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Biomedical subjects

P Friberg

Publications and source records attributed to P Friberg.

At least 145 records · Page 8Linked to original sources

Sympathetic and parasympathetic influence on blood pressure and heart rate variability in Wistar-Kyoto and spontaneously hypertensive rats.

The relative influence of sympathetic and parasympathetic nervous control of heart rate and heart rate variability, of mean arterial pressure (MAP) and MAP variability was investigated in young spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). An on-line computerized system was used for continuous intra-arterial measurements of MAP and heart rate every 2.5 min in freely moving rats with indwelling arterial catheters. Variability was expressed as the standard deviation in each rat. Heart rate and MAP showed clear diurnal rhythms, both in WKY and SHR. Blood pressure variability was clearly higher in SHR than in WKY, both during dark active hours and during light hours of relative sleep, and it did not change in response to either beta-adrenoceptor or vagal blockade. Structural vascular changes with the consequent increase in vascular reactivity may be one explanation for the elevated blood pressure variability in SHR. Heart rate variability was clearly reduced in SHR compared with WKY. This may be due to a reduced tonic vagal discharge in SHR, whereby a vagally mediated tachycardia is eliminated. The vagal withdrawal is part of the defence reaction, which is more easily elicited in SHR than in WKY.

Animals↗

Mechanisms behind myocardial depression in rat renal hypertension.

Cardiac function in rat renal hypertension has been shown repeatedly to be depressed. The reason for this impairment has not been fully understood, although cardiac hypertrophy and increased collagen content have been claimed as possible causes. To further unravel the mechanisms underlying the deterioration of left ventricular function in rat renal hypertension, we investigated cardiac function, myocardial morphology, myosin iso-enzymes, plasma renin activity and levels of myocardial high-energy compounds in hearts from rats exposed to renal and reversed renal hypertension. Maximal cardiac function was unaltered in hearts exposed to antihypertensive therapy from the time of renal artery clipping compared with untreated hypertensive rats. The observed alterations of iso-enzyme pattern, plasma renin activity levels and myocardial morphology among the groups showed to be of less importance with respect to cardiac performance. Together with previous results from our laboratory, the present findings suggest that some negative inotropic agent of renal or non-renal origin is released during two-kidney, one clip renal hypertension, which counteracts the enhanced left ventricular performance induced by cardiac hypertrophy.

Adenine Nucleotides↗

Effects of voluntary physical exercise on cardiac function and energetics in spontaneously hypertensive rats.

The influence of voluntary physical exercise in running wheels on myocardial function, cardiac oxygen utilization and cardiovascular response to emotional stress was analysed in the spontaneously hypertensive rat. After 6 weeks of exercise, a significant increase in resting cardiac output was found, which was due to an elevation of stroke volume. However, voluntary training for 12 weeks had no effect on resting blood pressure or on the blood-pressure response to mental stress. Cardiac function was also examined in vitro. At a low aortic diastolic pressure, it was markedly augmented in trained spontaneously hypertensive rats. At high aortic diastolic pressure, maximal cardiac function was similar in the two groups. Myocardial oxygen consumption (mumol min-1 g-1) for a given level of external work was reduced in trained, compared with non-exercised control spontaneously hypertensive rats. Chronic physical exercise thus greatly improved myocardial function at a subnormal perfusion pressure, suggesting better nutritional supply to the myocardium, probably created by an increased capillary surface area.

Animals↗

Newly detected molecules in dense interstellar clouds.

The last year or so has seen the identification of several new interstellar molecules, including C2S, C3S, C5H, C6H, and (probably) HC2CHO in the cold, dark cloud TMC-1; and the discovery of the first interstellar phosphorous-containing molecule, PN, in the Orion "plateau" source. Further interesting results include the observations of 13C3H2 and C3HD, and the first detection of HCOOH (formic acid) in a cold cloud.

Astronomical Phenomena↗

Methanol in dark clouds.

We report observations, for the first time, of the 2(0) - 1(0)A+ and E, 2(-1) - 1(-1) E, and 1(0) - 0(0)A+ lines of methanol (CH3OH) in three dark cold clouds, TMC1, L134N, and B335. The CH3OH emission is extended in these clouds and shows a complex velocity structure. Clear indications of non LTE excitation are observed in TMC 1. Estimated column densities are a few 10(13) cm-2. Although less abundant than formaldehyde (H2CO), methanol is almost an order of magnitude more abundant than acetaldehyde (CH3CHO), in these clouds. Dimethyl ether was searched for in L134N, to an upper limit of 4 10(12) cm-2 (3 sigma). Implications for dark cloud excitation and chemistry are discussed. A new, more accurate, rest frequency 96741.39(0.01) MHz is determined for the 2(0) - 1(0) A+ E line of methanol.

Acetaldehyde↗

Observations of OCS and a search for OC3S in the interstellar medium.

Observations of OCS and a search for OC3S are reported, with particular reference to cold dust clouds. OCS has been detected for the first time in dark clouds with a mean fractional abundance relative to hydrogen of approximately 3 x 10(-9); this is approximately 4 times greater than that observed for giant molecular clouds. This results is discussed in the context of molecule formation mechanisms. Observations of the J = 1 --> 0 transition of OCS indicate that this transition is amplifying the background continuum radiation in the direction of Sgr B2.

Astronomical Phenomena↗

Myocardial energetics and diastolic dimensions of the heart in experimental hypertension.

The present study examined changes in left ventricular design and function in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY), and in SHR exposed to voluntary physical exercise in running wheels (R-SHR) and their respective sedentary controls (C-SHR). End-diastolic volumes were obtained in vitro by determining the pressure-volume relationships of isolated hearts arrested in diastole. Cardiac function and myocardial oxygen consumption were also assessed in vitro by means of an antegrade working heart perfusion technique. Compared with WKY and C-SHR respectively, ordinary SHR and R-SHR had increased end-diastolic volumes, whereas the ratios between wall thickness and internal radius were relatively unchanged. Maximal cardiac performance was elevated in the structurally enlarged SHR heart compared with WKY, whereas it remained unchanged after chronic physical exercise. Long-term voluntary running in SHR caused an elevation of cardiac output due to an increased stroke volume, while arterial pressure was unaltered. The stimulus for the cardiac redesign to a structurally enlarged heart can probably best be explained by a chronic elevation in cardiac filling. Hence, enlarged left ventricles can then produce higher stroke volumes for given degrees of myocardial fibre shortenings. Thus, despite structurally enlarged left ventricles in SHR and in R-SHR and also increased arterial pressure in SHR compared with WKY (thereby elevating systolic wall stress), cardiac function was maintained and even augmented, which was not associated with an increase in total myocardial oxygen consumption.

Animals↗

Effect of spontaneous running on blood pressure, heart rate and cardiac dimensions in developing and established spontaneous hypertension in rats.

The effect of chronic voluntary exercise on resting blood pressure and heart rate was measured in two different age groups of spontaneously hypertensive rats (SHR). In the younger group, left ventricular dimensions were also measured. The younger group was 9 weeks old at the start of the experiment and was in a period of rapid blood-pressure rise. The older group, 13 weeks old at the start of the experiment, already had established hypertension. During a period of 6 weeks, the animals ran spontaneously in wheels mounted in their cages and reached a maximum of 6-7 km per 24 h. Age-matched, sedentary SHR were used as controls. Both groups of runners showed a decrease in body weight in comparison to controls. The younger runners exhibited a delayed onset of hypertension. They also showed a significantly increased left ventricular (LV) end-diastolic volume for every measured end-diastolic pressure between 7.5 mmHg and 20 mmHg (P less than 0.05). This suggests the development of a structural growth-dependent increase of the internal LV radius while LV weight and wall-to-lumen ratio were largely unaltered in younger runners compared with controls. In SHR with established hypertension, physical training did not reduce arterial blood pressure but heart rate was significantly lower than in the controls. These results thus indicate that an early onset of physical exercise in SHR may delay the development of hypertension. In addition, a more favourable cardiac design could also be seen.

Age Factors↗

Myocardial and vascular structural adaptation to chronic pressure overload.

Left ventricular (LV) function and end-diastolic dimensions were determined during antegrade and retrograde perfusions, respectively. Isolated hearts from spontaneously hypertensive rats (SHRs) and renal hypertensive rats and SHRs to which either feldopine, nifedipine, alpha-methyldopa, or a combination of felodipine and metoprolol was administered were used. Maximal cardiac function [cardiac output x (aortic pressure - left atrial pressure)] was elevated in SHRs, but depressed in those with renal hypertension. The diastolic pressure-volume relationships revealed eccentric rather than concentric LV hypertrophy in the SHRs. Renal hypertension in SHRs caused concentric LV hypertrophy. Antihypertensive therapy with calcium antagonists (but not with alpha-methyldopa) caused reduction of LV wall thickness, but increased LV end-diastolic volume (EDV). In SHRs, coronary flow was reduced at any given level of aortic pressure. At low aortic pressures (and hence, limited coronary perfusion), cardiac function was attenuated in SHRs. This reduction could be reversed by administration of antihypertensive therapy. These results suggest an improvement in maximal stroke work in SHRs as a result of eccentric hypertrophy which allows increased stroke volume for a given degree of myocardial shortening. Structural coronary vascular changes, which can be reversed by antihypertensive therapy, can limit coronary perfusion--and hence, cardiac performance--at low aortic pressures in SHRs. Maintenance of maximal cardiac function in treated SHRs, despite a reduction in LV wall thickness, may be due to an increase in LV end-diastolic volume.

Animals↗

Cardiac dimensions in spontaneously hypertensive rats following different modes of blood pressure reduction by antihypertensive treatment.

The present study examined changes in left ventricular design in spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats in response to different types of antihypertensive therapy. Blood pressure was reduced for 12 weeks by either peripheral vasodilators [hydralazine or felodipine (calcium antagonist)] or by sympatholytic drugs (alpha-methyldopa or metoprolol). End diastolic volumes (EDV) were obtained in vitro by determining the diastolic pressure-volume relationships of isolated perfused hearts, arrested in diastole by excluding calcium from the perfusate. Wall thickness (w) and internal radius (ri) were calculated from a ventricle considered as a spherical model. Compared with WKY, untreated SHR had elevated EDV and w. Vasodilator therapy, particularly felodipine, increased EDV but reduced w, while sympatholytic therapy with alpha-methyldopa reduced EDV in SHR. It is suggested that cardiac design is affected not only by the prevailing arterial pressure level which will affect w, but also by the haemodynamic situation. Vasodilators turn such a situation into one characterized by increased cardiac output and hence increased cardiac filling, whereas sympatholytic drugs by venodilatation will turn the haemodynamic situation towards a state characterized by reduced cardiac filling. Left ventricular EDV (ri) therefore seems to adapt to long-term filling conditions, while w adapts to bring w:ri ratio in balance with the pressure load.

Animals↗

Influence of long-term antihypertensive therapy on cardiac function, coronary flow and myocardial oxygen consumption in spontaneously hypertensive rats.

The relationships between cardiac performance, coronary flow, coronary vascular resistance at maximal vasodilatation and myocardial oxygen consumption were determined in isolated hearts from spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY) and from SHR given metoprolol (beta 1-selective blocker) and felodipine (selective calcium antagonist) for 35 weeks. A working heart perfusion system was used. An oxygen electrode allowed continuous measurement of oxygen tension in the venous coronary effluent. Blood pressure was reduced close to normal levels in treated SHR. Treatment also caused a substantial reduction of left ventricular weight. In both treated and untreated SHR, maximal cardiac performance, expressed as peak stroke volume, was enhanced above that of WKY at high perfusion pressures, while performance at low perfusion pressures was clearly reduced in the former groups. At a given workload, myocardial oxygen consumption (mmol O2/min per g) was reduced in both groups of SHR. This suggests a physiological structural adaptation to an elevated cardiac load in hypertension, where more myofibrils contribute to produce a given amount of work and therefore less oxygen is consumed per unit muscle mass. Coronary flow was reduced at any given perfusion pressure and oxygen extraction was increased in untreated SHR versus WKY. By causing regression of hypertensive structural vascular changes, treatment markedly increased coronary flow and correspondingly decreased oxygen extraction. Thus, by enhancing the myocardial nutritional supply with antihypertensive treatment, the reduced cardiac function at low perfusion pressure in untreated SHR was almost normalized.

Animals↗

Functional, morphological and metabolic characteristics of isolated hearts from normotensive and spontaneously hypertensive rats before, during and after renal hypertension.

It has been much discussed whether left ventricular hypertrophy (LVH) in hypertension implies improved or impaired cardiac performance, mainly because experiments in various hypertensive models have given controversial results. It has, for example, been suggested that increased collagen content may depress LV function both in renal and spontaneous hypertension (SHR) in rats. For such reasons cardiac performance was studied both in SHR and in normotensive control rats (NCR) before and during superimposed two-kidney, one clip Goldblatt hypertension, and also 1 week after reversal of hypertension by unclipping. The LV function of the isolated hearts was determined in an antegrade working heart perfusion system. Further, myocardial morphology, with regard to fibrous tissue infiltration and energy metabolic status, were evaluated in the renal hypertensive rats before and after unclipping. Compared with NCR, maximal cardiac performance was elevated in the hypertrophied SHR hearts, but depressed when renal hypertension was superimposed, even though this led to further LVH. However, one week after reversal of renal hypertension, when LVH was still considerable, cardiac function was increased well above the control level, even though the stores of high energy compounds and the content of myocardial fibrous tissue was almost the same as during renal hypertension. It is concluded that LVH generally enhances cardiac performance, but that concomitant renal hypertension exerts a cardio-depressive influence which can neither be ascribed to an increased fibrous tissue content nor to a reduced energy charge potential. It is therefore suggested that some negative inotropic agent of renal or extrarenal origin is released during two-kidney, one clip renal hypertension, which offsets the enhanced performance induced by the left ventricular hypertrophy.

Animals↗

The effects of varying sodium diets on haemodynamics and fluid balance in the spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) were given either 'low' (LNa; 0.5 mmol Na 100 g-1 food), 'control' (CNa; 12 mmol) or 'very high' (vHNa; 120 mmol) sodium diets from 5 to 13-14 weeks of age, to explore how these 240-fold variations in Na intake affected body weight, cardiac, renal and adrenal weights, overall water-electrolyte equilibrium and haemodynamic balance during rest, mental stress and blood loss. Body growth was retarded both in vHNa and LNa SHR presumably reflecting disturbed appetite due to the greatly altered dietary Na contents. Compared with CNa SHR, both cardiac and renal weights 100 g-1 body wt were slightly increased in vHNa and decreased in LNa SHR, with opposite changes of adrenal weights. Total body water, haematocrit and plasma Na-K levels were largely equal in the three groups. Furthermore, cardiac output (CO), stroke volume (SV) and central blood volume (CBV) did not differ significantly between groups; if anything, CO and SV were higher and CBV lower in vHNa and LNa SHR than in CNa SHR. However, while mean arterial pressure (MAP) was only marginally elevated in vHNa compared with CNa SHR, both MAP and total peripheral resistance (TPR) were lowered about 15% in LNa SHR with signs of increased sympathetic activity to the heart also during rest. Despite an apparently normal volume and cardiac output balance in LNa SHR, the latter changes suggest a disturbed neuro-hormonal cardiovascular control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cardiac design and pressure-volume characteristics of the left ventricle in normotensive (WKY) and hypertensive (SHR) rats after various dietary sodium treatments.

Normotensive (WKY) and hypertensive rats (SHR) from 5 to 13-14 weeks of age were given 'low' (LNa; 0.5 mmol Na 100 g-1 food), 'control' (CNa; 5 or 12 mmol), 'high' (HNa; 50 mmol) and in SHR also 'medium low' (mLNa; 2 mmol) and 'very high' (vHNa; 120 mmol) sodium diets, to explore how such 240-fold variations in Na intake affect cardiac design. This was assessed in isolated perfused, temporarily-arrested hearts by recordings of left ventricular (LV) diastolic pressure-volume relationships (P/V), LV and RV weights, and by calculations of the ratio between LV wall thickness and internal radius (w/ri), after in vivo recordings of awake mean arterial pressure (MAP) and heart rate (HR). In WKY, where MAP was the same in all diet groups, the HNa group showed an increased w/ri due to a 20% reduction of LV diastolic volume, with signs of reduced wall compliance compared with CNa. The LNa WKY showed less marked changes in the same direction. In the SHR LNa group, where MAP was lowered about 20 mmHg, LV diastolic volume was reduced nearly 20% at a modest w/ri increase, while HNa and Cna SHR had equal MAP, LV weights, P/V and w/ri relationships. However, in vHNa SHR, where MAP was elevated about 25 mmHg, the LV showed a mainly eccentric hypertrophy with 15% increase of diastolic volume at a slight increase of w/ri. These differentiated, and in WKY and SHR partially differing structural cardiac adaptations consequent to changes in Na intake, can hardly be ascribed only to the respective pre- and afterload alterations, suggesting that also altered neuro-hormonal profiles may have contributed with 'trophic' influences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Structural and functional adaptations within the myocardium and coronary vessels after antihypertensive therapy in spontaneously hypertensive rats.

The relationships between cardiac performance, coronary flow, minimal coronary vascular resistance and myocardial oxygen consumption (MVO2) were explored in isolated hearts from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) and in hearts from SHR given a combination of metoprolol and felodipine (selective calcium antagonist) for 35 weeks. Antihypertensive therapy markedly reduced arterial pressure and caused a substantial regression of left ventricular hypertrophy. An antegrade working-heart perfusion system was used, allowing measurements of stroke volume, coronary flow and MVO2 at varying pre- and afterloads. In untreated SHR cardiac function was reduced at low and enhanced at high perfusion pressure compared with WKY. Minimal coronary vascular resistance, which was greatly increased in SHR, was significantly reduced by treatment, allowing higher coronary flow for any given perfusion pressure and consequently a lower degree of oxygen extraction. In addition, at a given workload, MVO2 was reduced in both untreated and treated SHR. These results stress the importance of having adequate coronary perfusion within a hypertensive structurally redesigned coronary vascular bed in order to maintain cardiac performance. With antihypertensive therapy in SHR, an improved coronary flow capacity was created due to regression of the hypertensive vascular changes.

Animals↗

Tricarbon monoxide in TMC-1.

We report the measurement of three new lines of C3O in TMC-1. The observed peak antenna temperatures, appropriately corrected for atmospheric and telescope losses, are found to be consistent with a large velocity gradient radiative transfer model whose parameters span the range of standard values for this cloud. The derived fractional abundance for C3O is 1.4 x 10(-10), comparable with the results predicted from a model calculation based on a gas-phase ion-molecule reaction scheme. The results of negative searches for C3O in six other sources are not inconsistent with expected conditions in these clouds.

Astronomical Phenomena↗

Astronomical identification of the C3H radical.

The C3H radical, a linear carbon chain with a 2 pi electronic ground state, has been identified in the millimeter-wave spectra of two astronomical sources, IRC +10216 and TMC-1, and conclusively confirmed (accompanying Letter) in a laboratory glow discharge. In IRC +10216 four rotational transitions have been observed, three in the lower fine-structure ladder (2 pi 1/2) and one in the upper (2 pi 3/2), each a resolved or partially resolved lambda-doublet. In TMC-1, both lambda components of the lowest lying 3/2 --> 1/2 transition of the 2 pi 1/2 ladder have been observed, each with well-resolved hfs. In IRC +10216 the excitation of C3H is similar to that of SiCC: the rotational temperature Trot within the 2 pi 1/2 ladder is low (8.5 K), owing to rapid radiative decay, while Trot across the ladders is high (approximately 52 K) because interconnecting far-IR radiative transitions are only weakly permitted. The column density of C3H in IRC +10216 averaged over the estimated source diameter of 84" is 2.8 x 10(13) cm-2, an order of magnitude less than that of C2H and C4H. A determination of the spectroscopic constraints of C3H that permitted the entire radio spectrum of this molecule to be calculated to high accuracy has been derived from analysis of the combined astronomical and laboratory data presented in the accompanying Letter.

Astronomical Phenomena↗

The detection of acetaldehyde in cold dust clouds.

Observations of the 1(01) --> 0(00) rotational transitions of A and E state acetaldehyde are reported. The transitions were detected, for the first time in interstellar space, in the cold dust clouds TMC-1 and L134N, and in Sgr B2. This is also the first time acetaldehyde has been found in a dust cloud and is the most complex oxygen-bearing molecule yet known in this environment. We find a column density of 6 x 10(12) cm-2 in TMC-1, comparable to many other species detected there, and an approximately equal column density in L134N. In the direction of Sgr B2, the CH3CHO profile appears to consist of broad emission features from the hot molecular cloud core, together with absorption features resulting from intervening colder material. We also report the possible detection of HC9N toward IRC +10 degrees 216 through its J = 33 --> 32 transition. Implications for cold dust cloud chemistry and excitation are discussed.

Acetaldehyde↗