Conus medullaris injury due to herniated disk and intraoperative positioning for arthroscopy.

This report discusses the occurrence of a cauda equina syndrome from a herniated L1-L2 disc following knee arthroscopy.

Cardiac output increase and gas exchange at start of exercise.

To determine the rapidity of increased gas exchange resulting from increased cardiac output (Q) following exercise onset, subjects performed multiple rest-exercise transitions on a cycle ergometer: the early dynamics of pulmonary gas exchange were measured during 1) rhythmic breathing with ventilation kept constant at the resting level (controlled ventilation) and 2) prolonged constant airflow exhalation. With controlled ventilation, PACO2 increased and PAO2 decreased, typically beginning in the first exercise breath. After 15 s, PACO2 had increased and PAO2 decreased by 4.5-6.2 and 8.7-12.1 Torr, respectively, graded within these narrow ranges as functions of work rate (0-100 W). Exercise starting during a prolonged exhalation caused the slopes of the alveolar phases for O2 and CO2 to increase immediately or within 2-5 s following exercise onset. Work rate had little effect on the delay or the change of alveolar gas tension slope during the subsequent 10-15 s. Thus, increased gas exchange due to increasing Q occurred very rapidly following exercise onset so that it would coincide with the first or second breath of exercise in free-breathing subjects.

Ventilatory responses to cardiac output changes in patients with pacemakers.

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Role of neural afferents from working limbs in exercise hyperpnea.

To determine the role of reflex discharge of afferent nerves from the working limbs in the exercise hyperpnea, 1.5- to 2.5-min periods of phasic hindlimb muscle contraction were induced in anesthetized cats by bilateral electrical stimulation of ventral roots L7, S1, and S2. Expired minute ventilation (VE) and end-tidal PCO2 (PETCO2) were computed breath by breath, and mean arterial PCO2 (PaCO2) was determined from discrete blood samples and, also in most animals, by continuous measurement with an indwelling PCO2 electrode. During exercise VE rose progressively with a half time averaging approximately 30 s, but a large abrupt increase in breathing at exercise onset typically did not occur. Mean PaCO2 and PETCO2 remained within approximately 1 Torr of control levels across the work-exercise transition, and PaCO2 was regulated at an isocapnic level after VE had achieved its peak value. Sectioning the spinal cord at L1-L2 did not alter these response characteristics. Thus, reflex discharge of afferent nerves from the exercising limbs was not requisite for the matching of ventilation to metabolic demand during exercise.

Carbonic anhydrase activity of the cat hind leg.

The accessibility of tissue carbonic anhydrase to plasma was studied in five surgically isolated cat hind legs. After the leg was skinned and the paw circulation occluded with a tourniquet, it was perfused with a solution that contained neither red cells nor carbonic anhydrase. Solutions containing either H14CO3- or 14CO2 were injected with 125I-albumin, 22Na+, and 3H2O into the femoral artery and the concentrations of each were measured in the femoral venous outflow. Under control circumstances the outflow patterns of H14CO3- and 14CO2 were very similar. However, after carbonic anhydrase inhibition with 20 mg/l acetazolamide in the perfusion solution, the initial exchange of H14CO3- ("extraction") was greatly decreased, whereas the extraction of 14CO2 was slightly increased. Because there was insignificant carbonic anhydrase activity in the venous outflow, these data suggest the presence of carbonic anhydrase at a readily accessible site, possibly bound to the endothelial surface. In this location it would promote CO2 exchange and minimize disequilibrium between plasma HCO3- and CO2.

Determinants of gas exchange kinetics during exercise in the dog.

Following exercise onset, CO2 output (VCO2) and O2 uptake (VO2) increase exponentially, but with appreciably different time constants. To determine the sensitivity of the time courses of these variables to altered ventilatory kinetics, rhythmic exercise was induced abruptly in anesthetized dogs by bilateral stimulation of the peripheral ends of the cut sciatic and femoral nerves. This increased the metabolic rate by 83 +/- 25 (SD) %. The dogs were ventilated with a constant-volume pump, the frequency of which was changed exponentially from the start of the exercise up to the ventilation that returned arterial CO2 and O2 pressure (PCO2 and PO2) in the steady state to resting levels. The time constant (tau) of the increase in ventilation (VE) was varied among trials. VCO2, VO2, end-tidal PCO2 and PO2, and arterial PCO2 were measured breath by breath. tauVO2 was constant at approximately 18 s regardless of alterations in tauVE. In contrast, tauVCO2 was strongly dependent on tauVE, apparently due to the larger body stores for CO2; the transitions were isocapnic when tau VE was approximately 40 s. We conclude that ventilatory dynamics can markedly influence the dynamics of CO2 exchange during exercise, but has no appreciable effect on O2 uptake dynamics.

Ventilation and gas exchange during phasic hindlimb exercise in the dog.

To investigate the importance of the major neural afferent component from the exercising extremities in exercise hyperpnea, rhythmic contraction of hindlimb muscles was produced in the dog, by electrically stimulating the peripheral cut ends of the sciatic and femoral nerves, bilaterally, for 4- to 5-min periods. VE, VCO2, and VO2 were computed breath-by-breath and PaCO2 was monitored continuously with an indwelling arterial electrode. During exercise, VO2 and VCO2 were approximately doubled in the steady state, rising with t1/2 of 25 +/- 2 and 35 +/- 4 s, respectively. VE increased within five breaths after exercise onset, and thereafter rose to a steady state with a t1/2 of 37 +/- 5 s. Mean PaCO2 increased transiently within the 1st min of stimulation but was not significantly different from control in the steady state. We conclude that the major neural afferent component from the contracting muscles is not an obligatory requirement for normal ventilatory response in the steady state of phasic exercise.

Sympathetic vasomotor outflows to hindlimb muscles of the cat.

Blood flow to the hindlimb muscles of chloralose-anesthetized, paralyzed cats was monitored with an electromagnetic flowmeter on the femoral artery. The functional pathways of the sympathetic constrictor and dilator innervations to the vasculature of these muscles were determined by measuring changes in vascular conductance during electrical stimulation of 1) ventral roots T12-L7 (exit of preganglionic fibers from the spinal cord and entrance into the sympathetic chain), 2) the distally intact sympathetic chain at successive levels between the L1 and L7 ganglia (presence of caudally running vasomotor fibers in the chain at each level), and 3) isolated sympathetic ganglia L2-L7 (exit of postganglionic vasomotor fibers from the chain at each level). Our results indicate that vasoconstrictor fibers emerge from ventral roots T12-L4 with maximum functional outflow at L1-L3; the fibers course downward through the sympathetic chain to exit from the chain mainly at L5-L7 or below. In contrast, the preganglionic origin of cholinergic vasodilator fibers, tested after blocking the constrictor fibers with bretylium, is limited to ventral roots L2-L5, with maximum outflow at L4. The vasodilator fibers leave the sympathetic chain to enter the spinal nerves at the same levels as the vasoconstrictor fibers.

Mechanisms of vascular changes in skeletal muscle during asphyxia in the cat.

Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.

Vascular response to short-term systemic hypoxia, hypercapnia, and asphyxia in the cat.

Acute systemic hypoxia, hypercapnia, or asphyxia was produced in ketamine-anesthetized, paralyzed cats by ventilating them for 2-4 min with appropriate gas mixtures. A sustained rise in arterial pressure occurred in all cases. Vascular responses to hypoxia (7% O2, 10% 02, or 14% O2) included muscle constriction, cutaneous (hindpaw) dilatation (no change with 14% O2), renal constriction (unchanged flow), and unchanged intestinal resistance. Asphyxia (hypoxia + 10% CO2) produced a similar pattern, except that intestinal dilatation occurred. Hypercapnia (10% CO2 + 21% O2) produced muscle constriction, renal constriction (unchanged flow), intestinal dilatation, and no change in cutaneous resistance. Intestinal dilatation seemed in all cases a response to elevated CO2 only. Hypercapnia augmented the effects of hypoxia in skin and skeletal muscle. The variation of responses in different vascular beds suggests a patterning of sympathetic discharge, and varying responsivity to local and humoral factors.