A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.
To investigate the role of sympathoadrenergic activity on glucose production (Ra) during exercise, eight healthy males bicycled 20 min at 41 +/- 2 and 74 +/- 4% maximal O2 uptake (VO2max; mean +/- SE) either without (control; Co) or with blockade of sympathetic nerve activity to liver and adrenal medulla by local anesthesia of the celiac ganglion (Bl). Epinephrine (Epi) was in some experiments infused during blockade to match (normal Epi) or exceed (high Epi) Epi levels during Co. A constant infusion of somatostatin and glucagon was given before and during exercise. At rest, insulin was infused at a rate maintaining euglycemia. During intense exercise, insulin infusion was halved to mimic physiological conditions. During exercise, Ra increased in Co from 14.4 +/- 1.0 to 27.8 +/- 3.0 mumol.min-1.kg-1 (41% VO2max) and to 42.3 +/- 5.2 (74% VO2max; P < 0.05). At 41% VO2max, plasma glucose decreased, whereas it increased during 74% VO2max. Ra was not influenced by Bl. In high Epi, Ra rose more markedly compared with control (P < 0.05), and plasma glucose did not fall during mild exercise and increased more during intense exercise (P < 0.05). Free fatty acid and glycerol concentrations were always lower during exercise with than without celiac blockade. We conclude that high physiological concentrations of Epi can enhance Ra in exercising humans, but normally Epi is not a major stimulus. The study suggests that neither sympathetic liver nerve activity is a major stimulus for Ra during exercise. The Ra response is enhanced by a decrease in insulin and probably by unknown stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
The adrenocortical and hyperglycemic responses to hysterectomy were studied in five groups of patients receiving: general anesthesia (group I), general anesthesia + epidural analgesia extending from Th10-S5 (group II), general anesthesia + epidural analgesia extending from Th8-S4--5 (group III), general anesthesia + epidural analgesia extending from Th4--6-S5 (group IV) and epidural analgesia extending from Th4-S5 without general anesthesia (group V). The results showed that the cortisol response was abolished in group V, inhibited in group IV and normal in groups II and III. The hyperglycemic response to surgery was inhibited in groups II, III and IV, and abolished in group V. Epidural analgesia from Th4 to S5, preventing the adrenocortical and hyperglycemic responses to hysterectomy, and possibly also inhibiting other components of the endocrine-metabolic response to surgery, may have important applications in further studies of the physiologic significance of the endocrine-metabolic response to surgery.
SUMMARY1. In order to evaluate the importance of afferent neural feedback from the working muscles for cardiovascular and ventilatory responses to dynamic exercise, epidural anaesthesia was induced at L3-L4. Six healthy males cycled for 20 min at 57 % of maximum oxygen uptake and for 8-12 min at increasing work intensities until exhaustion at 238 + 30 W without as well as with epidural anaesthesia.2. Presence of afferent neural blockade was verified by cutaneous sensory analgesia below T10-T11 and attenuated post-exercise ischaemic pressor response (45 + 8-24 + 6 mmHg). Efferent sympathetic nerves appear to be intact since basal heart rate and blood pressure as well as the cardiovascular responses to a Valsalva manoeuvre and to a cold pressor test were unchanged.3. During dynamic exercise with epidural anaesthesia, blood pressure was lower than in control experiments; however, ventilation and heart rate were not affected.4. The results indicate that afferent neural activity from the working muscles is important for blood pressure regulation during dynamic exercise in man but may not be necessary for eliciting the ventilatory and heart rate responses.
Elevated arterial carbon dioxide tension, induced by the administration of CO2 via the respiratory air or by hypoventilation, entailed a gradual increase in the IOP in patients without eye diseases under general anaesthesia. A sudden cessation of CO2 administration or hyperventilation caused such a rapid, simultaneous fall in IOP to values below the initial level that the pressure variations must be of vascular nature, presumably related to changes in choroidal blood volume. The above-mentioned procedures always cause a change in the central venous pressure (CVP) simultaneously with the IOP changes. Alterations of the CVP induced by hydrostatic factors in postural changes, placing the head 15 degrees above or below the horizontal level while keeping the PaCO2 constant, caused IOP changes of the same configuration and magnitude as described above. It is concluded, therefore, that presumably the CO2-conditioned IOP changes are due predominantly to changes in central venous pressure, being one link in a CO2-conditioned action upon the general circulation, entailing passive secondary changes in the choroidal venous blood volume and thereby an influence upon the IOP. On the basis of the present results it appears rational to recommend hyperventilation to keep the PaCO2 between 25 and 30 mm and a 15 degree anti-Trendelenburg position in operations on the eye under general anaesthesia, since both procedures afford a low central venous pressure and consequently a low pressure in the posterior segment of the eye, with its attendant advantages as regards vitreous complications and the insertion of intraocular lenses. Owing to the risk of an unacceptable fall in BP in the combined procedure, a frequent checking of the BP is needed.
The effects of subarachnoid administration of 0.5% bupivacaine 4 ml in 8%, 5% or 0% glucose were investigated in a double-blind study in 30 women undergoing laparotomy through a lower abdominal incision. The onset time for maximum segmental spread of analgesia was 10-15 min for all solutions. Cephalad segmental spread of analgesia was three to four segments higher with the hyperbaric solutions (T4-5 v. T7-8). Time of onset of complete motor blockade of the lower limbs was 5-10 min for all solutions. The glucose-free solution did not produce sufficient surgical anaesthesia because of too low cephalad spread. Duration of motor blockade generally decreased with increasing glucose concentration, only the hyperbaric solutions providing useful for abdominal surgery, with a duration of 1-1.5 h. Anaesthesia (halothane) was required in seven of 10 patients in the glucose-free group and in five of 20 in the hyperbaric groups. No occurrence of "post-spinal headache" was recorded in the study.
Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 +/- 2.7 min (mean, SE) (fatigue) and oxygen uptake (VO2) increased to 1.90 +/- 0.13 1 min-1. Compared with voluntary exercise at the same VO2, increases in heart rate (HR) (135 +/- 7 vs. 130 +/- 9 beats min-1) and cardiac output (16.9 +/- 1.1 vs. 17.3 +/- 0.91 min-1) were similar, and ventilation (54 +/- 5 vs. 45 +/- 41 min-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 +/- 4 (rest) to 119 +/- 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 +/- 3 (rest) to 95 +/- 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.
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