Cutaneous Vascular Resistance Research Articles

Vascular effects of arginine vasotocin in toad skin.

Fluid balance in amphibians is regulated, in large part, by arginine vasotocin (AVT). One important action of this hormone is to facilitate water uptake by increasing the water permeability of the skin. Cutaneous blood flow also affects water uptake, but the effects of AVT on skin perfusion are unknown. This study tested the hypothesis that AVT facilitates water uptake, not only by increasing cutaneous water permeability, but also by promoting cutaneous blood flow. The effects of AVT on blood flow through the ventral pelvic skin, a region specialized for water uptake, were assessed in Bufo marinus by determining the conductance of the skin to acetylene (GsAc), an index of cutaneous blood flow. A pump-perfused skin preparation was used to study the effects of AVT on the cutaneous vascular resistance (CVR) of the ventral pelvic skin and the dorsal skin (a region not normally involved in water uptake). Bolus AVT injections (iv) of 10 pmol/kg and below had no significant effect on GsAc (P > 0.45). However, 100 and 300 pmol/kg of AVT decreased GsAc by 39 +/- 7 (P < 0.001) and 63 +/- 6% (P < 0.001), respectively. The higher AVT doses increased mean arterial pressure. AVT increased CVR in both pump-perfused preparations. The lowest concentration of AVT tested that significantly raised CVR was 1 x 10(-10) M for the dorsal skin (P = 0.006) and 3 x 10(-10) M for the ventral pelvic skin (P = 0.038).(ABSTRACT TRUNCATED AT 250 WORDS)

Thermoregulatory response to passive body heating in borderline hypertension.

Sweating and vasodilatation in the cutaneous circulation were investigated during passive body heating in eight borderline hypertensive subjects and in eight normotensive controls, matched for age, sex and body mass. Blood flow through the finger and forearm was examined in relation to changes in oral temperature; blood pressure, heart rate and sweating in the forehead and forearm were also measured. Systolic blood pressure decreased in borderline hypertensive subjects during the early stages of heating and then returned to baseline, but increased in normotensives. Increases in skin blood flow and decreases in cutaneous vascular resistance were similar in both groups. Thus, cutaneous vasodilatation during moderate body heating did not differ between normotensive subjects and subjects with mildly elevated blood pressure. These findings do not rule out attenuation of cutaneous vasodilatation in mildly hypertensive subjects during more intense heating.

Differential effects of isometric exercise on the cutaneous circulation of different regions.

Studies have been made in healthy human subjects of the changes evoked by isometric hand grip in arterial pressure, heart rate and cutaneous red cell flux, the latter being recorded using a laser Doppler meter. Hand grip for 2 min evoked increases in arterial pressure and heart rate, the magnitude of which were graded with the force of contraction (75, 50, or 25% maximum voluntary contraction). Cutaneous red cell flux in the contralateral forearm decreased significantly during 25 and 50% maximum voluntary contraction, while the cutaneous vascular resistance (arterial pressure/cutaneous red cell flux) increased to extents that were graded with the maximum voluntary contraction, indicating graded vasoconstriction. By contrast, cutaneous red cell flux in the face tended to increase, this reaching significance at 75% maximum voluntary contraction. Cutaneous vascular resistance in the face increased in some subjects, but decreased in others, vasodilator responses being most common during 75% maximum voluntary contraction when sweating commonly appeared on the face. In the dorsum of the foot, red cell flux did not change during 75% maximum voluntary contraction, although foot cutaneous vascular resistance increased significantly by the end of the first minute of contraction. At 50 and 25% maximum voluntary contraction most subjects showed an increase in foot cutaneous vascular resistance, but the remainder showed a decrease. We propose that isometric hand grip causes vasoconstriction in the cutaneous circulation of the contralateral forearm, the face and foot, that this response is strongest in the forearm and weakest in the face, and that in the face and foot, the vasoconstriction may be overcome by vasodilatation secondary to sweating.

Local deterioration of the cutaneous venoarterial reflex of the hand in cirrhosis.

Cutaneous focal blood perfusion and an index of cutaneous vascular resistance were determined on the dorsum and palm of the hand of 34 patients with liver cirrhosis and of 24 healthy control subjects. Tests were performed with a laser-Doppler technique before and during stimulation of the vasoconstrictor venoarterial reflex, performed by means of venous occlusion of the forearm. The mean arterial blood pressure of the cirrhotics turned out to be lower than that of the controls. On the dorsum of their hands a normal blood perfusion and a reduced vascular resistance were verified, suggesting the intervention of a local autoregulatory phenomenon of the blood flow. The blood perfusion turned out to be higher, whereas the vascular resistance was lower than the norm on the palm of the hands of cirrhotic patients who had palmar erythema, showing the presence of an anomalous non-autoregulatory vasodilation. The extent of venoarterial reflex on the dorsum of the hand turned out to be identical in the patients and controls, whereas that on the palm turned out depressed. This anomaly was present also in patients without palmar erythema, although less marked than in those with erythema. The data obtained suggest the presence of a disturbance in the functioning of the arteriovenous anastomoses (numerous in the palm but very scarce in the dorsum), superimposed on the venoarterial reflex. It may depend on the existence, in hepatic cirrhosis, of an impairment of the specialized autonomic nervous mechanisms that control temperature loss.

Sympathetic regulation of cutaneous circulation in the rat

The purpose of the present study was to characterize, in vivo, the function and origin of peripheral α-adrenergic mechanisms in acral regions of the cutaneous microvasculature. Laser-Doppler flowmetry was used to continuously monitor changes in local cutaneous microvascular perfusion (CP) measured at the plantar surface of the terminal phalange in the rat. In ketamine-anesthetized rats, the intravenous administration of phentolamine (a nonselective α-adrenoceptor antagonist) elicited a dose-dependent (0.01–1.0 mg/kg, i.v.) increase in CP, a decrease in mean arterial pressure (MAP) and a marked reduction in cutaneous vascular resistance (CVR). These results demonstrate a high degree of endogenous α-adrenergic tone in the cutaneous microvasculature of the rat. In pithed rats, cutaneous vasoconstriction could be evoked by ganglionic stimulation with DMPP or by electrical stimulation of the peripheral cut end of the sciatic nerve trunk. DMPP and sciatic nerve responses were not altered by propranolol or atropine, but were inhibited by phentolamine. In addition, the effects of DMPP on CP were abolished by bilateral adrenal demedullation, but were unaltered by hindlimb denervation. These results suggest that the predominant vasoconstrictor tone in the cutaneous vasculature is mediated by a humoral action of circulating catecholamines at postjunctional α-adrenoceptors. The adrenal medulla appears to be the origin of this humoral tone. Postganglionic sympathetic nerves play an insignificant role in mediating cutaneous vasoconstriction elicited by ganglionic stimulation.

Analysis of vascular responses evoked in the cutaneous circulation of one hand by cooling the contralateral hand

In 11 healthy human subjects, cutaneous red cell flux in the thenar eminence of the left hand was measured by a Laser Doppler meter, while the right hand was transferred sequentially from water at 33°C, to water at 16°C for 5 min, to water at 33°C (1st experimental run) and then to water at 16°C for 2 min (2nd experimental run). Red cell flux decreased from 33 ± 10 (mean ± SEM) to 19 ± 5 ∗ perfusion units (pu) by the end of the 2nd min of cooling ( ∗ P < 0.05 paired t-test ), but had returned to 27 ± 8 pu by the 5th min. Arterial pressure, measured by sphygmomanometry from the left arm at the 5th min (1st run) and 2nd min (2nd run) did not change, indicating the changes in red cell flux reflected changes in cutaneous vascular resistance. By contrast, when these experiments were repeated with a cuff on the right arm inflated to 56–62 mmHg to impede venous outflow from the cooled limb, there were no changes in red cell flux in the contralateral hand, nor in arterial pressure. Occlusion per se had no effect on red cell flux. Thus, we propose that cooling one hand evokes a short-lasting reflex constriction in the cutaneous circulation of the contralateral hand which is mainly mediated by core thermoreceptors affected by a reduction in blood temperature, rather than by peripheral thermoreceptors in the cooled hand. The contrast between this proposal and views based on earlier studies [14] is discussed.

Autonomic regulation of cutaneous vascular resistance in the bullfrog Rana catesbeiana

To gain a better understanding of the regulation of cutaneous blood flow in the bullfrog, the vascular innervation, vasoactivity and adrenoceptor types of the cutaneous vasculature were investigated using a pump-perfused skin preparation. Stimulation of cranial nerve I, the vagal ganglion, sympathetic ganglion 1 and sometimes sympathetic ganglion 2 caused cutaneous vascular resistance (CVR) to increase. Stimulation of cranial nerve IX and spinal nerves 1 and 2 had no effect on CVR. The response to stimulation of sympathetic ganglion 1 was antagonized by phentolamine but not by atropine. Phentolamine, atropine and alpha,beta-methylene ATP had no effect on the response to vagal stimulation. Both epinephrine (EPI) and norepinephrine (NE) increased CVR, with EPI being more potent than NE. The minimum concentrations of EPI and NE required for a significant change in CVR were much higher than plasma catecholamine levels reported for resting bullfrogs. Phentolamine antagonized, but propranolol had no effect on, the responses to the catecholamines. Isoproterenol caused small decreases in CVR which were abolished by propranolol. Acetylcholine was a weak vasodilator. The results indicate that the cutaneous vasculature has two types of vasomotor nerves: sympathetic nerves that are probably adrenergic, and other nerves that are non-adrenergic/non-cholinergic and which do not use ATP as a transmitter. Although catecholamines are vasoactive, the sensitivity of the cutaneous vasculature to EPI and NE is probably too low to allow a direct regulatory role of these hormones on CVR. There is no evidence for cholinergic regulation of CVR. Both alpha- and beta-adrenoceptors are present in the cutaneous vasculature. alpha-Adrenoceptors mediate the constrictor responses to sympathetic nerve stimulation and catecholamine administration. It is unlikely that beta-adrenoceptors play a significant role in regulating CVR.

Cutaneous Vascular Responses Evoked in the Hand by the Cold Pressor Test and by Mental Arithmetic

1. Laser Doppler flowmetry has been used to study changes in cutaneous erythrocyte flux produced in the hand (i) on successive immersion of the contralateral hand in water at 20 degrees C (cold test) and then in water at 0-4 degrees C (cold pressor test), and (ii) by mental arithmetic. 2. In 11 subjects, placing the right hand in water at 20 degrees C for 2 min induced a significant decrease in cutaneous erythrocyte flux in the contralateral hand and a significant fall in mean arterial pressure. Cutaneous vascular resistance, calculated as arterial pressure/cutaneous erythrocyte flux, showed no significant change. Thus, the decrease in erythrocyte flux was apparently due to a fall in perfusion pressure. 3. Subsequent immersion of the right hand in water at 0-4 degrees C for 2 min caused a significant decrease in erythrocyte flux in the contralateral hand and a significant rise in mean arterial pressure. It is concluded that the cold pressor response evoked from one hand elicited a substantial reflex vasoconstriction in the skin of the other hand; accordingly, calculated cutaneous vascular resistance increased significantly. 4. Eight subjects performed mental arithmetic for two periods of 2 min separated by a rest period of 2 min. By the end of the second minute of each period of mental arithmetic there was a significant decrease in erythrocyte flux. Mean arterial pressure increased significantly in the first period only, but calculated cutaneous vascular resistance increased in both periods, consistent with cutaneous vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic differences between carvedilol and labetalol in the cutaneous circulation

The effects of labetalol and carvedilol on local cutaneous microvascular perfusion and calculated local cutaneous microvascular resistance were investigated in anesthetized rats at submaximal doses that produced equivalent reductions in blood pressure and heart rate. Labetalol decreased cutaneous perfusion (-25% +/- 3%) without significantly affecting cutaneous vascular resistance (-6% +/- 3%). In marked contrast, carvedilol dramatically increased cutaneous perfusion (+64% +/- 9%) and significantly reduced cutaneous vascular resistance (-57% +/- 3%). These results suggest that carvedilol and labetalol possess differences in the mechanisms by which they produce vasodilation in vivo.

Local cutaneous hemodynamic effects of carvedilol and labetalol in the anesthetized rat

The effects of labetalol and carvedilol and local cutaneous microvascular perfusion and calculated local cutaneous microvascular resistance were investigated in anesthetized rats at submaximal doses that produced equivalent reductions in blood pressure and heart rate. Labetalol decreased cutaneous perfusion (-25 ± 3%) without significantly affecting cutaneous vascular resistance (-6 ± 3%). In marked contrast, carvedilol dramatically increased cutaneous perfusion (+64 ± 9%) and significantly reduced cutaneous vascular resistance (-57 ± 3%). These results suggest that carvedilol and labetalol possess differences in the mechanisms by which they produce vasodilation in vivo.

Effect of Arotinolol on Hemodynamics and Plasma Atrial Natriuretic Peptide at Rest and During Stress in Spontaneously Hypertensive Rats

We investigated the effects of chronic treatment with arotinolol, a beta-blocker with weak alpha-blocking potency, on hemodynamics and plasma levels of catecholamines and atrial natriuretic peptide (ANP) at rest and during stress in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. At rest, arotinolol treatment decreased mean arterial pressure (MAP), cardiac index (CI) and heart rate (HR), with no changes in total peripheral resistance index or regional hemodynamics in SHR. Acute stress caused more remarkable hemodynamic changes in SHR. During stress, arotinolol decreased MAP, CI and HR, and reduced myocardial and skeletal muscle flow and splanchnic, renal, cerebral and cutaneous vascular resistance in SHR. Arotinolol's effects were much less in WKY. Stress also increased the plasma catecholamine and ANP levels in SHR. Arotinolol raised these hormones in both strains at rest and in SHR during stress. Thus, arotinolol treatment exerted greater suppressive effects on the resting and stressed hemodynamics in SHR, with associated increases in the plasma catecholamine and ANP levels.

Evaluation of the dilator capacity of skin blood vessels of hypertensive patients by laser doppler flowmetry

Knowledge of regional circulation in the skin of hypertensive patients is largely incomplete. We examined the vasodilator capacity of skin blood vessels in the foot in 20 hypertensives and in 20 age- and sex-matched normal control subjects. Vasodilator capacity was assessed by measuring skin blood flow (laser doppler flowmetry) and cutaneous vascular resistance at rest and at the peak of the postocclusive reactive hyperemia response. Skin blood flow was higher in hypertensive patients than in controls at rest (69.4 ± 23.6 vs 44.2 ± 17.5 mV; P < 0.003), but did not differ significantly after reactive hyperemia (89.2 ± 23.5 vs 88.2 ± 25.4 mV; N.S.). Calculated cutaneous vascular resistance was higher in controls at rest (2.99 ± 1.06 vs 2.22 ± 0.81 a.u.; P < 0.3), but lower after reactive hyperemia (1.43 ± 0.44 vs 1.64 ± 0.43 a.u.; N.S.). Laser Doppler flowmetry is a technique suitable for studying the alterations in cutaneous microcirculation induced by hypertension. These data are compatible with structural changes in the vascular wall of hypertensive patients.

Effects of taurine on stress-evoked hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.

Cardiovascular hemodynamics (microspheres) and plasma norepinephrine and epinephrine levels at rest and during short-term shaker stress were investigated in conscious spontaneously hypertensive rats and Wistar-Kyoto rats, with or without oral taurine (1.5%) treatment for 8 weeks. Taurine effects were evaluated by comparing data on the taurine-treated and untreated rats. Taurine affected neither the resting hemodynamics nor the resting plasma catecholamine levels in spontaneously hypertensive and Wistar-Kyoto rats. Taurine slightly but significantly reduced the left ventricular/body weight ratio in the spontaneously hypertensive rats (p less than 0.05) and caused an insignificant 10 mm Hg decrease in the resting mean arterial pressure. Spontaneously hypertensive and Wistar-Kyoto rats responded in a qualitatively similar manner to stress, as evidenced by resistance-dominated increases in mean arterial pressure and increases in heart rate, with a blood flow redistribution from splanchnic, cutaneous, and testicular to skeletal muscle and cerebral circulations and by increases in plasma norepinephrine and epinephrine levels. These changes were more marked in the spontaneously hypertensive rats. Taurine significantly reduced the stress values of mean arterial pressure (untreated, 189 +/- 4 (SE) mm Hg; treated, 166 +/- 4 mm Hg in the spontaneously hypertensive rats; p less than 0.05), while it significantly reduced stress values of heart rate in spontaneously hypertensive and Wistar-Kyoto rats (p less than 0.05). Taurine also blunted the stress values of splanchnic, testicular, and cutaneous vascular resistance in the spontaneously hypertensive rats. There were no or only slight regional effects in the Wistar-Kyoto rats. Taurine substantially decreased plasma levels of norepinephrine (untreated, 615 +/- 76 pg/ml; treated, 383 +/- 49 pg/ml) and epinephrine (untreated, 892 +/- 187 pg/ml; treated, 232 +/- 59 pg/ml) during stress in the spontaneously hypertensive rats. These results indicate that chronic taurine treatment attenuates short-term shaker stress-induced hemodynamic and plasma catecholamine changes in spontaneously hypertensive rats.

Evidence that serotonin receptors mediate the cutaneous vasoconstriction produced by 5-hydroxytryptamine in canine forelimbs.

The effects of local intra-arterial infusions of serotonin (5 or 25 micrograms base/min) or norepinephrine (1 or 5 micrograms base/min) on cutaneous (skin) and skeletal muscle vasculatures were investigated in canine forelimbs perfused at constant flow in dogs anesthetized with pentobarbital. Norepinephrine produced dose-related constriction of the skin and skeletal muscle vasculatures. In the cutaneous vascular circuit, norepinephrine produced large artery, small vessel, and large vein constriction. The increase in cutaneous vascular resistance was primarily due to an increase in small vessel resistance. Serotonin did not increase skeletal muscle vascular resistance but produced marked cutaneous vasoconstriction subsequent to large artery and large vein constriction. The small vessels, if anything, tended to dilate. The skin and skeletal muscle vascular responses to serotonin and norepinephrine were similar in innervated and acutely denervated forelimbs. Phentolamine pretreatment completely blocked all vascular actions of norepinephrine, and largely inhibited the cutaneous vasoconstriction produced by the infusion of the low dose of serotonin. However, the cutaneous large artery and large vein constriction produced by the infusion of the high dose of serotonin was not affected by phentolamine pretreatment. Cyproheptadine pretreatment blocked or largely inhibited the cutaneous vasoconstriction produced by serotonin only in doses which also inhibited norepinephrine and vasopressin cutaneous vasoconstriction. Pretreatment with methysergide blocked or largely inhibited the cutaneous large artery and large vein constriction produced by infusions of serotonin. Norepinephrine and vasopressin produced significant vasoconstriction in the presence of methysergide. These data suggest that the cutaneous large artery and large vein constriction produced by serotonin is not due to the activation of postjunctional alpha-adrenergic receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Dependence of transcutaneous oxygen tension on local arteriovenous pressure gradient in normal subjects.

1. We studied the relationship between transcutaneous oxygen tension at the foot and local arteriovenous pressure difference in 15 normal men and women; arteriovenous pressure difference was varied by changing the height of the foot with respect to the heart and by applying external pressure to the foot. 2. Control transcutaneous oxygen tension was 67 +/- 9 SD mmHg (8.9 +/- 1.2 kPa) at a control arteriovenous pressure difference of 80 +/- 6 SD mmHg (10.6 +/- 0.8 kPa). 3. In every subject transcutaneous oxygen tension fell non-linearly with a decrease in arteriovenous pressure difference; transcutaneous oxygen tension was relatively insensitive to changes in arteriovenous pressure difference when arteriovenous pressure difference was high, but always fell sharply to zero at some positive arteriovenous pressure difference [range 13-34 mmHg (1.7-4.5 kPa)]. 4. An analysis of the data indicated that transcutaneous oxygen tension varied with arteriovenous pressure difference approximately as the oxygen tension of cutaneous venous blood under the sensor varied (in the absence of changes in cutaneous vascular resistance and oxygen consumption). 5. This analysis was supported by studies in three subjects in whom the oxygen tension of superficial venous drainage from a warmed hand or foot was measured along with transcutaneous oxygen tension while arteriovenous pressure difference was varied.

Effect of morphine on limb capacitance and resistance vessels.

1. The actions of 15 mg of intravenous morphine on hand and forearm capacitance and resistance vessels were studied with venous occlusion plethysmography. 2. In contrast to a 5% increase in forearm venous volume, intravenous morphine caused a 26% decrease in hand venous volume. This hand venoconstriction was confirmed by finding an increase in hand venous tone. The effects of morphine on hand veins were attenuated by intraarterial phentolamine and blocked by intravenous naloxone. 3. Whereas morphine had no significant effect on forearm resistance vessels, it caused a 70% reduction in hand vascular resistance. 4. Intra-arterial morphine had no local action on hand capacitance or resistance vessels. 5. Though the contrasting actions of morphine on hand and forearm capacitance vessels resulted in no important change in limb venous capacitance, the large reduction of cutaneous vascular resistance may contribute to haemodynamic benefit in patients with pulmonary oedema.

Effects of simultaneous alcohol and toluene poisoning on the cardiovascular system of rats

A group of rats was fed a control liquid diet while another group was fed a liquid diet containing alcohol up to 36% of the total caloric intake. One-half of both groups was placed in an inhalation chamber supplied with fresh air; the other two half-groups were made to inhale air containing 4000 mg toluene/m 3 for 6 hr daily, 5 days a week, for a period of 4 weeks. After exposure the ECG, hematocrit, histological structure of the heart, blood pressure, cardiac output, distribution of the cardiac output to the organs, nutritive blood flow and circulatory resistance of the organs were studied in these groups of animals. The ECG, hematocrit values, and histological and histochemical structure of the heart did not change in any of the groups. Toluene inhalation increased myocardial vascular resistance and reduced cerebral nutritive blood flow. Alcohol ingestion reduced the arterial blood pressure, the cardiac index, and nutritive blood flow to the myocardium, kidney, skin, and carcass, while myocardial and cutaneous vascular resistance as well as the cerebral blood flow fraction increased. It was concluded that the cardiovascular sites of action of toluene and alcohol were not identical.

Effects of isolated right and left ventricular stretch on regional arteriolar resistance.

In order to evaluate right and left ventricular stretch receptors without concomitantly stimulating those of the contralateral ventricle, 12 dogs were placed on total cardiopulmonary bypass. Balloons connected to compliant reservoirs were introduced into the right and left ventricles. Changes in systemic, gracilis muscle, and paw perfusion pressure at a constant flow were used as indices of systemic, muscle, and cutaneous vascular resistance. To induce left ventricular stretch, the balloon in that chanber was rapidly inflated from a mean pressure of 1.33 kPa (10 mmHg) to a mean pressure of 7.32 kPa (55 mmHg) for 15s (6.00 kPa [45mmHg] increment). For right ventricular stretch, the pressure was increased from 0.67 to 4.00 kPa (5 to 30 mmHg) for 30 s (3.34 kPa [25 mmHg] increment). Both left and right ventricular stretch produced a significant fall in systemic (-4.92 kPa [-37 mmHg], -36%) and gracilis muscle (-5.59 kPa [-42 mmHg], -30%) perfusion pressure, with only minimal changes in cutaneous vascular resistance (-0.80 kPa [-6 mmHg], -4%). This reflex was found to be vagally mediated, to have a low threshold for stimulation (left ventricle, 0.67 kPa [5 mmHg] increment; right ventricle, 1.33 kPa [10 mmHg] increment), and to have a neurogenic sympathetic alpha-adrenergic efferent limb. The low threshold for stimulation suggests that these reflexes may play a physiological role with changes in body position and may be important in such pathological conditions as semilunar valvular stenosis and myocardial infarction.

Physiological Evaluation of Pulmonary Dilutional and Enzymatic Activity on Blood-Borne Catecholamines in Cardiocirculatory Performance

Although the lung is a rich source of monamine oxidase and related catecholamine metabolizing and transporting enzymes, their physiologic role in cardiocirculatory regulation by affecting the properties of blood-borne sympathetic neurotransmitters is unclear. Accordingly, the present study evaluated the possibility that effects of pulmonary vasculature on systemic actions of catecholamines might be due to dilutional influences rather than to enzymatic activity. The experimental design was to compare left atrial (LA) and right atrial (RA) injections of norepinephrine (NEP) to ascertain a specific injection site effect, and upon documenting such a difference, to delineate whether the lesser RA injection effect could be accounted for by dilutional instead of enzymatic considerations. Thus, 0.2 µg/kg NEP was rapidly injected into RA or LA of 17 vagotomized open-chest intact canine preparations, and changes were observed in systemic blood pressure (BP), myocardial contractility (left ventricular dp/dt at 50 mm Hg pressure) and cutaneous vascular resistance (perfusion pressure of isolated hind-paw). TheLA bolus increased peak BP more (p 0.05) in peripheral resistance. However, when pulmonary vascular bed dilutional effects were obviated by steady state infusion (0.1 NEP µg/kg/min) into RA or LA, no

Potentiating effect ofβ-adrenergic stimulant on the response of the cutaneous vascular resistance toβ-adrenergic stimulant

Die Wirkung von Noradrenalin auf den peripheren vaskulären Widerstand wurde am isolierten Kaninchenohr untersucht und festgestellt, dass die Wirkung einer α-adrenergen Stimulation durch β-adrenerge Stimulation verstärkt wird.