ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09698.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Eight healthy and regularly physically active men, 44–69 years old, performed one‐ and two‐legged dynamic knee extension exercise at increasing work intensities, including one leading to exhaustion. Leg blood flow increased linearly in relation to work rate, reaching a peak value of 5.1 ±0.4 1 min‐1. With a mean weight of quadriceps femoris of 2.2 ±0.1 kg, a peak perfusion of 2.3 ±0.11 kg‐1min‐1was attained. The maximal leg oxygen uptake was 0.72 ±0.071 min‐1(0.33 ±0.03 1 kg‐1min‐1). At submaximal work the elevation in limb oxygen uptake accounted for between 70 and 100% of the rise in pulmonary oxygen uptake. Comparing two‐ with one‐legged knee extension the cardiac output was 1.5 1 min‐1higher at each work level, reaching 13.7±0.7 and 12.3 ± 1.0, respectively at exhaustion, leaving 3.5 and 7.2 1 min‐1of blood flow to the remaining body (cardiac output –leg blood flow). The mean arterial pressure was 119 ±5 mmHg at rest and increased to 155 mmHg for both test modes at the maximal work rate. The femoral arterial and venous plasma concentrations of lactate, ammonia and noradrenaline were significantly higher for two‐legged as compared with one‐legged exercise at the maximal load performed. However, the rate of release per leg, for both lactate and ammonia, did not differ between the two test conditions.It is concluded that physically active middle‐aged men, with a well‐retained muscle mass, can maintain a high skeletal muscle perfusion, similar to that of young males. However, the blood flow is achieved with a higher mean arterial pressure and an elevated sympathetic activity, as reflected by noradrenaline in pl

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09699.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Cardiac output and superior mesenteric arterial flow in five healthy young men were followed using Doppler ultrasound techniques at rest and during 4 min bouts of bicycle exercise in both a pre‐ and a post‐meal situation. The meal given was mixed and heavy, with an energy content (related to body size) of about 1400–1600 kcal (5.9‐6.9 MJ). Two levels of exercise, 50–65 W and 150–200 W (about 75% ofVotmax), were tested, with the subjects cycling in a reclining position.Superior mesenteric arterial flow increased threefold, to about 1.11 min‐1, after the meal. During exercise in the fasting situation there were only modest changes in splanchnic vascular conductance, and moderate increases in superior mesenteric arterial flow were actually recorded. Exercise in the post‐prandial state caused appreciable reductions in splanchnic vascular conductance, and a 38% reduction was observed during the most heavy exercise. However, not even such a decrease in conductance resulted in any definite reduction in superior mesenteric arterial blood flow, which was maintained at the pre‐exercise level.Cardiac output increased by about 1.3 1 min‐1after the meal. The exercise‐inducedincreasesin cardiac output were of the same order in the fasting and in the post‐prandial state. Variance analyses showed the high cardiac output levels reached during postprandial exercise to be no different from levels that would be reached by pure summation of the changes caused by eating alone and by exercise alone.It is concluded that blood flow to the splanchnic organs in reclining man retains its high pre‐ and post‐prandial priority during short exercise

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09700.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

A marked decrease in splenic vascular resistance, with an increase in blood flow to the spleen, occurs already 5 min after an acute and severe hypotensive bleeding in awake rats. This response is virtually abolished in rats pretreated with a β‐adrenergic blocking agent. We have now studied the contribution of the sympathetic vasomotor innervation and of adrenal gland‐derived catecholamines to the splenic vasodilation.Splenic blood flow was determined with the microsphere method in heavily bled (1.5% of body weight) awake rats. The sympathetic neurones in one group of rats had been chemically destroyed with 6‐hydroxydopamine. In another group of rats we had removed the adrenal glands.In the control and in sympathectomized rats, splenic vascular resistance fell to 35 and 64%, respectively, of baseline 5 min after bleeding. Splenic blood flow about doubled during this period in the control rats, and then declined gradually to baseline over the next 24 h. In the sympathectomized rats, splenic blood flow decreased gradually over the first 12 h to reach 66% of baseline. The removal of the adrenal glands did not appreciably influence the splenic vascular response to bleeding.We conclude that an increased activity in the splenic sympathetic vasomotor neurones is a prerequisite for the observed vasodilation and concomitant large increase in splenic blood flow after haemorrhage in intact, awake rats. Catecholamines from the adrenal glands did not contribute detectably to the splenic vasodi

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09701.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Experiments were designed to determine the effects of sub‐zero temperatures on the function of the noradrenergic innervation of a peripheral blood‐vessel. The central ear‐artery of the rabbit was used for this purpose. The ear was exposed to temperatures of – 6, –9 or –18oCin vivofor 15 min. After 1 day (24 h) or 6 daysin vivo, the central ear‐artery was dissected free, incubated in [3H]‐noradrenaline (NA) and stimulatedin vitrowith high potassium (75 mM) for 5 min to evoke release of [3H]‐NA. The release of [3H]‐NA was Ca2+‐dependent. One day after exposure to –6, –9 or –18CC, increases of 45–57 and 44–72% and a reduction of 12–35% were observed, respectively, in three successive potassium‐evoked NA‐releases. After 6 daysin vivoan increase of 30–34% was observed following exposure to –6oC, while no alteration was observed after exposure to –9oC. A reduction of 84–89% was recorded after exposure to – 18oC. Following this exposure to – 18oC, there was also a great reduction in the evoked release of [3H]‐NA compared with the spontaneous release, whereas this correlation did not change after exposure to – 6 and – 9oC. The total uptake of [3H]‐NA was unchanged after freezing the tissue at – 6oC, but was substantially reduced after exposure to –9 and –18oC. A short period ofin vivorestoration (6 days, enhanced the uptake of [3H]‐NA. Rapid thawing, within approximately 3 min, after freezing at – 9oC (1 dayin vivo)resulted in a normal, potassium‐evoked, release of [3H]‐NA and a higher uptake of [3H]‐NA than after a longer, standardized, thawing procedure of approximately 10 min. These results demonstrate that both the evoked and the spontaneous releases of [3H]‐NA from the sympathetic nerves were increased after freezing at moderate freezing temperatures (±– 9oC), while rapid thawing resulted in a normalization of the potassium evoked released of [3H]‐NA. Exposure to –18oC reduced both the uptake and release of neurotransmitter.

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09702.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

The membrane ‘labilizer’ veratridine (3.7 ± 10‐6m) which potentiates the contractions at twitch (0.1 Hz) stimulation due to multiple discharges, inhibited the tetanic contractions (50 Hz in 10 s) and the simultaneously recorded electromyogram in a use‐dependent way, leading to fading of tetanic tension. The effect was equal during indirect and direct stimulation, and could therefore be localized to the excitable sarcolemma. This was confirmed by intracellular recording of action potentials, showing a marked veratridine‐induced fallout of action potentials during continuous 50 Hz stimulation, whereas endplate potentials were unaffected. Accordingly, veratridine probably caused a use‐dependent inhibition of the Na+channels of the excitable sarcolemma. The tetanic fade was unaffected by K+depolarization, increased by hyperpolarization in K+‐free solution, and decreased by high Ca2+. All these changes of the ionic concentrations inhibited the twitch potentiating effect of veratridine. Since hyperpolarization and increasing the electric field in the membrane with high Ca,+had opposite effects on the tetanic fade, the field change was probably not the cause of the antagonism in high Ca2+. Instead, a membrane stabilizing effect of high Ca2+is suggested, since the neutral local anaesthetic benzocaine (1.5 ± 10‐4m), which is also a membrane stabilizing drug, had the same effects as high Ca2+on the veratridine‐induced tetanic fade. The effect of veratrine during tetanic stimulation was partly reversible upon washing. The reversibility was enhanced by hig

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09703.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

A new, sensitive assay for the quantitative determination of AMP deaminase activity in human skeletal muscle is presented. The method is based on the determination of the direct product of the AMP deaminase reaction, the formed IMP, by high performance liquid chromatography (HPLC). In order to evaluate the relationship between AMP deaminase activity on the one hand and the contractile and metabolic characteristics of the muscle and the physical performance on the other, muscle biopsies were taken from 20 male subjects. The subjects also performed a 30 s sprint test on a cycle ergometer. The inter‐individual variation in AMP deaminase activity was large, ranging from 5.4 to 27.4 μkat g‐1dry muscle. AMP deaminase was positively correlated with phosphofructokinase (PFK), the marker of the glycolytic capacity of the muscle, but there was no correlation with enzymes of oxidative metabolism, such as 3‐hydroxyacyl‐CoA dehydrogenase and citrate synthase, or with the activity of myokinase and lactate dehydrogenase. There was no significant correlation between AMP deaminase activity and the proportion of the different muscle fibre types. A weak positive correlation was found between the sprint performance and the AMP deaminase activity. In conclusion, the HPLC assay was found to be a fast, sensitive and reliable method for the quantitative determination of AMP deaminase activity in muscle. A direct relationship between AMP deaminase activity on the one hand and glycolytic capacity and sprint performance on the other was found. However, no relationship to oxidative capacity or contractile properties w

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09704.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

The objective of this study was to investigate the role of nitric oxide and oxygen in the regulation of pulmonary vascular resistance, especially by means of substitution with nitric oxide after inhibition of endogenous nitric oxide formation. In artificially ventilated open‐chest rabbits pulmonary vascular resistance at normoxic ventilation (F102= 21%) was 56±6cmH2O ml‐1mim‐11000‐1(mRUL).Nw‐nitro‐L‐arginine methyl ester (l‐NAME, 30 mg kg‐1), an inhibitor of NO synthase, increased pulmonary vascular resistance to 122±17 mRULat normoxic ventilation. In response to l‐NAME there was also an increase in mean arterial blood pressure. Exogenous nitric oxide (0.014‐9 p.p.m. in the inhaled air) dose‐dependently and reversibly counteracted the effect of l‐NAME on pulmonary vascular resistance at normoxic ventilation, without affecting systemic blood pressure. In addition, the L‐NAME‐induced vasoconstriction was critically dependent on oxygen. Thus, during hypoxic ventilation (F1O2= 10%) the pulmonary vascular resistance was increased approximately four‐fold by the presence of L‐NAME (30 mg kg‐1), and increments in F,02(21–100%) dose‐dependently and reversibly counteracted the effect of L‐NAME on pulmonary vascular resistance.Taken together these findings demonstrate that inhalation of low doses of NO may act as a replacement when endogenous NO synthesis is inhibited, and that pulmonary vasoconstriction induced by NO synthesis inhibition is likely to be the result of interference with oxygen‐dependent regulatory mechanisms. Endogenous NO cooperates with oxygen to evoke a vasodilator component of the pulmonary hypoxic pressor response, balan

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09705.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Histamine is released from the heart during ischaemia‐reperfusion injury. As histamine has cardiac effects, we investigated the role of histamine in ischaemia‐reperfusion injuryofisolated rat hearts. A Langendorff‐model with 30 min global (37oC) ischaemia followed by 60 min reperfusion was employed. The effects of ischaemia alone (n= 10, group 1.1+n = 10, group 2.1, 2 different series), and ischaemia with H1‐ and H2‐receptor blockade with cimetidine (10 μM, n= 10), chlorpheniramine (10 μm,n= 8), terfenadine (10 μM,n= 8), and promethazin (10μM,n= 9), or both cimetidine and chlorpheniramine (n =8), were studied. Histamine was measured in the coronary effluent and cardiac tissueofgroup 1.1. Release of histamine increased from 6.5 ± 1 pmol min‐1before ischaemia to 19 ± 3 pmol min‐1at the start of reperfusion. Ischaemia decreased left ventricular developed pressure to 18 ± 11 % (1.1) and 50 ± 11 % (2.1) of initial value (mean ± SEM) at the start of reperfusion. Left ventricular end‐diastolic pressure increased from 0 to 79 ± 8 mmHg (1.1) and 39 ± 9 (2.1) mmHg, while left ventricular systolic pressure was unchanged (101 ± 12% in 1.1 and 101 ± 10% in 2.1). Severe arrhythmias were induced in 90 (1.1) and 30 (2.1)% of the hearts, while coronary flow decreased during reperfusion. H2‐blockade did not modify the changes in left ventricular pressures, coronary flow, or heart rate induced by ischaemia. Three different Hj‐blockers increased left ventricular systolic pressure, inhibited the decrease of developed pressure, attenuated the increase of end‐diastolic pressure, and totally inhibited reperfusion arrhythmias. The effect of both blockers together was similar to that of H1‐blockers alone. Coronary flow was increased during reperfusion in two of the groups with Hj‐blocker compared with ischaemic controls. Increased release of histamine from ischaemic‐reperfused rat hearts concurred with depression of left ventricular function and arrhythmias during early reperfusion. Cardiac dysfunction during reperfusion was attenuated

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09706.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY

摘要:

Ischaemic preconditioning by brief ischaemic episodes could be explained by reduced cellular calcium ion (Ca2+) influx, reduced cytosolic Ca2+overload and delayed cell‐injury during subsequent long‐lasting ischaemia. L‐type calcium channels (LCC) regulate sarcolemmal Ca2+influx in myocardial cells. The aim of this study was to investigate if preconditioning was associated with reduced density or altered state of LCC in the preconditioned region of the heart. To test this we compared the density and the dissociation constant of (4‐)‐[3H]isradipine binding to LCC in membranes from preconditioned and control regions of porcine hearts. Eight porcine hearts were regionally preconditioned by two 10‐min occlusions of the mid left anterior descending artery, and each occlusion was followed by 30 min of reperfusion. Biopsies were taken from the preconditioned regions and control regions supplied by the circumflex artery at the end of the last reperfusion, and (+)‐[3H]isradipine binding to membranes made from the biopsies was measured. The differences in density and dissociation constant of (4‐)‐[3H]isradipine binding to LCC in membranes from preconditioned and control regions were not significant. In conclusion, the proposed effect of ischaemic preconditioning to reduce Ca2+influx, does not involve local changes in density or state of LCC that could be detected by (+)‐[3H

ISSN:0001-6772    

DOI:10.1111/j.1748-1716.1994.tb09707.x

出版商:Blackwell Publishing Ltd    

年代:1994

数据来源: WILEY