Head-up tilt effect on glomerular filtration rate, renal plasma flow, and mean arterial pressure in spinal man.

Changes in glomerular filtration rate (GRF), renal plasma flow (RPF), and mean arterial pressure (MAP) were measured in subjects tested in supine and head-up tilt positions with various levels of spinal cord lesion and thus with different degrees of supraspinal sympathetic vasomotor control. Responses of paraplegic subjects to head-up tilt were not significantly different from those of normal controls but GFR and RPF were significantly lower in quadriplegics in the supine position. With tilt, MAP and RPF decreased significantly, but the fall in GFR was not significant. In all 3 groups, the GFR during head-up tilt was similar, indicating that in spite of the great loss of supraspinal sympathetic control, quadriplegic subjects apparently equally-constrict their afferent and efferent renal arterioles during orthostatic stress and thus prevent excessive fall of GFR.

Spinal cord injury: effect of thyrocalcitonin on calcium, magnesium and phosphorus in paraplegic rats.

Calcium, magnesium and phosphorus balances were studied in 20 paraplegic rats (T5) fed ad libitum an 18% casein diet. Ten of the paraplegic animals were treated daily with 4MRC (Medical Research Council) units of thyrocalcitonin. Ten sham-operated rats served as controls. Spinal cord transection caused an immediate increase in urinary excretion of calcium, 550 +/- 70 micrograms/24 hr, compared with controls levels, 257 +/- 85 micrograms/24 hr. Paraplegia also resulted in an elevated excretion of fecal calcium, 39 +/- 5 mg/24 hr, phosphorus, 42 +/- 7 mg/24 hr, and magnesium, 4.6 +/- 0.8 mg/24 hr, compared with that of controls, 26 +/- 6 mg/24 hr, 32 +/- 6 mg/24 hr and 2.7 +/- 0.8 mg/24 hr for calcium, phosphorus and magnesium, respectively. Administration of thyrocalcitonin to paraplegic rats further increased urinary excretion of calcium, 835 +/- 186 micrograms/24 hr. However, fecal losses of calcium, 19 +/- 5mg/24 hr, phosphorus, 31 +/- 6mg/24 hr, and magnesium, 2.6 +/- 0.4mg/24 hr, which were elevated following spinal cord transection, were markedly reduced after thyrocalcitonin treatment. As a result, balances of these compounds, which were depressed in rats following spinal cord transection, were "normalized" after treatment with thyrocalcitonin. It would seem, therefore, worthwhile to study the effect of thyrocalcitonin in spinal cord injured humans in an effort to determine whether or not it would be helpful in improving mineral balances.

Pituitary-testicular axis dysfunction in spinal cord injury.

Concentrations of testosterone, luteinizing hormone (LH), and follicle-stimulating hormone (FSH) in serum and 17-ketosteroids (17-KS) in urine of 10 paraplegic and 10 quadriplegic subjects were measured from onset of injury and followed once a week for 4 months. Compared with age-matched normal controls, paraplegic subjects showed significantly lower serum levels of LH and FSH for 2 weeks and of testosterone for 6 weeks after spinal cord trauma, following which periods of time these hormones attained normal levels. By contrast, in quadriplegic subjects, serum testosterone concentrations remained significantly lower than those of the controls during the entire 4-month testing period. Furthermore, in another group of 10 chronic (1 to 6 years after onset of injury) paraplegic and 10 chronic quadriplegic subjects, serum testosterone and FSH concentrations were comparable to those of the normal controls. Serum LH concentrations were at control levels in chronic paraplegic but significantly depressed in chronic quadriplegic subjects. The concentrations of urinary 17-KS exhibited sharp fluctuations over the 4-month period and were below control levels in paraplegic but within control limits in quadriplegic subjects. The results indicate that the function of the hypothalamic-pituitary-gonadal axis is disturbed for at least 4 months in quadriplegic subjects.

Mineral metabolism in spinal cord injury.

In 10 paraplegic and 10 quadroplegic subjects, bone resorption was investigated by determining urinary excretion of hydroxyproline, calcium, and phosphorus. Measurements were performed weekly from the onset to 4 months after injury. During the first 7 weeks following injury, urinary excretion of calcium in paraplegic and quadriplegic subjects reached the highest level (380 +/- 180 mg/24hr). From 7 to 16 weeks after injury average urinary excretion of calcium (245 +/- 72 mg/24hr) remained significantly greater than that in controls (100 +/- 25 mg/24hr; p less than 0.05). Urinary hydroxyproline was elevated in paraplegic subjects (80 +/- 18 mg/24hr) for 8 weeks and in quadriplegic subjects (102 +/- 37 mg/24hr) for the entire 16 weeks following injury compared with that in controls (48 +/- 12 mg/24hr; p less than 0.05). Both paraplegic and quadriplegic subjects excreted more phosphorus (1.6 +/- 0.4 gm/24hr) than controls (0.85 +/- 0.2 gm/24hr; p less than 0.05) only during the first 2 weeks following spinal cord injury. During the acute phase of the injury (0-3 months), urinary excretion of calcium and magnesium was significantly higher (p less than 0.05) in subjects with complete compared with incomplete spinal cord lesions.

Spinal cord injury: effect of thyrocalcitonin on periarticular bone formation in three subjects.

Sodium fluoride 18F scintimetry was performed before and after 1 month of salmon thyrocalcitonin treatment of 3 spinal cord injured patients with periarticular ossification of the hips and knees. Thyrocalcitonin therapy caused a marked diminution of 18F uptake in 1 patient with long-standing periarticular bone of both hips. Clinically, the range of motion in this subject increased by 25 degrees and there was a marked decrease in pain locally. The results were, however, not duplicated in the 2 patients with periarticular bone formation of short duration.

Hypertensive crises in quadriplegic patients. Changes in cardiac output, blood volume, serum dopamine-beta-hydroxylase activity, and arterial prostaglandin PGE2.

The syndrome of autonomic dysreflexia often occurs in quadriplegic subjects and is characterized by paroxysmal hypertension, headache, vasoconstriction below and flushing of the skin above the level of transection, and bradycardia. These attacks may cause hypertnesive encephalopathy, cerebral vascular accidents, and death. In five patients during crises, the mean arterial pressure changed from 95 to 154 mm Hg, heart rate 72 to 45 beats/min, cardiac output 4.76 to 4.70 L/min, and peripheral resistance 1650 to 2660 dynes.sec.cm-5. In eight subjects the control plasma, red cell, and total blood volumes were 19.1, 10.5, and 29.6 ml/cm body height, respectively, and when hypertensive, the plasma protein concentration increased by 9.9% and the hematocrit by 9.5%. Plasma volume was only reduced by an estimated 10-15%. At that time, arterial dopamine-beta-hydroxylase (DbetaH) activity increased 65% and prostaglandin E2 concentration by 68%. Thus, the augmented DbetaH activity presented primarily an elevated sympathetic tone and not hemoconcentration of that protein. The rise in prostaglandin may contribute to the severe headaches during hypertensive episodes.

Bone mineralization in the distal forearm of hemiplegic patients.

Bone mineral content was measured by single photon absorptiometry using a modified bone densitometer (Packard) with 125I as the source. In 42 hemiplegic subjects, matched for sex and age, the bone density was compared bilaterally on the radius and ulna 2 cm and 4 cm above the wrist. The nonparalyzed side served as a control for the paralyzed side. The results indicate a consistent, general loss of bone mineral on the paralyzed side compared with the nonparalyzed side. The extent of demineralization in females was greater than in male subjects. Right-dominant left-paralyzed patients showed a greater loss of bone density than right-dominant right-paralyzed subjects. The absorption ratio of the paralyzed vs the nonparalyzed sides revealed that there was a 5.3% and 7.4% decrease in the average bone density at 4 and 2 cm above the wrist, respectively. There was a progressive loss of bone mineral content relative to time after the onset of paralysis, amounting to an average of 6.4% approximately three months after the onset of injury. It was estimated that before the onset of paralysis there was an excess of bone mineral on the dominant vs the nondominant side of +5.4% and +3.2% for males and females, respectively.