Biomedical subjects
Publications and source records attributed to O Henriksen.
Magnetic resonance imaging offers new possibilities in the investigation of the prostate. The current results of imaging and tissue discrimination in the evaluation of prostatic disease are reviewed. Magnetic resonance imaging may be of value in the staging of carcinoma of the prostate.
Pure sensory stroke (PSS) is typically caused by a lacunar infarct located in the ventral-posterior (VP) thalamic nucleus contralateral to the paresthetic symptoms. The lesion is usually so small that it cannot be seen on computerized tomography (CT), as illustrated by our case. In our moderately hypertensive, 72-year-old patient with PSS, CT scanning and conventional nuclear magnetic resonance imaging (NMRI) scanning using a 7-mm-thick slice on a 1.5 Tesla instrument all failed to visualize the thalamic infarct. Using the high-resolution mode with 2-mm slice thickness it was, however, clearly seen. In addition, NMRI unexpectedly showed diffuse periventricular demyelinization as well as three other lacunar infarcts, i.e., findings characteristic of subcortical arteriosclerotic encephalopathy (SAE). This prompted psychometric testing, which revealed signs of mild (subclinical) dementia, in particular involving visiospatial apraxia; this pointed to decreased function of the right parietal cortex, which was structurally intact on CT and NMRI. Single photon emission computerized tomography by Xenon-133 injection and by hexamethyl-propyleneamine-oxim labeled with Technetium-99m showed asymmetric distribution of cerebral blood flow (CBF), with an 18% lower value in the right parietal cortex compared to the left side; this indicated asymmetric disconnection of the cortex by the SAE. Thus, the tomograms of the functional parameter, CBF, correlated better with the deficits revealed by neuropsychological testing than by CT or NMRI.
From a 7-day food recording in 29 morbidly obese patients two groups of six patients each were selected: a high-energy-intake group (HEI) and a low-energy-intake group (LEI). The groups were otherwise comparable. Five lean subjects served as controls for some observations. Oral glucose tolerance tests showed that all patients in the HEI group and the lean controls had normal glucose tolerance, whereas it was abnormal in all subjects in the LEI group. The fasting metabolic rate did not differ between the obese groups but was significantly lower in the lean group. The glucose-induced thermogenesis during 180 min expressed as a percentage of the energy content of the glucose load was lower in both obese groups compared with the lean controls (lean: +11.5 per cent, HEI: +5.3 per cent and LEI: -4.2 per cent, HEI vs lean: P = 0.04 and LEI vs lean: P = 0.005), and lower in the LEI group compared with the HEI group (P = 0.02). The integrated increase in leg oxygen consumption after glucose was also smaller in the LEI group than in the HEI group (15 +/- 269 vs 987 +/- 356 ml, P less than 0.05). The arterial noradrenaline response to glucose was significantly diminished in both obese groups compared with the lean controls. Glucose induced a similar increase in leg noradrenaline release in both obese groups, whereas the arterial adrenaline level was lower in the LEI group compared with the HEI group and with the lean controls (P = 0.04). Among the obese subjects the degree of glucose intolerance was inversely correlated with the post-glucose arterial adrenaline level (r = -0.55, and P = 0.04), and positively correlated with the fractional leg adrenaline extraction (r = 0.71, and P = 0.003). The results suggest that patients who are obese in spite of a fairly low energy intake have a reduced glucose-induced facultative thermogenesis, and that the defect is at least in part located in skeletal muscle. Since the sympathetic nervous system is partly responsible for the glucose-induced thermogenesis, the reduced thermogenic response in the obese patients may be due to an impaired activation of the sympathetic nervous system. It is hypothesized that the reduced arterial adrenaline level in the LEI group is caused by hyperglycaemic suppression of the adrenomedullary secretion and further that this may be a link connecting deterioration of glucose tolerance and a thermogenic defect in obesity.
A technique for noninvasive determination of cardiac output by aid of first-pass radionuclide cardiography is described. After intravenous injection of 10-15 mCi technetium-99m-(99mTc) labeled red blood cells the method requires acquisition of a first passage time-activity curve recorded with a gamma camera over the left ventricle, the background corrected left ventricular count rate recorded after complete mixing of the tracer in the circulation, and determination of the distribution volume of the tracer. The method was applied in 14 patients with heart disease of various origins and evaluated against the conventional tracer dilution technique with arterial sampling of blood activity. Cardiac output determinations by external counting ranged from 2.30 to 8.56 l/min, mean +/- s.d. 4.50 +/- 1.66 l/min and by arterial blood sampling from 1.88 to 8.96 l/min, mean +/- s.d. 4.52 +/- 1.71 l/min. An excellent correlation was demonstrated between the two techniques, r = 0.978 (p less than 0.001). When no background subtraction was applied to the left ventricular counts at equilibrium, radionuclide cardiac output values were approximately 40% higher than those obtained by arterial sampling. The new first-pass radionuclide cardiographic technique may prove a useful tool in the noninvasive evaluation of cardiac function, especially in patients with arrhythmias and/or valvular incompetence.
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Relative changes in blood flow and vascular resistance in arm and leg muscle during head-up tilt at 45 degrees were studied in eight patients with complete cervical spinal cord transection and in 13 healthy volunteers. Muscle blood flow was measured by the local 133Xe washout method. In forearm muscle kept at heart level blood flow remained constant in the tetraplegic patients during head-up tilt, in contrast to that seen in the normal subjects, where blood flow decreased by 30%. In the dependent leg muscle, head-up tilt caused a decrease in blood flow of 46% and 40% in the patients and normals, respectively. Abolition of the local veno-arteriolar axon reflex, by inducing local counter-pressure to prevent venous distension in the dependent leg muscle, reduced the decrease in blood flow to 24% and 23%, respectively. Thus, the vascular response to head-up tilt differed significantly in forearm muscle between the two groups, whereas no difference was seen in the leg muscle. The absence of the vasoconstrictor response in forearm muscle indicates that postural sympathetic reflexes to this region depend on sympathetic reflexes integrated in centres located rostrally to the spinal cord. The results further suggest that local veno-arteriolar axon reflexes as well as spinal reflexes contribute to the observed vasoconstriction in the leg muscle.
Left ventricular end-diastolic and end-systolic volumes were determined in 17 patients with different levels of left ventricular function by magnetic resonance imaging (MRI). A 1.5 Tesla Magnet was used obtaining ECG triggered single and multiple slices. Calculated cardiac outputs were compared with those measured simultaneously by a classical physiological indicator dilution technique. There was good agreement between cardiac output as measured by MRI and the indicator dilution method, when the multislice technique was used (r = 0.87, p less than 0.001). A poor correlation between the two methods was seen when the single slice technique was used (r = 0.06, p greater than 0.80). The results indicate that MRI is a reliable method for left ventricular volume determination when the multislice technique is used.
The effect of moderate hypoxemia upon postural sympathetic vasoconstrictor reflexes in skeletal muscle was studied in five healthy young students, aged 20-30 years. The vasoconstrictor response to head-up tilt was studied in brachio radial muscle kept at heart level and in the anterior tibial muscle. The local sympathetic veno-arteriolar axon reflex was studied in the anterior tibial muscle placed at heart level and lowered 30-50 cm below heart level. Muscle blood flow was measured by the local 133Xe wash-out technique. The measurements were carried out with the subject breathing atmospheric air and with the subject breathing 10-11% oxygen. No sign of orthostatic intolerance was seen during hypoxaemia as arterial blood pressure remained constant in the tilted position. Hypoxaemia did not alter the head-up tilt induced vasoconstriction in brachio-radial and anterior tibial muscles. The vasoconstriction elicited by the local veno-arteriolar reflex was slightly reduced during hypoxaemia. The results suggest that central orthostatic vasoconstrictor reflexes to muscle are essentially normal during moderate hypoxaemia, but local veno-arteriolar reflexes are slightly attenuated. This does not, however, significantly alter blood pressure control during head-up tilt.
In sodium deplete subjects forearm (FBF) and splanchnic (SBF) blood flows were measured at rest and during lower body negative pressure (LBNP) before and during angiotensin II (ANG II) blockade. Both FBF and SBF were reduced by LBNP. Forearm blood flow and forearm vascular resistance were unaffected by ANG II blockade (intra-arterial saralasin, n = 6; i.v. enalapril, n = 9) both at rest and during LBNP. In contrast, resting SBF increased and splanchnic vascular resistance decreased after i.v. enalapril (n = 10). The low resistance was completely unchanged during the following LBNP. It is concluded that acute ANG II blockade has no influence on the vascular resistance in the human forearm, but increases basal SBF in sodium depleted subjects and 'paralyses' the vasoconstrictor response to LBNP.
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Autoregulation of blood flow in subcutaneous tissue was studied at the level of the lateral malleolus in eight long-term Type 1 (insulin-dependent) diabetic patients with clinical microangiopathy, eight short-term Type 1 diabetic patients without clinical microangiopathy and seven healthy control subjects. Blood flow was measured by the local 133Xenon washout technique. Mean arterial blood pressure was reduced by a maximum of 23 mmHg by elevating the limb above heart level and elevating to a maximum of 70 mmHg by head-up tilt; in the latter position venous pressure was kept constant and low by activation of the leg muscle vein pump (heel raising). Mean arterial blood pressure was thus varied between 60 and 160 mmHg. In normal and short-term diabetic subjects blood flow remained within 10% of control values during the changes in arterial blood pressure. In six of the eight Type 1 diabetic patients with clinical microangiopathy, autoregulation of blood flow was impaired, blood flow changing approximately 20% per 10 mmHg change in arterial blood pressure; the slope of the autoregulation curves was significantly higher compared with the two control groups (p less than 0.02). Resting mean arterial blood pressure was significantly elevated in long-term diabetic patients (median: 107 mmHg) compared with short-term diabetic (median: 85 mmHg) and control subjects (median: 91 mmHg) (p less than 0.01 and p less than 0.02, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)
Capillary permeability of 131I-albumin in skeletal muscle was determined by applying the "single injection, residue detection" method to the autoperfused cat gastrocnemius muscle preparation. Experiments at zero venous pressure gave an average capillary extraction fraction, E, of 0.028 at a plasma flow of about 3 ml X (100 g)-1 X min-1. The permeability-surface area product, PS, was on average 0.075 ml X (100 g)-1 X min-1. Experiments at a venous pressure of 10 mm Hg gave essentially the same PS product (0.070 ml X (100 g)-1 X min-1. Further experiments demonstrated that stagnant intravascular pools of 131I-albumin were not present. The free diffusion coefficient in water at 37 degrees of the purified 131I-albumin was 0.0631 X 10-5 cm2 X sec-1). The distribution volume for 131I-albumin in the interstitial space was 3.5 ml X (100 g)-1 X sec-1. Assuming a capillary surface area of 70 cm2 X g-1 the permeability coefficient was calculated to be 18 X 10(-8) cm X sec-1 which is about 3 to 10 times higher than values obtained by lymph sampling methods. The results indicate that the predominant transcapillary transport mechanism for 131I-albumin is diffusion. When analyzed according to the theory of restricted diffusion the results are compatible with transcapillary diffusion through pores with an effective equivalent pore radius of 145 A.
Local blood flow regulation was studied on the forefoot by the 133-Xenon wash-out method. In 21 normal limbs blood flow decreased 36% when the foot was lowered 40 cm below heart (local vasoconstrictor response). During elevation blood flow was constant to 20 cm, and flow decreased only 10% at further elevation to 40 cm, corresponding to a drop in vascular resistance of 15% (autoregulation of blood flow). In six sympathetically denervated limbs blood flow decreased only 6%, significantly less than in the normal limbs. Autoregulation of blood flow was preserved in these limbs. In 22 limbs with intermittent claudication blood flow decreased only 19%, significantly less than in the normal limbs. However, taking into account the additional increase in arterial pressure that occurs, when a limb with arterial occlusion is lowered there was no significant difference (p = 0.26) in the increase in vascular resistance between the two groups. During elevation vascular resistance decreased significantly in the claudicants indicating preservation of autoregulation. In limbs with rest pain blood flow increased 28% during lowering, and when the additional increase in arterial blood pressure was accounted for, a significant increase in vascular resistance of 21% was noted. During elevation blood flow decreased significantly, and the estimated vascular resistance in this group did not decrease significantly. The study suggests that the increase in blood flow and the relief of ischaemic rest pain induced by lowering are due to an additional increase in arterial pressure rather than due to dilatation of arterioles.
The study was performed in order to determine the effect of venous pressure elevation induced by unilateral partial renal venous ligation upon total renal blood flow and filtration fraction in the dog kidney. An anaesthesia with no known inhibitory effect on sympathetically mediated vasoconstriction was used. During control conditions instantaneous increase in renal venous pressure to 60 mmHg induced a decrease in renal blood flow (66 +/- 4%) corresponding to an ipsilateral vasoconstriction which was completely abolished following (1) surgical denervation of the kidney, (2) local alpha-receptor blockade of the kidney, and (3) application of lidocaine on the kidney surface. The most striking feature during step increase in renal venous pressure to 40 mmHg was an increase in renal vascular conductance. Renal venous pressure elevation of more than 40 mmHg induced a vasoconstriction, but the vasoconstrictor response was less pronounced as compared with that observed during instantaneous increase in renal venous pressure to the same level. The results strongly suggest that venous stasis of more than 40 mmHg activates an adrenergic sympathetic vasoconstrictor reflex comprising the spinal cord. The reflex is probably elicited from stretch receptors located in the renal capsule. Changes in filtration fraction at venous stasis during the experimental conditions indicate that renal venous pressure elevation activates mechanisms other than neural ones accounting for the reduction in the filtration fraction.
Studies in man indicate that skeletal muscle blood flow is modulated via high pressure baroreceptors located in the carotid body. However, whether subcutaneous blood flow is influenced in this way remains controversial. Therefore, the aim of the present study was to determine whether subcutaneous as well as skeletal muscle blood flow was influenced by direct carotid body stimulation; this was done by means of neck suction. Six young healthy males were investigated. Subcutaneous and skeletal muscle blood flow in the forearm was measured by the local 133Xe washout technique. Neck suction of -20 mmHg was applied through a tight helmet covering the head and neck. In the supine position heart rate increased about 10%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged, but skeletal muscle blood flow increased about 70%. Measurements were repeated during neck suction, -20 mmHg, and 45 degrees head-up tilt (which is known to decrease subcutaneous blood flow and skeletal muscle blood flow by increasing sympathetic vasoconstrictor activity). Heart rate increased by about 20%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged and skeletal muscle blood flow increased about 100%. These results indicate that skeletal muscle blood flow is modulated through carotid baroreceptors. Subcutaneous blood flow seems not to be influenced by high pressure baroreceptor modulation, although a vasoconstrictor response to head-up tilt was demonstrated in this as well as other recent studies.
The effect of vascular surgical reconstruction or Buerger's exercises upon average subcutaneous blood flow for a 24-h period was studied in 14 patients with severe leg ischemia due to occlusive arterial disease. Blood flow was estimated proximally in the calf and in the foot by a 133Xe washout technique. Seven patients underwent vascular surgery. Postoperatively subcutaneous blood flow increased in the calf and the foot in all patients except one in whom a decrease in blood flow in the foot was seen. In this case a decrease in systolic blood pressure occurred following the operation. Buerger's exercises did not alter subcutaneous blood flow either in the calf or in the foot in the seven patients studied. Buerger's exercises seem to be of no value for these patients. The measurement of blood flow in subcutaneous tissue over a period of 24 h seems to be a useful test of the effect of different treatments.
The autoregulation of blood flow in subcutaneous tissue was investigated at the level of the lateral malleolus by the local 133Xenon washout technique. We have investigated eight long-term insulin-dependent diabetics and seven healthy controls. All diabetics had moderate diabetic nephropathy and retinopathy. The blood flow remained constant in all normal subjects, when the arterial perfusion pressure was varied between 70 and 150 mm Hg. All diabetics had impaired or reduced autoregulation of the subcutaneous blood flow. The blood flow increased and decreased almost linearly with the changes in arterial perfusion pressure. The mechanism underlying the defect autoregulation of blood flow in diabetics is uncertain; possibilities include structural changes of the arterioles and/or alterations of local metabolic factors.