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Biomedical subjects

J Lundvall

Publications and source records attributed to J Lundvall.

At least 55 records · Page 3Linked to original sources
PubMed1982

Impairment during marked hypotension of the plasma volume control in hemorrhage.

During hypovolemia extravascular fluid is transferred across the capillaries into the circulation in order to restore blood volume. Several studies have shown that this process, which mainly occurs in skeletal muscle, effectively can compensate for the blood loss. The preset investigation performed in the cat strongly indicates, however, that this vital compensatory mechanism is inactivated in situations of pronounced hypovolemia leading to hypotension levels of 30-40 mmHg, i.e. when the need for refill of the circulatory system is most in demand. It is suggested that the cessation of fluid transfer from skeletal muscle to blood during marked hypotension is causally linked to the evoked pronounced reduction of blood flow, due partly to the much reduced perfusion pressure and partly to the marked vasoconstriction. Pronounced vasoconstriction in the hemodynamically important vascular bed of skeletal muscle is obviously an essential part of the necessary resistance response evoked in the systemic circulation in order to avoid circulatory collapse already in the early phase of a large blood loss. However, the chances for the organism to survive is minimized if the vasoconstriction leads to impairment of the mechanisms for plasma volume regulation.

Animals↗
PubMed1982

beta 2-Adrenergic control of plasma volume in hemorrhage.

Hemorrhage is associated with absorption of extravascular fluid from skeletal muscle to blood in order to compensate for the loss of intravascular volume. Our previous studies have shown that this fluid gain is mainly linked to beta-adrenergic microvascular adjustments leading to decrease in capillary hydrostatic pressure and to precapillary 'sphincter' mediated increase in the capillary surface area available for fluid exchange. In the present study the importance of beta-adrenergic control of plasma volume in bleeding was confirmed by measurement of changes in plasma volume after graded hemorrhage in animals with intact and blocked vascular beta 2-adrenoceptors (i.v. administration of the 'selective' beta 2-blocking agent ICI 118, 551). With intact beta 2-adrenoceptors plasma volume was gradually restored after bleeding so that about 50% of the shed plasma volume (about 35% of the shed blood volume) had been compensated for at two hours after exsanguination of 20% as well as 40% of the blood volume. The corresponding figures in animals with blocked beta 2-adrenoceptors were only 14% of the shed plasma volume and 8% of the shed blood volume at both degrees of hemorrhage.

Adrenergic beta-Antagonists↗
PubMed1982

Influences on central hemodynamics in hemorrhage of beta 2-adrenergic vascular control mechanisms.

Central hemodynamic responses evoked by standardized hemorrhage (exsanguination of 20 ml x kg bwt-1) were followed during 2 h in cats with intact and blocked vascular beta 2-adrenoceptors using the 'selective' beta 2-blocker, ICI 118, 551. In the first 10 min after bleeding blood pressure and cardiac output (CO) decreased and total peripheral resistance (TPR) increased by the same amount in the 'intact' and beta 2-blocked animals. Whereas blood pressure later on reached approximately the same hypotension level in both groups, other hemodynamic variables were distinctly different. In the 'intact' animals there was a gradual, partial recovery of stroke volume (SV) and CO in the face of a restoration to control of TPR. In the beta 2-blocked animals TPR continued to increase in the face of a maintained low CO and declining SV. The lower SV in the latter group was ascribed to abolition of beta 2-adrenergic restoration of plasma volume via absorption of tissue fluid into the circulation. The gradual decline of TPR in the 'intact' animals was attributed to beta 2-adrenergic dilator interaction with constrictor influences on the resistance vessels. It is concluded that beta-adrenergic vascular control mechanisms help to improve nutritional tissue blood flow during hemorrhage by increasing plasma volume, and hence venous return and CO, and by decreasing TPR. These reflex, beta 2-adrenergic circulatory events are similar to those aimed at in current shock therapy by transfusion and vasodilator treatment.

Adrenergic beta-Antagonists↗
PubMed1982

beta-Adrenergic dilator effects in consecutive vascular sections of skeletal muscle.

Humoral and neurogenic beta-adrenergic dilatation that influenced the resistance function, the capillary exchange function, and to some extent the capacitance function was demonstrated in the vascular bed of cat skeletal muscle. The beta-adrenergic effects were mainly confined to the microcirculation, causing dilatation of the precapillary sphincters and the resistance vessels of small calibre. The microcirculatory effects were pronounced in response to epinephrine, but blood-borne and nerve-released norepinephrine also evoked marked effects. The beta-adrenergic inhibition of vascular tone in the microcirculation may serve in the intact organism to improve tissue nutrition by facilitating capillary diffusion exchange. It further seems to regulate transcapillary hydrodynamic exchange, partly by controlling the precapillary sphincters and the capillary hydrostatic pressure. The blood-borne catecholamines, especially epinephrine, also markedly affected total regional vascular resistance and thereby blood flow by dilator interaction with the concomitant alpha-adrenergic vasoconstrictor response.

Animals↗
PubMed1981

Hormonal and neurogenic adrenergic control of the fluid transfer from skeletal muscle to blood during hemorrhage.

During hemorrhage net transcapillary absorption of interstitial fluid from skeletal muscle into the intravascular space compensates effectively for the blood loss. This absorption of fluid is mainly linked to decrease of the capillary hydrostatic pressure (Pc), as caused by reflex adrenergic re-adjustment of the ratio of pre- to postcapillary resistance (ra/rv). The present study demonstrates the existence of both a neurogenic and a humoral component in the adrenergic control of the fluid transfer for skeletal muscle to blood. In the early period of bleeding (less than 5 min) reflex activation of the vasomotor fibres contributed significantly to the fluid absorption. The subsequent, main part of the fluid gain from the extra- to the intravascular space was due to the action of the blood-borne catecholamines. Both the neurogenic and the hormonal control of the fluid absorption process was mainly linked ot beta-adrenergic inhibition of vascular smooth muscle tone. This control was effected via two mechanisms, viz. by a relatively larger beta-adrenergic dilation of post- than precapillary resistance vessels, leading to adjustment of ra/rv and thereby to decrease of Pc, and via beta-adrenergic dilation of "precapillary sphincters' leading to increased capillary surface area available for fluid exchange.

Absorption↗
PubMed1981

Classification of beta-adrenoceptors in the microcirculation of skeletal muscle.

Nervous and humoral beta-adrenergic, postjunctional effects on microvascular resistance, on precapillary sphincter tone, and on transcapillary fluid exchange in cat skeletal muscle (Lundvall & Järhult 1974, 1976 a, Lundvall & Hillman 1978 a, b) were evaluated with regard to the beta 1- or beta 2-specificity of the adrenoceptors. Marked beta 2-dilator responses but no significant beta 1-effects were observed. The conclusion was therefore reached that neurogenic as well as humoral beta-adrenergic control of the microcirculation in skeletal muscle is exerted via activation of beta 2-adrenoceptors.

Animals↗
PubMed1980

Beta-adrenergic dilator interaction with the constrictor response in resistance vessels of skeletal muscle during hemorrhage.

A marked beta-adrenergic dilator interaction with the vasoconstrictor response in skeletal muscle during hemorrhage is described. The dilator influence corresponded to some 40% of the constrictor response both at mild and moderate as well as at large bleeding. In absolute resistance units, the beta-adrenergic dilator influence averaged no less than 14 mmHg/ml X min-1 X 100 g-1) at large bleeding (hemorrhagic hypotension of 50 mmHg). Comparison of the hemorrhage induced resistance effects in the autoperfused innervated muscle, in the autoperfused denervated muscle, and in the innervated muscle cross-circulated from a donor animal, showed that the beta-adrenergic dilator influence more or less completely was caused by blood-borne catecholamines, in all likelihood by adrenaline, which is known to be secreted in large amounts during hemorrhage. The described beta-adrenergic dilator mechanism may serve to maintain nutritional blood flow by counteracting the constrictor response. It deserves consideration also from the point of view that it obviously has to be taken into account for proper evaluation of other vascular control mechanisms brought into action in hemorrhage.

Animals↗
PubMed1978

Fluid transfer from skeletal muscle to blood during hemorrhage. Importance of beta adrenergic vascular mechanisms.

Vascular reactions in the cat lower leg in response to short-term (10 min) hemorrhagic hypotension (approximately 80 mmHg) were studied before and after regional blockade of the beta-adrenoceptors. In the muscle region with intact beta-adrenoceptors, hemorrhage raised vascular resistance by about 80% and caused a dilatation of the precapillary sphincters, the latter effect evidenced in terms of a 35% increase of the capillary filtration coefficient. Concomitantly, an absorption of extravascular fluid to the blood stream occurred, a process tending to compensate for the reduction of intravascular fluid volume. After regional beta-blockade there was quite a marked augmentation of the hemorrhage induced increase of vascular resistance whereas the inhibition of precapillary sphincter tone and the transcapillary fluid absorption were almost abolished. These observations indicate that bleeding is associated with a significant beta-adrenergic dilator influence in both the resistance vessels and precapillary sphincters of skeletal muscle and that the beta-dilator mechanism may be essential for the important, compensatory fluid gain from the extravascular to the intravascular space during hemorrhage. The observed beta-adrenergic mediation of the net transcapillary fluid absorption could be ascribed to resetting of the pre-/postcapillary resistance ratio, leading to decreased capillary hydrostatic pressure, and to the dilator influence in the precapillary sphincters, leading to an increased number of the patent capillaries available for the transcapillary fluid exchange.

Animals↗
PubMed1977

Reflex plasma hyperglycemia and hyperosmolality evoked by unloading of the carotid baroreceptors.

Hemorrhage is usually accompanied by a considerable increase in the plasma osmolality and glucose concentration due to an augmented release of glucose from the liver. In the present cat experiments an attempt was made to investigate the possible role of different vascular receptors in mediating this hyperglycemic (hyperosmolar) response. Bilateral vagotomy or stimulation of the carotid chemoreceptors by perfusion of the carotid sinus with venous blood at normal pressure only slightly increased the arterial plasma glucose concentration. On the other hand, when the sinus nerves were cut in the vagotomized animal, thereby simulating complete unloading of the carotid baroreceptors, the arterial plasma glucose concentration rose by about 8 mM/L and the arterial plasma osmolality by about 10 mOsm/kg H2O. Perfusion of the carotid baroreceptors with arterial blood at different levels of hypotension showed that the baroreceptor-induced hyperglycemia was graded in relation to the pressure level. Regional hypotension of the liver, pancreas, intestine, kidneys or brain did not significantly affect plasma glucose concentration or osmolality. We conclude that the reflex release of glucose from the liver during hemorrhage mainly is initiated from the unloading of arterial baroreceptors.

Animals↗
PubMed1977

Evidence for a rate-sensitive regulatory mechanism in myogenic microvascular control.

To reveal a possible rate-sensitive component in the myogenic control, changes of total and segmental vascular resistances in sympathectomized skeletal muscle in response to alteration of vascular transmural pressure (extravascular pressure) by 40 mmHg were compared when the pressure change was applied at two distinctly different rates (15 and 120 s). The papaverine-dilated vascular bed showed an entirely passive behaviour, whereas the normal, myogenically reactive vascular bed responded with active constriction upon transmural pressure increase and active dilation upon pressure decrease. These responses were especially pronounced in the microvessels where a clearcut two-component effector response was observed. The magnitude of the initial component was distinctly correlated to the rate at which the transmural pressure stimulus was applied, whereas the later steady state component during the static pressure change was rate-independent. At the high rate of pressure increase, the initial rate-dependent microvascular constrictor response was some ten times larger than the steady state response. These observations indicate the existence of a rate-sensitive as well as a static component in the myogenic response to changed transmural pressure, an interpretation strongly supported by a previous analogous study on isolated single-unit vascular smooth muscle (Johansson and Mellander 1975). It is concluded that the microvessels in skeletal muscle are highly responsive to myogenic stimuli and that emphasis should be placed on the dynamic rather than the static characteristics of the stimulus. Such rate-sensitivity in myogenic control would seem to facilitate prompt and proper vascular adjustments, for instance in myogenic autoregulation.

Animals↗
PubMed1976

Beta adrenergic dilator component of the sympathetic vascular response in skeletal muscle. Influence on the micro-circulation and on transcapillary exchange.

A neurogenic beta-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic beta-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1-16 Hz) before and after beta-adrenoceptor blockade. Beta-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the "micro-vessels" during stimulation was, however, clearly more pronounced in the beta-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, beta-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of alpha-blockade were observed at all rates of sympathetic stimulation.--The conclusion was reached that the beta-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the alpha-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic beta-dilator mechanism is primarily aimed at improving the transcapillary exchange.

Adrenergic beta-Antagonists↗
PubMed1976

Hyperglycemic and hyperosmolar responses to graded hemorrhage.

Changes of the arterial plasma osmolality and of the glucose concentration were followed during a 30 min period of graded hemorrhagic hypotension (80, 50, and 30 mmHg) in the cat. Bleeding evoked a significant plasma hyperosmolality at all three hypotension levles and the responses were quantitatively related to the degree of hypotension. An approximate steady state increase in the arterial plasma osmolality was reached about 20 min after the start of the bleeding and it then averaged 8. 20, and 25 mOsm/kg H2O at 80, 50, and 30 mmHg, respectively. Bleeding also evoked an increase in the plasma glucose concentration, which almost entirely accounted for the observed hyperosmolality, especially at 80 and 50 mmHg. In late stages of hypotension at 30 mmHg, elevated plasma lactate and potassium concentrations contributed to the overall hyperosmolality. --Previous hemorrhagic hypotension experiments at 50 mmHg (Järhult 1975 b) have shown that hyperosmolality serves as an important regulator of the plasma and extracellular fluid volumes during bleeding. The present results indicate that such an osmolar compensatory mechanism is operating over wide ranges of hemorrhagic hypotension.

Animals↗
PubMed1976

Tissue hyperosmolality as a causal factor in vasodilatation following sympathetic stimulation of the submandibular gland.

In a previous investigation, parasympathetic activation of the submandibular gland in the cat was found to cause a considerable increase of regional tissue osmolality, the degree of which was related to the evoked functional hyperemia; intra-arterial hypertonic infusion to the resting gland producing tissue hyperosmolality of similar magnitudes caused graded and marked dilatations (Lundvall and Holmberg 1974). It was concluded that hyperosmolality contributes significantly to the functional hyperemia response. In the present study evidence is presented to indicate that tissue hyperosmolality is a mediator of the dilatation associated with sympathetic activation as well. An increase of tissue hyperosmolality, as traced in the venous effluent, was found at all frequencies of sympathetic stimulation (2-16 Hz). At high stimulation rates it sometimes exceeded the resting control level by more than 20 mOsm/kg H2O. There was a direct relation between the degree of venous hyperosmolality and the hyperemia response observed immediately after cessation of stimulation. Comparison of the dilator effects evoked by sympathetic stimulation and by hypertonic infusion to the resting gland indicated that tissue hyperosmolality is an important causal factor for the nerve induced dilatation, especially at low and moderate stimulation rates.

Animals↗