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Biomedical subjects

D Gustafsson

Publications and source records attributed to D Gustafsson.

50 records · Page 3Linked to original sources
PubMed1988

Effects of calcium antagonists on myogenic and neurogenic control of resistance and capacitance vessels in cat skeletal muscle.

The effects of five different calcium antagonists (diltiazem, felodipine, nifedipine, nimodipine, and verapamil) on cat skeletal muscle resistance and capacitance vessels were studied in a whole organ preparation. These calcium antagonists seemed to have the similar qualitative effects on these vascular functions. Calcium antagonists were found to be potent inhibitors of myogenic vascular reactivity (here defined as the maximal increase in flow resistance evoked by a sudden rise of transmural pressure). Basal vascular tone and vascular tone induced by low frequency stimulation of sympathetic nerves were both less sensitive to these drugs than vascular tone induced by myogenic vascular reactivity. Sympathetically mediated vascular tone at high stimulation frequencies seemed to be least sensitive. Further, resistance vessels were much more sensitive to these drugs than capacitance vessels. Finally, basal tone in the large bore arterioles were more sensitive than in the small bore arterioles, a surprising finding which was interpreted with the aid of computer simulations using a mathematical model of local vascular control in cat skeletal muscle. The model suggested that this difference could be due to a delicate interaction between myogenic vascular reactivity and metabolic vascular control. It is suggested that the inhibition of myogenic vascular reactivity is a factor contributing to the edema formation of calcium antagonists.

Animals↗
PubMed1988

In vitro diagnosis of atopic allergy in children. A comparison between total IgE, conventional RAST and a new multi RAST (Phadiatop).

A new multi RAST (Phadiatop) was compared with conventional RAST and total IgE determination (PRIST) for the diagnosis of IgE-mediated allergy in children. Serum specimens were tested from 100 children with a suspected IgE-mediated allergy, restricted to the eyes and/or the respiratory tract, to inhalant allergens. Compared with a RAST panel of 12 allergens representing seven groups, the new multi RAST showed a sensitivity of 95% and a specificity of 100% with a predictive value for positive test of 100% and for negative test of 91%. Corresponding figures for total IgE elevated greater than 2 SD above mean determined with PRIST were 47%, 88% 84% and 56% respectively. We conclude that multi RAST might be a good adjunct to the clinical diagnosis of IgE-mediated allergy to inhalant allergens.

Adolescent↗
PubMed1987

Microvascular mechanisms involved in calcium antagonist edema formation.

The effects of calcium antagonists on microcirculation in cat skeletal muscle were studied using a plethysmographic technique. Nifedipine given locally intraarterially decreased vascular resistance in a dose-dependent way by means of vasodilatation that was relatively more pronounced in precapillary vessels than in postcapillary vessels. This led to an increase in capillary hydrostatic pressure, which was the main force for the concomitant transcapillary fluid filtration from blood to tissue. Capillary filtration coefficient, which reflects precapillary sphincter tone (and thus the capillary surface area available for fluid exchange) and specific capillary permeability, was not changed much by nifedipine, even when vasodilatation was pronounced. A comparison of five different calcium antagonists (diltiazem, felodipine, nifedipine, nimodipine, and verapamil) showed that at the same degree of vasodilatation these agents caused the same increase in capillary hydrostatic pressure and the same net transcapillary fluid transfer, but caused no change in capillary filtration coefficient. Nifedipine also interfered with local vascular control in the tissue, leading to an impairment of "autoregulation of capillary hydrostatic pressure" at variations in arterial blood pressure and an impairment of protection against increased hydrostatic load in dependent vascular beds. It is concluded that peripheral edema (usually ankle edema) during treatment with calcium antagonists may result from vasodilatation alone and an inhibition of local vascular (myogenic) control.

Animals↗
PubMed1984

Microsphere analysis of beta 2-adrenergic control of resistance in different vascular areas after hemorrhage.

In cats exposed to bleeding (exsanguination of 15 ml X kg bwt-1) the microsphere technique was used to determine regional vascular resistances in a large number of tissues before and after i.v. administration of the 'selective' beta 2-adrenoceptor antagonist ICI 118,551. beta 2-blockade significantly raised vascular resistance in the stomach (+ 26%), small (+ 25%) and large (+ 38%) intestine, pancreas (+ 29%), kidney (+ 39%), omental (+ 33%) and subcutaneous (+ 26%) fat, 'white' skeletal muscle (+ 19%), and skin (+ 24%). These findings indicate that, with intact beta-adrenoceptors, beta 2-adrenergic dilator interaction counteracted the hemorrhage evoked vasoconstrictor influences. beta 2-blockade also evoked quite a strong increase of total peripheral resistance (19%) and led to some redistribution of cardiac output. It is concluded that beta 2-adrenergic inhibition of vascular tone significantly seems to improve tissue perfusion during bleeding in several vascular areas. Such effects may be of special significance during severe hemorrhage. In the intestine, pancreas, and adipose tissue, for example, protection against excessive vasoconstriction may serve to minimize the severe metabolic disturbances with secondary release of toxic factors into the circulation reported during hemorrhagic shock.

Adrenergic beta-Antagonists↗
PubMed1984

Decrease in survival time in beta 2-adrenoceptor blocked cats exposed to bleeding.

Our previous investigations have indicated that beta 2-adrenergic regulatory mechanisms contribute to important compensatory hemodynamic adjustments in hemorrhage. In the present study an attempt was made to examine, by comparative observations after standardized fatal hemorrhage on cats with intact and 'selectively' blocked beta 2-adrenoceptors (ICI 118,551), whether such compensatory effects are crucial for survival. On the average, the survival time after bleeding was 686 min in cats with intact and 427 min in cats with blocked beta 2-adrenoceptors (p less than 0.05), the difference thus approaching 4.5 h. It is suggested that the reduced survival time after beta 2-blockade, at least partly, can be ascribed to interference with the circulatory beta 2-adrenergic control in hemorrhage aimed at improving tissue perfusion.

Adrenergic beta-Antagonists↗
PubMed1984

Central hemodynamic effects of adrenaline with special reference to beta 2-adrenergic influence on heart rate and cardiac afterload in anesthetized cats.

Central hemodynamic responses evoked by i.v. infusions of adrenaline and noradrenaline were studied in normovolemic anesthetized cats with intact adrenoceptors, after selective beta 2-blockade (ICI 118,551), and after nonselective beta-blockade propranolol). The results demonstrated the presence of an important beta 2-adrenergic component in the integrated response to 'physiological' doses of adrenaline contributing to increased cardiac output, decreased total peripheral resistance and virtually unchanged mean arterial blood pressure. Corresponding beta 2-adrenergic effects of noradrenaline were small. The beta 2-adrenergic effects of adrenaline on the heart seemed to be both direct and indirect. A moderate direct chronotropic response mediated by beta 2-adrenoceptors apparently was present but there was no evidence of a direct beta 2-adrenergic inotropic effect. An indirect, quite marked effect on the heart was accomplished by a beta 2-adrenergic vasodilator interaction with the alpha-adrenergic vasoconstrictor influence on the systemic resistance vessels. This caused a net decrease in total peripheral resistance, thereby preventing an undue increase in cardiac afterload (arterial pressure) which seemed to be essential for evoking 'optimal' increases in cardiac output. It is suggested that such adrenaline evoked indirect, beta 2-adrenergic improvement of cardiac performance is of functional importance in reflex sympatho-adrenal circulatory control.

Adrenergic beta-Antagonists↗
PubMed1984

Beta 2-adrenergic vascular control in hemorrhage and its influence on cardiac performance.

Cardiac output (CO), heart rate, stroke volume (SV), and total peripheral resistance (TPR) were followed in anesthetized cats with intact and selectively blocked beta 2-adrenoceptors. SV and CO decreased and TPR increased initially after bleeding in both groups. After this, animals with intact beta 2-adrenoceptors showed gradual recovery of SV and CO and gradual restoration to control of the initially raised TPR. In beta 2-blocked animals SV and CO instead remained low and TPR high. These patterns of response occurred after mild, moderate, and severe bleeding. Separate experiments indicated that the restoration of TPR with intact beta 2-adrenoceptors mainly can be attributed to beta 2-adrenergic dilator interaction with the vasoconstrictor influences. The previously described beta 2-adrenergic control of plasma volume in hemorrhage (Acta Physiol. Scand. 116: 175-180, 1982) suggests that the increases in SV and CO with intact beta 2-adrenoceptors, in turn, probably are indirect effects on cardiac performance due to improved cardiac filling. A synthesis of present and previous findings thus suggests the existence of a beta 2-adrenergic vascular control in hemorrhage favoring tissue perfusion via decreased resistance and via increased plasma volume and hence SV and CO.

Adrenergic beta-Antagonists↗
PubMed1983

Possible benefit of selective beta 2-blockade in orthostatic hypotension a 'model' study in the cat.

In anesthetized cats head-up tilt was associated with a marked beta 2-adrenergic dilator interaction with the evoked constrictor response in the resistance vessels. The beta-adrenergic inhibition of vascular tone was revealed by measurements of total peripheral resistance and of regional resistance in skeletal muscle and in the intestine. Tentatively, the results may suggest that 'selective' blockade of vascular beta 2-adrenoceptors can be beneficial in states of orthostatic hypotension.

Adrenergic beta-Antagonists↗
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↗
PubMedDate not supplied

Superoxide dismutase and catalase do not improve recovery of regional myocardial contractile function when given at the time of reperfusion after reversible regional ischemia in anesthetized dogs.

Earlier studies have demonstrated an improvement in the recovery of the regional myocardial function after reversible myocardial ischemia when dogs were treated with superoxide dismutase (SOD) + catalase (CAT). In all these studies, drug administration was started prior to the ischemic period. The aim of this study was to investigate the effects of SOD and CAT on the recovery of the regional contractile function in anesthetized beagle dogs when the drugs were administered at the time of reperfusion. The animals were subjected to 20 min of left coronary artery occlusion followed by 3 h reperfusion. The regional myocardial contractile function, measured as subendocardial segment shortening (SS, sonomicrometry) decreased to below zero and the regional blood flow in the ischemic subendocardium was reduced to about 5% of pre-ischemic values during the coronary artery occlusion period. The size of the occluded bed was similar in the two groups. Saline (n = 8) or SOD (10 mg/kg) + CAT (3.4 mg/kg) (n = 8) were infused into the left atrium from 2.5 min prior to until 20 min after the start of reperfusion. The peak plasma level of SOD was 102 +/- 15 mg/l at 20 min reperfusion. There were no significant differences in the arterial blood pressure, cardiac contractile function and regional blood flow between the two groups at any time during the experiment. During reperfusion in the dogs given vehicle, SS recovered to 48 +/- 7% (mean +/- SEM) after the first hour of reperfusion, and to 51 +/- 6% of pre-ischemic values after 3 h of reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗