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Biomedical subjects

S E Ricksten

Publications and source records attributed to S E Ricksten.

At least 91 records · Page 5Linked to original sources
PubMed1986

Sympathetic nerve activity and central haemodynamics during mechanical ventilation with positive end-expiratory pressure in rats.

The aim of this study was to examine the effects of mechanical ventilation with increasing levels of positive end-expiratory pressure (PEEP) on sympathetic nerve activity (SNA), cardiac output (CO), stroke volume (SV), heart rate (HR), central blood volume (CBV), total peripheral resistance (TPR), mean arterial pressure (MAP), pulse pressure (PP) and right and left atrial transmural pressure in chloralose anaesthetized rats before and after vagotomy. Changing ventilatory pattern from spontaneous breathing (SB) to artificial ventilation with 10 cm H2O PEEP in intact animals caused a significant fall in CO, SV and CBV (42, 48 and 17%, respectively) and an increase in SNA, HR and TPR (90, 13 and 83%, respectively). The MAP increased slightly but significantly from 103 +/- 4 to 107 +/- 4 mmHg while PP decreased from 48 +/- 2 to 37 +/- 3, from spontaneous breathing (SB) to 10 cm H2O PEEP. Transmural left atrial pressure decreased significantly from 4.5 +/- 0.3 to 3.0 +/- 0.4 mmHg. After vagotomy, MAP and CO were significantly lower at 10 cm H2O PEEP and PP and SV were significantly lower at all levels of positive end-expiratory pressure than the corresponding prevagotomy values. In spite of a greater fall in MAP and PP during PEEP after vagotomy, the absolute and relative increase of SNA was significantly lower compared to corresponding prevagotomy values. We conclude that reflex cardiovascular adjustments elicited by ventilation with PEEP are not solely due to unloading of arterial baroreceptors as has been claimed by others. Unloading of cardiac receptors with tonically active inhibitory afferents in the vagi is probably also of great importance for the excitation of the sympathetic nervous system during mechanical ventilation with PEEP.

Animals↗
PubMed1986

Effects of periodic positive airway pressure by mask on postoperative pulmonary function.

Postoperative pulmonary complications, alveolar-arteriolar oxygen difference ([A-a]O2-diff), peak expiratory flow (PEF) and forced vital capacity (FVC) were compared in patients using continuous positive airway pressure (CPAP) and positive expiratory pressure (PEP) administered by face mask against those of a control group using a deep-breathing device (Triflo). Forty-three consecutive, randomized patients undergoing elective upper abdominal surgery were included. CPAP, PEP and Triflo were administered for 30 consecutive breaths in every waking hour for three days postoperatively. The (A-a)O2-difference increased equally and significantly in the three groups after surgery, reaching a maximum on the first postoperative day. After this day, however, (A-a)O2-diff decreased in the CPAP and PEP groups, being significantly lower in the PEP group compared to the control group, two days postoperatively (p less than 0.05) and significantly lower in both the PEP and CPAP groups three days postoperatively (p less than 0.001 and p less than 0.05, respectively.) PEF did not differ significantly between the groups before or after surgery, while FVC was significantly higher in the PEP and CPAP groups, compared to control, on the third postoperative day (p less than 0.05). Atelectatic consolidation was observed in six of 15 patients in the control group three days postoperatively, the incidence being significantly lower in both the PEP group (0 of 15, p less than 0.001) and the CPAP group (one of 13, p less than 0.05). We concluded that periodic face mask administration of CPAP and PEP are superior to deep breathing exercises with respect to gas exchange, preservation of lung volumes and development of atelectasis after upper abdominal surgery. We also conclude that the simple and commercially available PEP mask is as effective as the more complicated CPAP system.

Abdomen↗
PubMed1986

On the role of atrial natriuretic peptide in cardiovascular regulation in the spontaneously hypertensive rat.

Atrial natriuretic peptide ANP(1-23) reduced mean arterial pressure (MAP), cardiac output (CO), central blood volume (CBV) and stroke volume (SV) when given i.v. (100 pmol/min) to spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). In SHR, total peripheral resistance (TPR) was significantly lowered. The major cause of the fall in blood pressure in WKY was reduction in CO and in SHR reduction in TPR. Acute 20% volume expansion increased plasma immunoreactive ANP (IR-ANP) in WKY as well as in SHR. However, the ANP release in SHR was blunted compared with WKY. After chronic high salt intake, ANP release in SHR was even further reduced in relation to an acute volume load. We conclude that the release of ANP as well as the haemodynamic responses to exogenous ANP is altered in SHR.

Animals↗
PubMed1985

Plasma atrial natriuretic peptide and haemodynamics in conscious normotensive and spontaneously hypertensive rats after acute blood volume expansion.

The atrial natriuretic peptides (ANP) are a family of newly discovered peptides which are released from atrial tissue and have potent diuretic/natriuretic, vasodilating and aldosterone inhibitory properties. Plasma concentration of ANP was measured and related to haemodynamic changes after acute blood volume expansion (10 and 20%) in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Acute blood volume expansion resulted in an increase in central (CBV) and peripheral blood volume (PBV), central venous pressure (CVP), stroke volume (SV) and cardiac output (CO), while total peripheral resistance (TPR) and heart rate (HR) were decreased. Mean arterial pressure (MAP) was unchanged. There were larger increases in CBV, CVP and CO in SHR than in WKY rats. In contrast, the increase in PBV and the decrease in HR were more marked in the WKY rats. Basal plasma ANP concentrations were similar in both groups. Blood volume expansion caused a linear increase in plasma ANP in the WKY rats, while the increase in plasma ANP concentration was attenuated in the SHR. It is concluded that acute blood volume expansion is more centralized in the SHR than in the WKY rats. Interestingly, the ANP release in response to blood volume expansion seems to be attenuated in SHR compared with WKY rats, as maximal plasma ANP concentrations were found at 10% volume load.

Animals↗
PubMed1984

Renal sympathetic activity in spontaneously hypertensive rats and normotensive controls, as studied by three different methods.

Recordings of sympathetic activity from multifibre preparations of renal nerves have produced conflicting results concerning the presence or absence of an increased sympathetic discharge in spontaneously hypertensive rat (SHR) compared to normotensive Wistar-Kyoto rats (WKY). Therefore, recordings of single fibre activity to the kidney were performed in anesthetized SHR and WKY in comparison with multifibre recordings in conscious, undisturbed rats. A new method of estimating sympathetic discharge by analyzing the variability of "cycle activity" in multifibre nerve recordings was also used. The average nerve activity in a great number of cardiac cycles was then expressed in relation (in per cent) to the nerve activity in a small number of cardiac cycles with the highest and lowest nerve activity in each rat. Single fibre recordings showed a significantly higher sympathetic activity to the kidneys in SHR (3.8 +/- 0.3 Hz) than in WKY (1.7 +/- 0.2 Hz; p less than 0.001). Also average "cycle activity" was significantly higher in conscious SHR (34 +/- 1%) than in WKY (26 +/- 2%, p less than 0.01). This was due to the larger number of cardiac cycles in SHR with high sympathetic activity while WKY showed more of "silent" cardiac cycles which lacked nerve impulses. Further, the recordings of rectified multifibre renal nerve activity also showed an elevated sympathetic activity in conscious SHR rats. The increased renal sympathetic activity appears to reflect the "primary" central nervous "hyperreactivity" characterizing SHR hypertension. It is suggested that the increased renal sympathetic activity may be of particular importance for the development of primary hypertension in SHR and perhaps also in man.

Animals↗
PubMed1984

Interaction between "mental stress" and baroreceptor reflexes concerning effects on heart rate, mean arterial pressure and renal sympathetic activity in conscious spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) were compared concerning the interactions between cortico-hypothalamic alerting responses and baroreflex influences on neurogenic cardiovascular control. For this purpose mean arterial pressure (MAP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were continuously recorded during night time in conscious, otherwise undisturbed rats. Baroreceptor sensitivity was assessed as percentage HR and RSNA reductions per mmHg MAP elevation when a standardized phenylephrine infusion was performed. A state of acute "mental stress" could be induced by a likewise standardized sudden blowing of air. These two opposing influences on neurogenic cardiovascular control were also experimentally superimposed in various ways and the effects on MAP, HR and RSNA followed. During "rest" RSNA was higher in SHR than in WKY and it also increased more during "mental stress". The baroreflex sensitivity was clearly reduced in SHR and WKY concerning HR reduction (0.44 +/- 0.06 vs. 0.78 +/- 0.08%/mmHg; p less than 0.01) but not so concerning RSNA, which was similar in SHR and WKY (2.6 +/- 0.2 vs. 2.9 +/- 0.4%/mmHg). If expressed (HR + 1 +/- 3%; p less than 0.025 vs. SHR and RSNA + 11% +/- 10, p less than 0.01 vs. SHR). These results) (0.10 +/- 0.02 vs. 0.06 +/- 0.01 microV/mmHg; p less than 0.12). Also single fibre recordings in anaesthetized rats showed the same principle difference between SHR and WKY.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Spontaneous variations in arterial blood pressure, heart rate and sympathetic nerve activity in conscious normotensive and spontaneously hypertensive rats.

In the present study we have recorded spontaneous variations in mean arterial blood pressure (MAP), heart rate (HR) and mean rectified splanchnic nerve activity (SNA) in conscious undisturbed normotensive Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). The variability in blood pressure was not significantly different but HR variability tended to be lower in SHR. The variability in SNA expressed as % change from mean value was not significantly different between SHR and WKY. By computer techniques the correlation between HR, MAP and SNA could be calculated during spontaneous variations of these parameters. The slope of the regression line correlating HR and SNA was significantly steeper in SHR than in WKY (0.73, 0.47 resp.). Thus a certain change in HR was associated by a greater change in SNA in SHR compared with WKY. Spontaneous changes in SNA could be divided in principally two different patterns. One typical pattern was a rise in SNA in parallel with a drop in MAP. This pattern was most likely triggered by the arterial baroreceptors and was called a "baroreceptor-pattern". Marked spontaneous excitations in SNA and HR was also observed during natural behaviours such as eating, drinking and explorative behaviour, a so called "centrally mediated pattern".

Animals↗
PubMed1983

Diastolic properties of the hypertrophied left ventricle in spontaneously hypertensive rats.

The influence of myocardial hypertrophy on left ventricular volume compliance was studied in vitro in isolated hearts of 4 and 19 month old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). In both SHR groups diastolic volume compliance was similar to that in the controls, despite the presence of left ventricular hypertrophy. This seems to be mainly due to an altered geometric situation, since with increased wall thickness to internal radius ratio (w/ri), which was at hand, the less are outer myocardial layers stretched at a given increase in ventricular volume. This may imply that these layers will only little interfere with luminal distension (and thereby with diastolic volume compliance) in SHR. It was also observed that the progressive increase of ventricular hypertrophy from 4 to 19 months of age did not further increase w/ri in SHR, indicating an increase in overall ventricular size with age. Left ventricular end diastolic pressure (LVEDP) was also measured in conscious 5 week and 4 month old SHR compared with matched controls. LVEDP increased with the development of hypertension and was significantly elevated in 4 month old SHR. This will increase also the average diastolic pre-stretch of the SHR left ventricle and mobilize the "Starling mechanism" to maintain a normal stroke volume against the increased afterload for the heart in established hypertension. This seems particularly important since the hypertrophic w/ri increase (about 20%) is smaller than the great elevation of mean arterial pressure (40-50%) in SHR.

Age Factors↗
PubMed1983

Structurally based changes of renal vascular reactivity in spontaneously hypertensive and two-kidney, one-clip renal hypertensive rats, as compared with kidneys from uninephrectomized and intact normotensive rats.

Renal vascular beds from spontaneously hypertensive rats (SHR) at different stages of hypertension, from two-kidney, one-clip renal hypertensive rats (RHR) and from uninephrectomized rats (UNR) were in constant-flow, paired perfusions compared with kidneys from normotensive control rats (NCR) concerning vascular smooth muscle sensitivity to noradrenaline (NA) and resistance vessel reactivity, as reflected by the position, respectively the shape, of the dose-resistance response curves. None of these kidney variants differed significantly from controls concerning smooth muscle sensitivity to NA during in vitro perfusion. However, both the steepness and maximal pressor responses of the renal resistance curves increased progressively with age in SHR, to become ultimately much enhanced when related to age-matched controls. It suggests a well preserved smooth muscle contractility and a progressive elevation of the average wall/lumen ratio in the SHR renal resistance vessels. Also the untouched, "high-pressure" RHR kidneys showed increased vascular reactivity, while it was somewhat reduced in the clipped, "low-pressure" RHR kidneys and unchanged in the hypertrophied but normotensive UNR kidneys. These results, when combined with other findings concerning renal vascular design (Göthberg & Folkow 1982a), illustrate how the renal resistance vessels readily adapt structurally to hypertension, hypotension, kidney hypertrophy and also with age, and in directions which tend to chronically "autoregulate" glomerular blood supply and filtration.

Age Factors↗
PubMed1983

Renal denervation and sodium balance in young spontaneously hypertensive rats.

In 7-week-old male, spontaneously hypertensive rats (SHR) and matched normotensive control rats, Wistar Kyoto Rats (WKY), a bilateral renal denervation was performed. In two additional groups of rats a sham denervation was done (SHRS, WKYS). The animals were then kept in metabolic cages during a 10-day period during which sodium intake, urine volume, urinary sodium excretion, fecal sodium excretion, urinary aldosterone excretion and plasma renin activity were determined. Fractional urinary excretion of sodium was higher in the denervated SHR (p less than 0.1) and WKY (p less than 0.05) during the first 3 days after denervation, but during the following 3-day periods no difference between denervated and sham-operated groups was noted. The difference in fractional urinary excretion of sodium initially was due to a diminished urinary sodium excretion in the sham-operated groups since both SHRS and WKYS exhibited a significant increase between the first and the last 3-day period. Urine volume increased significantly in both SHR and WKY after denervation. Urinary aldosterone excretion on the 7th day after denervation was significantly lower in SHR compared to WKY, but there was no significant difference between the denervated and sham-operated groups. PRA was also significantly lower in SHR but no significant decrease was seen after denervation.

Aldosterone↗
PubMed1983

Interaction between mental stress and baroreceptor control of heart rate and sympathetic activity in conscious spontaneously hypertensive (SHR) and normotensive (WKY) rats.

Spontaneously hypertensive (SHR) and Wistar-Kyoto rats (WKY) were compared with regard to the interaction between cortico-hypothalamic alerting responses and the baroreflex influences on neurogenic cardiovascular control. Baroreceptor sensitivity was assessed as heart rate (HR) and renal sympathetic nerve activity (RSNA) reduction per mmHg mean arterial pressure (MAP) increase by phenylephrine infusion. Response to 'mental stress' was studied. Addition of 'mental stress' during baroreceptor activation (30 mmHg MAP increase) was also performed. RSNA was higher in SHR than in WKY during rest and increased more during stress. Baroreflex sensitivity was reduced in SHR compared with WKY concerning HR (0.44 +/- 0.06 versus 0.78 +/- 0.08%/mmHg). Percentage RSNA reduction was similar, while RSNA reduction appeared greater in SHR in comparison with WKY (0.10 +/- 0.02 and 0.06 +/- 0.01 microV/mmHg, P less than 0.12). During baroreflex activation 'mental stress' increased both HR (+24 +/- 7%) and RSNA (+114 +/- 21%) in SHR with almost no changes in WKY. The results suggest an increased cortico-hypothalamic activity in SHR, which is clearly augmented during 'mental stress' and readily overcomes baroreflex inhibitory influences on sympathetic activity.

Animals↗
PubMed1982

Sodium balance during development of hypertension in the spontaneously hypertensive rat (SHR).

Sodium balance was studied in 7 and 16 week old male spontaneously hypertensive rats (SHR), in matched normotensive Wistar rats (NCR) and in Wistar Kyoto rats (WKR). The animals were placed in metabolic cages and given diets with either normal sodium content (5.35 mmol sodium/100 g food) or with a sodium content 3 or 10 times the normal. Whether on normal or increased sodium diet we did not observe any increased sodium retention in either SHR age group. However, in both SHR groups urinary sodium excretion was correspondingly increased compared with the controls. This shift of sodium excretion from kidneys to gastrointestinal tract in SHR did not reflect any 'primary' inability of the SHR kidneys to excrete sufficient sodium amounts since on high sodium diet they excreted the increased sodium load as readily as the normotensive controls. The present results do not support the concept that a primary renal retention of sodium and water should be of pathogenetic importance for the SHR variant of primary hypertension.

Age Factors↗
PubMed1981

Renal nerve activity and exaggerated natriuresis in conscious spontaneously hypertensive rats.

Exaggerated natriuresis upon volume loading occurs in both human and animal hypertension and is mainly due to suppressed tubular reabsorption. To explore whether altered renal sympathetic activity contributes to this response, conscious male spontaneously hypertensive rats (SHR) were exposed to isotonic saline loading in comparison with normotensive male Wistar Kyoto rats (WKR). After a 60 min control hydropenic period, during which mean arterial pressure, heart rate, renal sympathetic nerve activity and urinary sodium excretion were followed, a 60 min period of intravenous volume expansion with isotonic saline (0.2 ml/min X 100 g b.w.) was started followed by a 60 min hydropenic recovery period. Already during the control period sodium excretion was significantly higher in SHR. During the volume load and subsequent recovery period a clearly exaggerated natriuresis occurred in SHR compared with WKR. Further, volume loading reduced renal sympathetic nerve activity in all animals, but significantly more in SHR. Moreover, volume loading reduced mean arterial pressure and heart rate in both groups. It is suggested that the accentuated reflex inhibition of renal sympathetic activity in SHR upon volume loading emanates from cardiac mechanoreceptors and partly explains the exaggerated natriuresis in SHR. This augmented "volume' reflex response is probably due to reduced systemic venous compliance in SHR with a consequently increased central filling and cardiac receptor activation.

Animals↗
PubMed1981

Peripheral and central vascular compliances in conscious normotensive and spontaneously hypertensive rats.

Changes of left atrial (LAP) and right atrial pressure (RAP) upon 10% and 20% blood volume expansion were studied in conscious spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKR) with intact nervous cardiovascular control. In a separate series the changes of central (CBV) and peripheral (PBV) blood volumes upon similar increases of total blood volume (TBV) were measured as well, throughout using male, adult SHR and WKR in both series. During volume expansion both LAP and RAP increased significantly more in SHR than in WKR, as did CBV, while PBV increased significantly less in SHR than in WKR. Total "effective' vascular compliance, defined as delta TBV/delta RAP, was significantly lower in SHR. From the two series of measurements central (CBV/LAP) and peripheral (PBV/RAP) vascular compliances could be separately deduced. Central vascular compliance was nearly 50% lower in SHR than in WKR. However, "unstressed' volume of the peripheral compartment appeared to be rather normal in SHR compared to WKR. It is therefore suggested that the decreased total vascular compliance seen in essential hypertension and in SHR is mainly due to a decreased distensibility of the systemic capacitance vessels.

Animals↗
PubMed1980

Distensibility of the left atrial wall in spontaneously hypertensive rats compared with that in normotensive Wistar-Kyoto rats.

1. The cardiac mechanoreceptors, which in rats are mainly located in the left atrial wall, are reset in spontaneously hypertensive rats. The atrial pressure has to be almost twice as high in spontaneously hypertensive rats as in normotensive controls to produce similar receptors activations, as is apparent from previous studies. 2. The present study was performed to investigate whether this resetting is due to decreased distensibility of left atrial walls in the spontaneously hypertensive rats. 3. Static load-length relationships were investigated in vitro on left atrial strips, and pressure-volume relationships were studied on isolated left atria from spontaneously hypertensive and normotensive Wistar-Kyoto rats. 4. The force per cross-sectional area exerted during a relative length increase of 80% was significantly greater in spontaneously hypertensive rats. The dynamic but not in the static distensibility was significantly lower in these animals. 5. The decreased dynamic distensibility of left atrial walls in spontaneously hypertensive rats can at least partly explain the resetting of atrial receptor function.

Animals↗
PubMed1980

Reflex inhibition of sympathetic activity during volume load in awake normotensive and spontaneously hypertensive rats.

The reflex inhibition of the sympathetic activity in the splanchnic nerves was recorded upon volume expansion with blood in awake spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKR) at an age of 16-20 weeks. At 10% blood volume expansion SHR showed a significantly greater nerve inhibition (43%) in comparison with WKR (33%). This augmented reflex response was not caused by the arterial baroreceptors, because the sensitivity of the arterial baroreceptor reflex arch, if anything, tended to be lower in SHR and the increase in arterial blood pressure upon volume load was also lower in SHR. It is suggested that the reason for this increased reflex inhibition in SHR is an augmented low pressure receptor response. The mechanism behind this is discussed. The most likely explanation is a decreased distensibility of the venous system, the systemic and/or the pulmonary veins.

Adrenergic Fibers↗