摘要:

Contractile responses to phenylephrine and high‐K+were investigatedin vitroin microvascular preparations from the rat medial plantar artery, a branch from the saphenous artery, obtained after short‐term denervationin vivo. Two groups of animals were studied: (1) animals undergoing surgical resection of the saphenous nerve, and (2) animals undergoing surgical resection of both the sciatic and saphenous nerves. The animals were operated on one side only. Microvascular preparations (diameter about 325 μm) were obtained 10 days after surgery. Vessels from the non‐operated side served as controls. Immunocytochemistry showed a decreased number of both neuropeptide Y (NPY) and calcitonin gene‐related peptide (CGRP) immunoreactive nerve fibres in vessels after resection of the saphenous nerve only. Resection of both the saphenous and the sciatic nerve caused a complete loss of immunoreactive nerve fibres. Mechanical measurements were performed using a wire myograph. In vessels subjected to resection of the saphenous nerve the sensitivity to phenylephrine was similar to controls. Vessels denervated by resection of both the saphenous and sciatic nerves showed significant increases in phenylephrine and potassium sensitivity. When depolarized in high‐K+solution the denervated vessels showed an increased sensitivity to extracellular Ca2+. The results show that complete short‐term denervation of the rat medial plantar arteryin vivocauses a pronounced supersensitivity in the vascular smooth muscle. The supersensitivity appears not to be restricted to the sympatheticα‐receptors but also associated with changes in the cellular excitation‐contraction coupling. Such altered reactivity of the vascular smooth muscle may contribute to vascular disturbances observedin vivoafter nerve damage or s

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00177.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Forearm blood flow during mental stress (Stroop's colour word conflict test) was studied in 18 healthy men before and during regionalβ‐adrenoceptor blockade (propranolol 0.5 mg), muscarinic receptor blockade (atropine 0.2 mg) and combined blockade, and compared with results obtained in untreated controls. Forearm blood flow was measured with venous occlusion plethysmography, and forearm vascular resistance was calculated. Arterial and venous blood sampling was performed for determination of adrenaline and noradrenaline in plasma. Mental stress increased heart rate, systolic and diastolic blood pressures and forearm blood flow, and lowered the forearm vascular resistance, to the same degree as in our previously studied controls. Neither of the intra‐arterially administered drugs had any discernible systemic effects. Beta‐blockade increased forearm vascular resistance by 32% and decreased forearm blood flow by 21% compared with unblocked levels during mental stress, whereas forearm vasodilation was maintained throughout the stress test in the control group (P < 0.05). Intra‐arterial atropine had no certain effects. Arterial adrenaline levels during mental stress were similar in the receptor‐blocked and control groups. In conclusion, the sustained forearm vasodilation during mental stress appears to be partly mediated viaβ2‐adrenoceptor stimulation (i.e. by adrenaline), but we obtained no support for a cholinergic v

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00192.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Scorpion venom can induce in dogs severe haemodynamic changes leading to rapid rise in systemic blood pressure and cardiac output, followed by reduction of cardiac output and blood pressure within 1 h. The decrease in cardiac output is not related to myocardial dysfunction (Tarasiuket al.1994). We hypothesized that scorpion venom affects cardiac output by reducing venous return to the heart. Venous return was studied by steady‐state measurements of cardiac output, the pressure gradient and resistance to venous return, in 16 dogs following injection of 0.05 mg kg−1venom obtained from the scorpion speciesLeiurus quinquestriatus. In eight of the 16 dogs, atropine (0.1 mg kg−1) was given 15 min prior to venom injection (n = 4) or 85 min (n = 4) after venom administration. In five additional dogs, the stability of the preparation over time was evaluated following the same protocol without the injection of the venom. At 15 min, the venom induced an increase in blood pressure (80%) and cardiac output (250%) (P < 0.001) with little effect on heart rate. At 90 min, cardiac output and heart rate declined considerably below baseline (P < 0.001). Atropine prevented the decrease in heart rate, but did not affect the reduction of cardiac output. Five minutes after venom injection, mean circulatory pressure increased by 300% (P < 0.001), which was accompanied by a rightward shift of the venous return curve with no effect on resistance to venous return. At 120 min, mean circulatory pressure recovered and resistance to venous return remained at 40% (P < 0.01) above baseline. This study indicates that, in dogs, scorpion venom affects cardiac output by modifying the determinants of venous return. The initial increase in cardiac output is related to increased mean circulatory pressure since resistance to venous return did not change. The later fall in cardiac output is related to the reduction of mean circulatory p

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00202.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Synchronous contractions in the intramedullary venous vasculature have been postulated to assist in the discharge of hormones from the stimulated adrenal medulla in a manner analogous to the squeezing of a wet sponge. This study reports on two experimental approaches to support the hypothesis that contractions in the venous vasculature may contribute to the hormonal efflux. Firstly, the bovine adrenal medulla was perfused retrogradely via the bovine central adrenomedullary vein and changes in the vascular volume were assessed as changes in wet weight of the perfused tissue. Stimulation with acetylcholine and carbachol resulted in repetitive, transient weight losses, suggesting cholinergically mediated reductions in the vascular volume. Secondly, the contractile properties of the longitudinal layers of smooth muscle cells in the intramedullary venous system were characterized, using the bovine central adrenomedullary vein as a model. The results showed that the longitudinal layers of this vein were, similarly to the circular layers, selectively contracted by endothelin‐1 via an ETA‐like receptor, by neuropeptide Y and by membrane depolarization (high K+). However, the vein was insensitive to electrical stimulation, acetylcholine and carbachol, as well as to catecholamines. These results suggest neuropeptide Y, released from the cholinergically stimulated chromaffin cells, as the most likely mediator of stimulus‐evoked synchronous contractions of the venous vasculature in the bovine adrenal medulla. Together, these experiments provide support for the `wet sponge' hypothesis for hormonal discharge from the adrenal

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00213.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

The effect of serotonin (5‐HT) on the metabolism of infused 1‐methylxanthine (1‐MX), a putative substrate of capillary endothelial xanthine oxidase (XO), and on the distribution of infused fluorescent microspheres (15μm) by the artificially constant‐flow perfused rat hindlimb preparation was investigated. 1‐MX (5–100μM) caused a slight inhibition of oxygen uptake (V˙O2) but was not vasoactive, either alone or with 5‐HT. 1‐MX was converted to 1‐methylurate (1‐MU) and this conversion was inhibited by allopurinol and xanthine. 5‐HT (0.35μM), which caused vasoconstriction and decreased V˙O2, also inhibited the conversion of 1‐MX, indicated by a lowered venous perfusate steady‐state 1‐MU:1‐MX ratio from 1.14 ± 0.02 to 0.71 ± 0.02 (P < 0.001), which is equivalent to the rate of conversion decreasing from 0.83 ± 0.03 to 0.63 ± 0.05 nmol min−1 g−1. This change closely followed the time course for changes in V˙O2and perfusion pressure and all three changes reversed in parallel when 5‐HT was removed. Recoveries of 1‐MU plus 1‐MX at all times were high (100 ± 5%). 5‐HT did not act to inhibit XO. When compared with vehicle alone, 5‐HT had either no effect (plantaris, gastrocnemius white, tibialis, extensor digitorum longus, vastus and thigh), or increased microsphere content (soleus and gastrocnemius red,P < 0.05) of muscles with only bone showing a significant decrease (P < 0.05). Since 5‐HT did not inhibit XO or alter the net flow to individual muscles in this constant‐flow model, the inhibition of conversion of 1‐MX to 1‐MU is concluded to be the result of a 5‐HT‐mediated decrease in the access of 1‐MX to capillary XO within individual muscles. Possibilities include the redirection of flow to capillaries either in muscle or in connective tissue closely associated with muscle, where resi

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00215.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Thoracic impedance consists of a constant baseline componentZ0and a time‐variable component ΔZwhich represents the impedance change related to the cardiac cycle. The maximum part of ΔZ[ (dZ/dt)max] represents the peak of the ascending aortic blood flow. Measurements of basal thoracic impedance are affected by structural and anatomical differences in the thorax related to sex and ageing. This component is a variable in the denominator of Sramek's formula which is used for calculating stroke volume. The aim of this study was to elucidate the question as to whether the age‐ and sex‐related variation in basal impedance may affect bioimpedance measurements of stroke volume.The study comprised 111 healthy subjects (55 males and 56 females) of ages between 20 and 69 years, divided according to age decades into five groups each of males and females. Stroke volume index (SI),Z0and (dZ/dt)maxwere measured in every subject, using transthoracic bioimpedance cardiography.Z0and (dZ/dt)maxhad significantly higher values in females than in males in every age group except the oldest one in the case ofZ0and the oldest two groups in the case of (dZ/dt)max. Stroke index showed no significant sex difference, although the higherZ0in females may underestimate the values of stroke index. Elevation of (dZ/dt)maxin females may therefore reflect a positive relation toZ0rather than higher flow rates. SinceZ0and (dZ/dt)maxare variants in opposite positions in Sramek's formula (denominator and numerator, respectively), this functional relationship may keep the bioimpedance measurements from being affected by the sex‐ and age‐related c

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.d01-1949.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

In a biventricular bypass preparation with constant‐flow perfusion, pulmonary arterial pressure (Ppa), average pulmonary capillary pressure (Ppc), venous pressure (Pv), extravascular lung water volume (EVWd) and capillary permeability‐surface area product for urea (PS) were determined in control animals and in animals subjected to alveolar hypoxia. During hypoxia,Ppaincreased in a biphasic manner, the site of hypoxic pulmonary vasoconstriction being located in the arterial upstream segment. At baseline,Ppcvalues were identical in control and experimental animals (3.4 ± 0.4 vs. 3.6 ± 0.2 mmHg). During 150 min of airway hypoxia, the rise inPpc(5.1 ± 0.3mmHg) did not exceed the rise inPpc(4.9 ± 0.5mmHg) recorded in control animals at same time interval during normoxic ventilation. EVWdincreased during hypoxia to values significantly higher than those obtained in control animals (0.559 ± 0.036 vs. 0.466 ± 0.027 mL water g−1lung). PS remained unchanged at baseline level throughout experiments in both groups of animals. Present data suggest that lung oedema formation during alveolar hypoxia may be caused by increased transcapillary fluid loss preferentially through transcellular hydrau

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00221.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Obstructive apnoeas could cause flow limitation to venous return, resulting in a decrease in cardiac output and a change in the distribution of flow from the upper and lower body. In 14 anaesthetized dogs, we studied the effects of obstructive apnoeas on inferior and superior vena caval flows under baseline conditions and with intra‐abdominal pressure increased by ≈5 torr by binding the abdomen. During obstructive apnoeas in the two groups, respiratory rate decreased by 30% (P < 0.02) and inspiratory airway pressure decreased by ≈15 torr (P < 0.01). At baseline, the ratio of inferior to superior vena caval flow was 2.4:1 and did not change with abdominal binding or apnoeas. During apnoeas there was no change in cardiac output or in the ratio of inferior to superior vena cava flow either with baseline or abdominal binding conditions. Preservation of total inferior vena caval flow during apnoeas and cardiac output occurred, even though inspiratory flow limitation was found with the abdomen bound. We conclude: (1) there was no change in either cardiac output or the distribution of venous return during apnoeas; (2) there was substantial inspiratory/expiratory variation in venous return during obstructive apnoeas. The large inspiratory increase in venous return may have implications for the development of pulmonary hypertension during obstru

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00208.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Impaired antioxidant defences may predispose to the increased resting and exercise‐induced oxidative stress found in patients with insulin‐dependent diabetes mellitus (IDDM). We investigated major erythrocyte antioxidant enzyme activities at rest and in response to sustained, moderate intensity physical exercise in young diabetic men (n = 9) previously reported to have markedly elevated plasma lipid peroxidation and blood glutathione levels compared with control men (n = 13) (Laaksonenet al.1996). At rest, erythrocyte glutathione reductase activity was 15% higher in the diabetic group (P = 0.049). Se‐glutathione peroxidase and glutathione‐S‐transferase activities were similar in both groups. Red cell Cu, Zn‐superoxide dismutase and catalase activities were lower in the IDDM group (P = 0.033 andP = 0.023, respectively). After 40 min of exercise at 60% of the subjects' peak oxygen consumption, Se‐glutathione peroxidase activity rose by about 14% in the control group (P = 0.003), but not in the IDDM group (P = 0.47). Exercise did not cause significant changes in other enzyme activities in either group. To conclude, lower erythrocyte Cu, Zn‐superoxide dismutase and catalase activity in young men with IDDM at rest may contribute to increased oxidative stress. On the other hand, increased glutathione reductase activity may represent a compensatory upregulation of glutathione homeostasis in response to increased oxidative stress. Upregulation of Se‐glutathione peroxidase activity in response to physical ac

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00200.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY

摘要:

Adenine nucleotides and glycogen are degraded in skeletal muscle during no‐flow ischaemia. Past investigations have ascribed these metabolic changes to the severe energetic stress which arises with the removal of exogenous substrates (principally oxygen). We tested this hypothesis by measuring the high‐energy phosphagen and glycogen contents of stimulated rat hindlimb muscles (1 twitch s−1) prior to and following 40 min of no‐flow ischaemia or hypoxic perfusion without glucose (Pao2= 4.6 ± 0.1 torr, plasma glucose = 0.3 ± 0.1 mmol L−1). Both experimental protocols eliminated exogenous substrate supply; however, the maintenance of flow during hypoxic perfusion ensured the removal of metabolic by‐products. A period of forty minutes of skeletal muscle ischaemia was characterized by reductions in the total adenine nucleotide pool, phosphocreatine and glycogen in the slow oxidative soleus, fast oxidative‐glycolytic plantaris and the fast glycolytic white gastrocnemius. Compared to ischaemia, the total adenine nucleotide pool was higher (by 7.2–13.3 μmol g−1dry wt) and the glycogen content lower (by 10.0–16.6 μmol g−1dry wt) in skeletal muscle exposed to hypoxic perfusion without glucose. The ability of hypoxic perfusion to attenuate TAN degradation and augment glycogenolysis can be attributed to metabolic by‐product removal. By limiting muscle lactate andPCO2accumulation, hypoxic perfusion without glucose attenuates cellular acidification; this could in turn limit AMP deaminase activation and glycogen phosphorylase inhibition. We conclude that the ischaemia‐induced alterations in adenine nucleotide and glycogen metabolism arise in response to the elimination of exogenous substrates

ISSN:0001-6772    

DOI:10.1046/j.1365-201X.1997.00210.x

出版商:Blackwell Science Ltd    

年代:1997

数据来源: WILEY