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Biomedical subjects

S E Ricksten

Publications and source records attributed to S E Ricksten.

106 records · Page 6Linked to original sources
PubMed1980

Distensibility of left atrium in normotensive and spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHR) left atrial mechanoreceptors are reset. Thus, left atrial pressure must be almost twice as high in SHR as in normotensive rats to produce comparable degrees of receptor activation and reflex sympathetic inhibition. The present study was performed to investigate whether this resetting is due to a decreased atrial distensibility in SHR. Static load-length relationships were therefore investigated on isolated left atrial strips from 11 pairs of male SHR and Wistar Kyoto rats (WKR). After each experiment the strips were fixed at a passive tension of 4 mN and the average wall thickness was determined histologically. Furthermore, pressure-volume relationships were studied on non-beating, isolated left atria from SHR and WKR. Distensibility was here defined as % volume increase when LAP was increased from 2.5 to 12.5 mmHg either rapidly (0.5--1 s, "dynamic" distension) or slowly (3 min, "static" distension). Atrial wall thickness did not differ significantly in SHR and WKR, but the passive force (mN) per cross sectional area exerted during elongation above 80% was greater (P less than 0.05) in SHR. Also the "dynamic", but not the "static" volume distensibility was significantly lower in SHR (P less than 0.01). The decreased dynamic distensibility of SHR left atrial walls can at least partly explain the resetting of the atrial receptors activated during the rapid filling phase.

Animals↗
PubMed1979

Cardiac reflexes in normotensive and spontaneously hypertensive rats.

Characteristics of left atrial receptors were studied in normotensive control (Wistar) and spontenaously hypertensive rats. The left atrial pressure was chronically elevated in spontaneously hypertensive rats and at the end of the expiratory phase was 10.3 mm Hg as compared with 4.6 mm Hg in normotensive control rats. The thresholds of the receptor endings were twice as high in the hypertensive as in the normotensive rats (10.2 and 4.6 mm Hg, respectively). In other experiments the reflex inhibition of renal sympathetic outflow was studied during plasma infusion in baroreceptor denervated normotensive and hypertensive rats was was inhibited at a lower left atrial pressure in the former. These differences are attirubted to decreased distensibility of the left atrium in spotaneously hypertensive rats. The reflex splanchnic nerve inhibition with volume load also was recorded in awake rats. At a 10 percent increase in blood volume, splanchnic outflow was more significantly decreased in spotaneously hypertensive than in normotensive rats. The mechanism underlying such a hyperreactive volume receptor response is unknown, but a less distensible venous system, centrally or peripherally, might be a contributing factor.

Animals↗
PubMed1979

Recordings of renal and splanchnic sympathetic nervous activity in normotensive and spontaneously hypertensive rats.

1. Recordings have been obtained from single sympathetic fibres to the left kidney in anaesthetized adult spontaneously hypertensive (SH) rats and Wistar-Kyoto normotensive (WK) rats. 2. Under control conditions SH rats had a mean sympathetic activity of 3.3 +/- SE 0.45 Hz and WK rats 1.6 +/- 0.23 Hz. During noradrenaline infusion single fibre discharge decreased gradually to low levels in both SH and WK rats. The absolute decrease in fibre activity/mmHg rise of arterial pressure was greater in SH rats than in WK rats, but the reverse was true when the discharge reduction was expressed as a percentage change. 3. Recordings have also been obtained from the left splanchnic nerve in awake SH and WK rats. Upon volume load with blood, in SH rats the sympathetic activity decreased significantly more than in WK rats. 4. Thus the sympathetic discharge to the kidneys is higher in SH rats than in WK rats. Upon volume load SH rats show an exaggerated reflex response, probably due to an augmented volume-receptor response.

Animals↗
PubMed1979

Apparent and true vascular resistances to flow in SHR and NCR kidneys as related to the pre/postglomerular resistance ratio.

In maximally vasodilated SHR and NCR kidneys, perfused with filtrable and non-filtrable perfusates, analyses have been performed concerning the extent of average renal tissue pressure (Pt) elevation which occurs upon glomerular filtration and causes passive autoregulation of flow. The results illustrate the great importance of distinguishing between 'apparent' (PA--PV/flow) and 'true' (PA--Pt/flow) renal resistance to flow. This is particularly so when the compared SHR and NCR renal vascular beds differ not only in true total renal resistance but also concerning the structurally determined ratio between the pre- and post-glomerular resistances. The combined results show that this ratio is considerably elevated in adults SHT kidneys because of structural vascular changes, which is perhaps the most efficient way of resetting the 'long term barostat function' of the kidneys in hypertension. It is also illustrated how the altered pre-/post-glomerular ratio in SHR in combination with Pt rises can so markedly distort the results of apparently precise in vitro comparisons of SHR and NCR renal vascular beds as to give entirely misleading results, with underestimations of the structurally based vascular hyperreactivity of the preglomerular section in SHR.

Animals↗
PubMed1979

Cardiac receptors with non-medullated vagal afferents in the rat.

The characteristics of 22 atrial receptors in 15 normotensive adult male Wistar rats were investigated. All the receptor afferents were included in the C-fibre group with conduction velocities from 0.4 to 1.2 m/sec. No atrial medullated receptors or ventricular C-fibre endings were found. Two receptors were located in right atrium and 2 receptors throughout left atrium. Upon elevation of the left atrial pressure the receptor discharge was markedly elevated with thresholds from 2.5 to 9 mmHg in mean left atrial pressure. Ten of the atrial receptors displayed a clear cardiac rhythmicity upon activation and the discharge correlated with the v-wave, indicating distension as the cause of receptor activation. The maximal firing rate in most receptors was very high (up to 70 Hz), but 8 receptors had maximal firing rates below 25 Hz. These low frequency receptors had higher threshold and showed a more irregular firing. Thus, there is a substantial population of atrial receptors with vagal non-medullated afferents in the rat heart and the thresholds for many of these receptors are so low that they are likely to be active during normal conditions.

Animals↗
PubMed1979

Inhibition of renal sympathetic nerve traffic from cardiac receptors in normotensive and spontaneously hypertensive rats.

The reflex inhibition of the sympathetic outflow to the kidney was examined during volume load with horse plasma in 6 normotensive rats (NCR) and 6 spontaneously hypertensive rats (SRH). The rats were anesthetized with chloralose and urethane. The arterial baroreceptors were denervated. The renal nervous inhibition was mediated via the vagal nerves and was mainly due to activation of receptors in the left side of the heart. The average thresholds in mean left artrial pressure for renal nervous inhibition was 5.4 mmHg for NCR and 9.2 mmHg for SHR indicating a clear resetting of the reflex arch in the hypertensive animal: The reason is probably a decreased distensibility of the wall of the left atrium due to a chronic elevation of left atrial pressure. This resetting of the atrial receptors in the hypertensive animals is probably of importance to allow an adequate filling pressure of the hypertrophied left ventricle and might also be of importance for the reflex neural control of renal function in these animals.

Adrenergic Fibers↗
PubMed1979

Performance of the hypertrophied left ventricle in spontaneously hypertensive rat. Effects of changes in preload and afterload.

Isolated hearts from adult spontaneously hypertensive rats (SHR; Okamoto 1969), with established hypertension, were investigated in an antegrade perfusion apparatus where preload and afterload could be varied independently. Frank-Starling curves were constructed at constant afterloads ranging from 50 mmHg to 150 mmHg. As earlier reported, the SHR hearts exhibited a rightward shift of their Frank-Startling relationships compared to those from the normotensive control hearts, though visible only at afterloads up to about 100 mmHg. At higher afterloads the SHR hearts performed significantly better then the NCR ones as their maximal stroke volume was significantly greater compared to that of controls. Thus, left ventricular hypertrophy obviously increases the work capacity of the heart, though at the cost of an altered Frank-Startling relation dependent on the reduced diastolic compliance. For such reasons the myocardial hypertrophy in established SHR hypertension must be considered a physiologic adaptation and not a degenerative phenomenon, though naturally degenerative processes may later become superimposed.

Animals↗
PubMed1979

Left atrial pressure in normotensive and spontaneously hypertensive rats.

The left atrial pressure in adult spontaneously hypertensive rats (SHR) of the Okamoto strain and normotensive control rat (NCR) was measured via chronically implanted catheters. In SHR left atrial pressure in end-expiration was more than twice as high (10.3 +/- 0.4 mmHg) as in NCR (4.6 +/- 0.3 mmHg). There was no difference in the intrapleural pressure between the two groups of rats, therefore the enhanced left atrial pressure in SHR represents a real rise in the diastolic filling pressure of its left ventricle. This is considered to be the most important compensation for the earlier reported rightward shift of the Frank-Starling curve in SHR (Hallbäck, Isaksson & Noresson 1975, Noresson et al. 1979a). Without this compensation the stroke volume would have been drastically reduced for the hypertrophied heart.

Animals↗
PubMed1979

Resetting of cardiac C-fiber endings in the spontaneously hypertensive rat.

The characteristics of 11 left atrial receptors in 9 adult male spontaneously hypertensive rats (SHR) were investigated. All the receptor afferents were non-medullated with conduction velocities from 0.5 to 1.5 m/s. Elevation of left atrial pressure during graded aortic occlusion always induced a marked increase in receptor discharge with maximal frequencies ranging from 29 to 70 Hz. The threshold for activation was from 7.5 to 13 mmHg in mean left atrial pressure (mean +/- S.E., 10.2 +/- 0.6 mmHg). Upon atrial distension all the receptors displayed a clear rhythmicity and the discharge correlated mainly with the v-wave, indicating distension as the cause of receptor activation. The relationship between the mean left atrial pressure and the frequency of discharge was constructed for all the receptors and compared with similar data obtained from normotensive control rats (NCR) (Thorén et al. 1979). It was then obvious that the left atrial receptors are reset in SHR probably secondarily to a decreased distensibility of the left atrium.

Afferent Pathways↗
PubMed1976

Hemodynamic consequences of resistance vessel rarification and of changes in smooth muscle sensitivity.

Alterations in resistance vessel design in form of an increased wall/lumen ratio appears to markedly influence the resistance control in primary hypertension (Folkow et al. 1973). The raised resistance has also been suggested to be a consequence of a rarification of resistence vessels or/and to an increased vascular smooth muscle sensitivity. Thus two series paired experiments were performed on matched normotensive rats, utilizing the responses of their hindquarter vascular beds during constant flow perfusion. In the first series, the precapillary resistance vessels section was first "rarified" by graded microplugging, thereby raising resistance at maximal dilatation about 50 per cent. Then the vascular responses to noradrenaline were studied to characterize the dose-response or "resistance curves". In the second series the vascular smooth muscle sensitivity to noradrenaline of one of the hindquarters was changed by infusion of phentolamine. The resistance responses were then recorded and the ensuing "resistance curves" compared. --These changes of resistance vascular architecture and vascular smooth muscle sensitivity, respectively, led to mutually different characters of the "resistance curves". Both of these differ, however, in virtually all important respects from those curves characterizing vascular beds of spontaneously or renal hypertensive rats.

Animals↗
PubMedDate not supplied

Vasodilator therapy after heart transplantation: effects of inhaled nitric oxide and intravenous prostacyclin, prostaglandin E1, and sodium nitroprusside.

BACKGROUND: Vasodilator therapy is frequently needed to treat pulmonary hypertension after heart transplantation. In the present study, the effects of intravenous sodium nitroprusside, prostacyclin, prostaglandin E1, and inhaled nitric oxide (5, 10, and 20 parts per million) on central hemodynamics, right ventricular function, and pulmonary selectivity were evaluated shortly after heart transplantation. METHODS: Hemodynamic measurements were made after surgery in the intensive care unit. The intravenous vasodilators were compared at equipotent infusion rates. Effects of inhaled nitric oxide were measured after 10 minutes inhalation at each dose level. RESULTS: Cardiac output, stroke volume, right ventricular end-diastolic volume, and central filling pressures were highest with prostacyclin (16 +/- 2 ng/kg/min) compared with both prostaglandin E1 (202 +/- 27 ng/kg/min) and sodium nitroprusside (1.0 +/- 0.2 microgram/kg/min). Systemic and pulmonary vascular resistance were lowest with prostacyclin. None of the intravenous vasodilators induced a selective pulmonary vasodilation. In contrast, nitric oxide inhalation induced a selective decrease in pulmonary vascular resistance, with no change in systemic vascular resistance. Cardiac output increased with nitric oxide, whereas mean pulmonary arterial pressure, transpulmonary pressure gradient, and central venous pressure decreased, with the most pronounced effect at an inhaled concentration of 20 parts per million. CONCLUSIONS: Prostacyclin is the best choice for intravenous vasodilator therapy after heart transplantation. However, inhaled nitric oxide is the only selective pulmonary vasodilator, which should be used in cases of pulmonary hypertension and severe right ventricular failure associated with systemic hypotension.

Administration, Inhalation↗
PubMedDate not supplied

Inhaled nitric oxide in the evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

The reversibility of elevated pulmonary vascular resistance in heart transplant candidates is currently evaluated with intravenous vasodilators. The aim of this study was to evaluate the effects of increased concentrations of inhaled nitric oxide (20, 40, and 80 ppm) on central hemodynamics and right ventricular function in heart transplant candidates with elevated pulmonary vascular resistance (> 2.5 Wood units). Comparison was made with intravenous vasodilators, sodium nitroprusside, and prostacyclin in doses that lowered the mean arterial pressure by about 15%. Inhalation of nitric oxide did not change systemic or pulmonary arterial pressure, cardiac output, right ventricular function, or systemic vascular resistance. Pulmonary capillary wedge pressure increased and transpulmonary pressure gradient and pulmonary vascular resistance decreased (-34% +/- 4% and -36% +/- 4%, respectively; p < 0.01) during 20 ppm nitric oxide, with no further effects at higher doses. Prostacyclin and sodium nitroprusside decreased pulmonary vascular resistance (-50% +/- 6% and -33% +/- 5%; p < 0.01). Prostacyclin reduced to some extent (p = 0.08) transpulmonary pressure gradient, which was not seen during sodium nitroprusside infusion. Systemic vascular resistance decreased during both sodium nitroprusside (-37% +/- 5%) and prostacyclin (-44% +/- 4%) infusion. The pulmonary vascular resistance/systemic vascular resistance ratio, used as an index of pulmonary selectivity, was decreased by nitric oxide (p < 0.01) but not by the intravenous vasodilators. Metabolic data indicate that inhaled nitric oxide is metabolized in the same way as that formed endogenously. In conclusion, inhaled nitric oxide is a selective pulmonary vasodilator that can be used safely in the hemodynamic evaluation of heart transplant candidates with elevated pulmonary vascular resistance.

Administration, Inhalation↗
PubMedDate not supplied

Pulmonary vasodilation after heart transplantation. A comparison among prostacyclin, sodium nitroprusside, and nitroglycerin on right ventricular function and pulmonary selectivity.

The aim of this study was to compare the effects of prostacyclin on central hemodynamics and right ventricular function to the more widely used vasodilators, sodium nitroprusside and nitroglycerin, and to investigate whether prostacyclin is more selective to the pulmonary vascular bed compared to sodium nitroprusside and nitroglycerin in patients after heart transplantation. Hemodynamic measurements were made after the operation in the intensive care unit with a pulmonary artery fast-response ejection fraction/volumetric thermodilution catheter. The aim was to maintain mean arterial pressure around 70 mm Hg with each drug. After a 10-minute infusion of each drug at a stable infusion rate, central hemodynamic variables and right ventricular end-diastolic volume, end-systolic volume, and ejection fraction were measured or derived in triplicate. The average infusion rates of sodium nitroprusside, nitroglycerin, and prostacyclin were 3.3 +/- 1.7 micrograms/kg/min, 6.6 +/- 1.8 micrograms/kg/min, and 12.4 +/- 1.7 ng/kg/min, respectively. Cardiac output, stroke volume, right ventricular end-diastolic volume, and central filling pressures were highest for prostacyclin compared to both nitroglycerin and sodium nitroprusside. Pulmonary vascular resistance was lower for prostacyclin compared to nitroglycerin but was comparable to that of sodium nitroprusside. Systemic vascular resistance was lowest for prostacyclin compared to both sodium nitroprusside and nitroglycerin. The pulmonary vascular resistance/systemic vascular resistance ratio used as an index of pulmonary selectivity did not differ between the vasodilators. The right ventricular ejection fraction did not differ among the three drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗