increments of 20 W x min(-1), on a cycle ergometer. The AT was determined by the V-slope-method. Respiratory movements of the thorax, and the electrocardiogram were monitored. The instantaneous frequency of the HF component of HRV and of the respiratory signal were obtained by the Hilbert transformation. Both frequencies were closely related, the cross correlation coefficient being between 0.84 and 0.99. Various patterns of HRV and respiration were observed during the protocol. Remarkably, however, in over 90% of these cases, a shift in the instantaneous frequency of the HF component occurred during the transition from aerobic to anaerobic work. The difference between the AT determined by gas analysis and the AT evaluated as the power output (ATf), calculated using the approximation of the curve of the instantaneous frequency of HF by hyperbolic tangent functions, varied between 2 and 14%. In conclusion, the present study demonstrates significant changes in the behavior of the instantaneous frequency of HF in the region of the AT.

Adult↗
PubMed2000

Blood pressure control in eNOS knock-out mice: comparison with other species under NO blockade.

Changes in arterial blood pressure (ABP) lead to changes in vascular shear stress. This mechanical stimulus increases cytosolic Ca2+ in endothelial cells, which in turn activates the endothelial isoform of the nitric oxide synthase. The subsequently formed NO reaches the adjacent vascular smooth muscle cells, where it reduces vascular resistance in order to maintain ABP at its initial level. Thus, NO may play an important role as a physiological blood pressure buffer. Previous data on the importance of eNOS for blood pressure control are reviewed with special emphasis on the fact that endogenous nitric oxide can buffer blood pressure variability (BPV) in dogs, rats and mice. In previous studies where all isoforms of the nitric oxide synthase were blocked pharmacologically, increases in blood pressure and variability were observed. Thus, we set out to clarify which isoform of the nitric oxide synthase is responsible for this BPV controlling effect. Hence, blood pressure control was studied in knock-out mice lacking specifically the gene for endothelial nitric oxide synthase with their respective wild-type controls. One day after surgery, under resting conditions, blood pressure was increased by 47 mmHg (P < 0.05), heart rate was lower (-77 beats min-1, P < 0.05), and BPV doubled (P < 0.05). Based on these results, we conclude that chronic blood pressure levels are influenced by eNOS and that there is a blood pressure buffering effect of endogenous nitric oxide which is mediated by the endothelial isoform of the nitric oxide synthase.

Animals↗
PubMed2000

Coupling of left ventricular and aortic volume elasticity in the rabbit.

Changes in volume elasticity (VE) of the left ventricle and aorta could be important for blood flow. A procedure is presented to rapidly assess VE of the left ventricle and aorta by analyzing changes in the eigenfrequency. Six control rabbits and 11 rabbits with atheromatosis (12 wk of high-cholesterol feeding) were studied. In control rabbits, during the first half of the systole, left ventricular VE continuously increased to +43% (P < 0.05). Then VE gradually declined to an end-diastolic minimum (20% of the average systolic levels, P < 0.05). Aortic VE changes were in the opposite direction to the ventricle. Aortic VE continuously decreased throughout the systole; the last value was 20% lower than at the beginning of the systole (P < 0.05). Conversely, diastolic VE of the aorta took on greater values. This inverse time course between ventricle and aorta may reduce energy requirements for conveying blood. High cholesterol-fed rabbits did not reveal the inverse behavior of ventricular and aortic VE, e.g., aortic VE increased during the systole (119%, P < 0.05).

Animals↗
PubMed2000

Blunted arterial baroreflex causes "pathological" heart rate turbulence.

Sudden cardiac death is the leading cause of cardiovascular mortality in developed countries. Recently, two post-myocardial-infarction risk predictors were introduced that are superior to all other presently available indicators: turbulence onset (TO) and turbulence slope (TS). These parameters characterize the behavior of instantaneous heart rate after a ventricular premature beat, i.e., they describe the reestablishing of heart rate control after an acute perturbation. We propose that the dysfunction of an important cardiovascular control mechanism, the arterial baroreflex, is the mechanism behind these new potent markers. The hypothesis is tested by means of a physiological model involving the excitation generation in the heart, the hemodynamic situation in the aorta, and baroreceptor feedback mechanisms. The data show that a blunted baroreceptor response of the heart resembles patterns of heart rate turbulence that correspond to pathological values of TO and TS. The results of the model suggest that the recently established risk parameters TO and TS characterize baroreflex function, a known risk stratifier in patients.

Adrenergic beta-Antagonists↗
PubMed2000

Vascular response to angiotensin II in atherosclerosis: role of the baroreflex.

High-cholesterol alimentation is associated with an induction of angiotensin-converting enzyme and angiotensin II receptor expression within the vascular wall of the aorta. Despite an enhanced pressure response to angiotensin II in atherosclerotic conscious rabbits, angiotensin II-induced contraction was reduced in isolated vascular rings from the aorta and unchanged in those from the iliac artery. We, therefore, investigated whether cholesterol-induced atherosclerosis enhances overall vascular responsiveness to angiotensin II in intact animals and whether an altered arterial baroreflex sensitivity can explain the discrepancy between experiments in intact animals and isolated blood vessels. Rabbits were maintained on a high-cholesterol diet (2 g/d cholesterol plus 20 mL/d sunflower seed oil, n=11) or on a standard diet (n=12) for 12 weeks. Total serum lipids markedly increased (P<0.05). Tissue examinations 6 weeks after termination of the high-cholesterol diet revealed distinct atherosclerosis and elevated cholesterol content in the aorta (P<0.05). A high-cholesterol diet did not change baseline hemodynamic parameters. However, angiotensin II-induced increases in total peripheral resistance were larger in the atherosclerotic animals (86.3+/-13.0 versus 41.9+/-9.7 mm Hg. L(-1). min, P<0.05). In addition, the blood pressure pulse interval relationship was markedly reduced (slope: 0.80+/-0.14 versus 0. 49+/-0.06 ms/mm Hg, P<0.05), which suggested that the baroreflex blunted the angiotensin II response to a lesser extent in atherosclerotic animals. In conclusion, the overall vascular responsiveness to angiotensin II is increased in the atherosclerotic rabbit as indicated by the larger increase in total peripheral resistance. An attenuation of the arterial baroreflex sensitivity may contribute to this effect.

Angiotensin II↗
PubMed1999

Rhythms and complexity of respiration during sleep in pre-term infants.

The aim of this study is to test rhythmic and complex properties of respiratory control in former ventilated, pre-term infants during quiet and active sleep. The children had a higher risk for sudden infant death due to bronchopulmonary dysplasia (BPD). Twelve infants suffering from BPD and 12 control infants, matched regarding their post-conceptional age, were examined polygraphically during quiet (QS) and active sleep (AS). The respiratory rate (RR), the ratio (LF/HF) between the low-frequency power (LF) and the high-frequency power (HF) of the spectra of the thoracic respiratory effort, and the frequency of the dominant peak within LF (LFF) and HF (HFF) were computed. The correlation dimension (D2) of the respiratory signal was calculated to determine the complexity of the respiratory control. The transcutaneous pO2 (tcpO2) and pCO2 and the oxygen saturation (sO2) were analysed. Infants with BPD had significantly higher RR and HFF during QS (median: BPD 48 breaths min-1; control 32 breaths min-1). tcpO2 and sO2 were significantly lower in the BPD group. No differences were found in LF/HF, LFF or D2 between groups, either in QS or in AS. D2 ranged between 1.8 and 3.8, showing significantly higher values during AS. LFF was found to be lower during active sleep (AS 0.04-0.05 Hz; QS about 0.06 Hz). We propose that in infants with BPD the lower lung compliance and the higher resistance, and possibly also the hypoxaemia, contribute to the acceleration of breathing. The behaviour of RR, spectral parameters and D2 indicates a specific, functional setting rather than a regulatory impairment in infants with BPD.

Bronchopulmonary Dysplasia↗
PubMed1999

Pressure-dependent renin release: effects of sodium intake and changes of total body sodium.

The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2-4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (-3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.

Animals↗
PubMed1999

Frequency response characteristics of sympathetic transmission to skin vascular smooth muscles in rats.

Sympathetic modulation of cutaneous vasomotor waves in humans is most effective at frequencies up to 0.1 Hz. In contrast, sympathetic modulation of mesenteric vasomotor waves in rats is strongest in the frequency band between 0.2 and 0.75 Hz. Therefore, we addressed the question as to whether these different frequency response characteristics are due to species- or organ-specific disparities. Eleven Sprague-Dawley rats were instrumented with catheters in the carotid artery and in the jugular vein, together with electrodes on the centrally sectioned left lumbar sympathetic trunk (LST) and laser Doppler flow probes directed to the plantar surface of the skin of the left and right hind paws. In anesthetized rats, the LST was electrically stimulated at eight different stimulation frequencies, and the responses in laser Doppler blood flow were recorded in the skin of the ipsilateral and contralateral paw. At stimulation frequencies <0.2 Hz, LST stimulation induced corresponding oscillations in skin blood flow in the ipsilateral, but not in the contralateral, paw. These dynamic responses to LST stimulation in the ipsilateral paw were strongest at 0.05 and 0.075 Hz. At higher stimulation frequencies a tonic vasoconstriction was observed. It is concluded that organ-specific disparities exist in sympathetic transmission to vascular smooth muscles, whereas no species-specific differences are apparent in sympathetic transmission to cutaneous blood vessels of humans and rats.

Animals↗
PubMed1999

Enhanced blood pressure variability in eNOS knockout mice.

It has been shown previously that endogenous nitric oxide can buffer arterial blood pressure variability in dogs and rats. In these former studies, all isoforms of the nitric oxide synthase were blocked pharmacologically and an increased blood pressure variability was observed. Thus the question as to which isoform of the nitric oxide synthase is responsible for the blood pressure buffering effect of endogenous nitric oxide remains unraveled. In the present study, we therefore compared blood pressure variability in knockout mice that lack specifically the gene for endothelial nitric oxide synthase with their respective wild-type controls. One day after carotid artery cannulation, blood pressure was recorded in these conscious mice. During resting conditions, blood pressure variability was markedly enhanced in knockout mice compared with wild-type mice (10.5+/-1.5 mm Hg2 vs 6.0+/-0.8 mm Hg2, P<0.05). Power spectral analysis revealed that this increase in blood pressure variability is manifested at low frequencies that range from 0.05 to 0.40 s-1 (Hz) (5.1+/-1.0 mm Hg2 vs 2.5+/-0.5 mm Hg2, P<0.05). On the basis of these results, we conclude that the blood pressure buffering effect of endogenous nitric oxide is mediated by the endothelial isoform of the nitric oxide synthase. In addition, endothelial nitric oxide is most effective in buffering blood pressure oscillations at frequencies that range from 0.05 to 0.40 s-1 (Hz) in conscious mice.

Animals↗
PubMed1999

Mechanically induced potentials in fibroblasts from human right atrium.

It has been shown that cardiac fibroblasts of the human heart are electrically non-excitable and mechanosensitive. The resting membrane potential of these cells is -15.9+/-2.1 mV and the membrane resistance is 4.1+/-0.1 G[Omega]. Rhythmic contractions of the myocardium associated with stretch of the surrounding tissue produce reversible changes in the membrane potential of cardiac fibroblasts. These mechanically induced potentials (MIPs) follow the rhythm of myocardial contractions. Simultaneous recording of the action potential of cardiomyocytes and MIPs of cardiac fibroblasts demonstrates a delay of 40.0+/-0.4 ms after the action potential before the appearance of the MIP. Contraction produces a MIP which is more positive or more negative than the reversal potential - the membrane potential due to current injection at which the MIP reverses its direction. Regardless of the initial orientation of the MIP, intracellular polarization increases the amplitude towards the reversal potential if the background MIP had depolarized the membrane or away from the reversal potential if the initial background MIP had hyperpolarized the membrane. Artificial intracellular polarization changed the amplitude but not the frequency of the MIP. The pool of electrically non-excitable mechanosensitive cells, which change their electrical activity during contraction and relaxation of the heart, may play a role in the mechano-electrical feedback mechanism which has to be taken into account in the normal function of the heart as well as in pathological processes.

Aged↗
PubMed1998

Electrophysiological properties of mechanosensitive atrial fibroblasts from chronic infarcted rat heart.

Electrically non-excitable but mechanosensitive right-atrial fibroblasts are thought to be involved in the chronotropic response of the heart to stretch. After myocardial infarction, altered chronotropic response may be due to the remodeling process which also involves the right atrium. Remodeling is associated with the development of hypertrophy of cardiomyocytes and proliferation of fibroblasts. Electrical properties of atrial mechanosensitive fibroblasts from chronic infarcted hearts and their possible role for altered chronotropic response has not, to our knowledge, been studied until now. Thus, resting membrane potential as well as mechanically induced potential of fibroblasts, action potential (AP) of cardiomyocytes, spontaneous frequency and mechanical activity of preparations from the sinus node region were studied 10 weeks after myocardial infarction induced by ligation of the left coronary artery in rats. The prolongation of AP repolarization (increases in APD50 and APD90) correlated closely to the infarct size (IS) and the degree of hypertrophy, respectively. Along with increasing IS, membrane potentials of fibroblasts were shifted to more negative values, with a peak of frequency distribution at -15 mV (control and very small IS), at -35 mV (intermediate IS), and -55 mV (large IS), and spontaneous electrical activity was decreased. Membrane resistance of fibroblasts also correlated to IS and was eight-fold greater at large IS than in control. We hypothesize that, in the infarcted heart, increased membrane potential and membrane resistance of fibroblasts may alter electrical activity of neighbouring myocytes in the sinus-venosus region via intercellular electrical coupling.

Animals↗
PubMed1998

Kinins modulate the sodium-dependent autoregulation of renal medullary blood flow.

OBJECTIVE: In the recent past it has become clear that the kallikrein-kinin system is closely intertwined with long-term blood pressure regulation. It was shown that a kinin B2 receptor blockade leads to a sodium-dependent rise in blood pressure. The underlying mechanisms of this phenomenon, however, remain unclear. The osmotic gradient of the renal medulla is a prerequisite for the preservation of volume and sodium by the kidney. We thus hypothesized, that a kinin dependent modulation of medullary blood flow accounts for the influence of sodium on blood pressure. METHODS: In 39 urethane anaesthetized rats pressure dependent regulation of whole kidney blood flow and cortical and medullary blood flow were estimated via laser-Doppler flux by a stepwise reduction of renal perfusion pressure to 30 mm Hg. RESULTS: In controls (n = 15), a reduction in renal perfusion pressure to 30 mm Hg lead to a concomitant reduction in whole kidney blood flow (25 +/- 3% of baseline) and cortical laser-Doppler flux (36 +/- 5% of baseline). In contrast, medullary laser-Doppler flux decreased only to 79 +/- 8% of the baseline level. Providing a 2% sodium chloride solution as drinking water over 5 days (n = 12), resulted in a significantly lower capability to autoregulate medullary flow (50 +/- 6% of baseline, P < 0.05). Acute subcutaneous administration of Hoe 140, a bradykinin B2 receptor antagonist (300 micrograms/kg bwt), restored autoregulation of medullary flow to almost normal levels (93 +/- 12% of baseline, P < 0.01 versus high sodium diet alone, n = 12). CONCLUSIONS: Our results indicate that B2 receptor blockade restores the attenuated autoregulation of medullary Doppler flux during sodium enriched diet. This, suggests that the kinin dependent impact of sodium on blood pressure regulation is mediated by modulations of medullary blood flow autoregulation.

Analysis of Variance↗
PubMed1998

Chaos in the cardiovascular system: an update.

Rhythmic changes of blood pressure, heart rate, and other cardiovascular measures have drawn the attention of several investigators, since these oscillations can shed light onto the activity of the underlying control network. The overwhelming proportion of circulatory variations, however, are not linear, i.e., they do not consist of perfectly rhythmic components. Thus, these fluctuations are more adequately analysed by non-linear techniques, most of which are adopted from chaos theory. A spotlight issue of 'Cardiovascular Research' (Vol. 31, 1996), focused on chaos in the cardiovascular system. This current review outlines today's understanding of this field by presenting the major discoveries and developments which have taken place since then.

Blood Vessels↗
PubMed1998

Correlation integral of blood pressure as a marker for exercise intensities.

The purpose of this study was to test the hypothesis that the correlation integral technique detects altered regulation of cardiovascular function during graded treadmill exercise. Arterial blood pressure (BP) was measured via telemetry before and during graded treadmill exercise in Sprague-Dawley rats. During treadmill running at mild, moderate, and heavy exercise intensities, the slope of the correlation integrals (SCI) continuously increased from 5.45 +/- 0.17 to 7.12 +/- 0.18, 7.92 +/- 0.23, and 8.40 +/- 0.23, respectively. However, corresponding changes in pulse interval, blood pressure, and systolic blood pressure with increasing workload were not consistently observed. Low-frequency, midfrequency, and high-frequency powers of BP were not different between adjacent exercise grades; only the low-frequency component of pulse interval was different between resting state and mild exercise, and BP variance was significantly different between mild and moderate grades. Comparison of the SCI values with those obtained from surrogate data sets suggests that these differences originate mainly from nonlinear components in the cardiovascular control system. These findings support the hypothesis that SCI detects alterations in cardiovascular regulation associated with graded exercise. Furthermore, SCI may be superior to linear techniques in detecting altered regulation with changing exercise intensities.

Animals↗
PubMed1998

Blood pressure variability and urine flow in the conscious dog.

Pressure-dependent urine production is considered to be a major factor in long-term blood pressure control. The phenomenon has been well characterized for fixed levels of renal perfusion pressure (RPP), but the influence of physiological fluctuations in RPP and spontaneous variations in renal blood flow (RBF) on short-term urine flow (UV) remain unclear. To clarify this issue, we studied the interdependence of RPP, RBF, and UV in 13 conscious foxhounds during a single-step pressure reduction, under normal conditions, and with induced pressure changes. Reducing RPP in a single step to approximately 80 mmHg revealed short response times of RBF (0.4 +/- 0.1 s, n = 7) as well as of UV (8.1 +/- 0.8 s, n = 7). Under control conditions, UV was coupled with spontaneous variations of RBF (r = 0.94, P < 0.001), in contrast to RPP, which showed no significant correlation with UV (r = 0.09, P = NS). To discern the pressure and blood flow dependency of UV at a reduced RPP, we induced 0.9-mHz blood pressure oscillations (80 +/- 10 mmHg), which phase shifted RPP and RBF. Conversely, under these conditions, UV was dependent on RPP (r = 0.95, P < 0.001). These results suggest that spontaneous fluctuations in RBF around a normal baseline level lead to concomitant changes in urine production, in contrast to physiological short-term oscillations in RPP, which are not correlated to changes in UV. However, during induced oscillations of perfusion pressure, the blood flow dependence was no longer observed and UV was entirely pressure dependent.

Animals↗
PubMed1997

Endogenous nitric oxide buffers blood pressure variability between 0.2 and 0.6 Hz in the conscious rat.

Shear stress is a potent stimulus for the formation and release of nitric oxide (NO). It seems, therefore, possible that a short-term increase in arterial blood pressure (ABP), which leads to a concomitant rise in endothelial shear stress, enhances NO release. The latter elicits a relaxation of vascular smooth muscle cells that, in turn, counteracts the initial rise in blood pressure (BP). Thus this chain of events may constitute a negative feedback loop reducing BP variability (BPV). To test this hypothesis, BP-time series were determined via telemetry in freely moving conscious Sprague-Dawley rats. Because it was reported recently that NO effects on ABP are more pronounced in females, the experiments were performed on 2 groups consisting of 10 female and 11 male animals. This was done under control conditions and after fixing NO plasma levels via an intravenous bolus of 15 mg/kg body wt N(G)-nitro-L-arginine methyl ester together with a continuous infusion of nitroprusside (15 +/- 0.8 microg/min). This combined infusion maintained mean ABP and heart rate at physiological levels, thus avoiding as much as possible interferences with other reflexes, e.g., the baroreflex. To quantitate BPV, fast Fourier transforms of the BP-time series were determined. The absolute power in the frequency range below 1 Hz increased during fixed NO to approximately 350% vs. control animals (female control, 2.1 x 10(9) +/- 1.5 x 10(8) mmHg2 vs. fixed NO, 8.0 x 10(9) +/- 1.3 x 10(9) mmHg2, P < 0.005; male control, 3.4 x 10(9) +/- 4.6 x 10(8) mmHg2 vs. fixed NO, 8.3 x 10(9) +/- 2.0 x 10(9) mmHg2, P < 0.05). This was mainly caused by a substantial rise in the power ranging from 0.2 to 0.6 Hz, which increased roughly fourfold in both females and males. It is concluded that the NO system is a potent buffer of spontaneous BP oscillations in the freely moving rat. This system is most efficient in buffering frequencies within the range of 0.2-0.6 Hz and shows no gender-specific differences with respect to its BP buffering capacity.

Animals↗
PubMed1997

Noninvasive analysis of renal artery blood flow dynamics with MR cine phase-contrast flow measurements.

It was the aim of this study to quantify the measurement of pulsatile flow in the renal artery with the noninvasive magnetic resonance cine phase-contrast (MRCPC) method and combine it with the simultaneous assessment of pulsatile flow with a transit-time ultrasound (TTUS) flowmeter. In seven foxhounds with a chronically implanted precalibrated TTUS flow probe, MRCPC flow measurements were made in the renal artery with a temporal resolution of 32 ms. Mean and pulsatile flow signal were compared by the simultaneous ipsi- or contralateral measurement of the renal blood flow signal by both methods (TTUS and MRCPC). In addition, comparative MRCPC and TTUS flow measurements were made with artificial renal artery stenosis and after the administration of angiotensin II. The mean flow data assessed by the noninvasive MRCPC flow measurements showed an excellent correlation with corresponding TTUS recording (r = 0.99). The MRCPC flow signal displayed a waveform of the renal artery flow profile that was very similar to the TTUS flow pulse. The hemodynamic changes induced by angiotensin II or due to renal artery stenosis were also reliably detected by MRCPC. MRCPC provides a reliable noninvasive method for the quantification of mean blood flow and the assessment of the pulsatile flow signal in the renal artery and proves to be sensitive to hemodynamic changes of pathophysiological importance. Alternatively, the method may be used for studies in physiology that demand a noninvasive approach.

Angiotensin II↗