Skeletal muscle oxygen pressure fields during controlled hypotension with adenosine and sodium nitroprusside A comparative study in the rabbit

The MDO (Mehrdraht Dortmund Oberfläche) multiwire oxygen electrode was used for studies of oxygen pressure fields in eight rabbit skeletal muscle preparations during controlled hypotension with adenosine and sodium nitroprusside (SNP). Tissue oxygen histograms were constructed from 120 simple tissue oxygen pressures (P_tO₂) samples that were collected during 5 min. Statistical analysis between histograms was performed with the two-sample Kolmogorov-Smirnov test. Mean arterial blood pressure was reduced to 60 mmHg with both drugs, corresponding to a 42–43% reduction during the 25-min hypotension period. SNP-induced hypotension caused significant reduction of muscle oxygenization (compared to normotensive controls) in six of the animals, while this occurred on three occasions during adenosine administration. When comparing the histograms during hypotension, the tissue oxygenation during adenosine infusion was higher than during SNP in five and equal to SNP in three animals. Low tissue oxygen pressure values (0-0.6 kPa) were four times more frequent during SNP than during adenosine hypotension, although systemic arterial oxygen pressures were unaffected. We conclude that controlled hypotension with adenosine preserves tissue oxygen pressures better than hypotension induced by SNP.     

Vectorcardiographic changes during laparoscopic cholecystectomy may mimic signs of myocardial ischaemia

Background: Laparoscopic surgery involves the use of intra-ab-dominal carbon dioxide insufflation (pneumoperitoneum). The increased intra-abdominal pressure causes marked haemodyn-amic changes, which may influence electrocardiographic monitoring. The aim of the present study was to elucidate the influence of pneumoperitoneum on vectorcardiographic recordings.
Methods: Vectorcardiographic changes (QRS vector difference= QRSVD, QRS loop area, QRS magnitude, ST vector magnitude, spatial ST vector change) were recorded continuously applying computerized vectorcardiography in 12 anaesthetised cardio-vascularly healthy patients, scheduled for laparoscopic cholecystectomy.
Measurements were made before and during pneumoperitoneum in three different body positions (supine, Trendelenburg and reversed Trendelenburg), also employing transesophageal echo-cardiography and invasive blood pressure monitoring. Results: Pneumoperitoneum significantly increased QRSVD, in parallel with an enlargement in loop area and magnitude. The magnitude was significantly increased in the transversal and frontal planes and there was a tendency to increase the magnitude in the sagittal plane. The increase in QRS-VD reached levels previously associated with the development of myocardial ischaemia in patients with coronary artery disease. The ST-variables were not changed by the pneumoperitoneum. The positional changes also influenced QRSVD significantly.
Conclusions: When computerized vectorcardiography is used for ischaemia monitoring during pneumoperitoneum, the ST-variables seem reliable. However, vectorcardiographic QRS changes should be interpreted with caution, as the QRS alterations found during pneumoperitoneum mimic the changes seen during myocardial ischaemia.     

ST Depression and Left Ventricular Haemodynamics during Exercise in Patients with Angina Pectoris

ABSTRACT. The mechanism of ischaemic ST depression and the cause of its low sensitivity to coronary artery stenosis are not well understood. Of 30 patients with severe stable effort angina, 19 (63%) showed ischaemic ST depressions after exercise (the STAE group) and 11 did not. The highest load during the symptom-limited exercise test and the heart rate on that load did not differ between the two groups. The clinical characteristics and angiographic findings were also similar, bat the findings at heart catheterization differed during exercise (in supine). Although the load was similar, the stroke index was significantly lower (38 vs. 53 ml/m² BSA) and the left ventricular end-diastolic pressure rose to a significantly higher value in the STAE group (40 vs. 32 mmHg). When STAE occurred, they were exclusively or concomitantly present in chest lead 5. These findings suggest that ischaemic STAE may not reflect regional ischaemia but the consequent left ventricular dysfunction. The mechanism may, for example, be that a sufficiently elevated left ventricular diastolic pressure causes a global subendocardial ischaemia.     

Skin reactions to primary irritants and predisposition to eczema

Fifty individuals with healed hand eczema were tested with nine primary irritants. The results were compared with those of carefully matched controls. An increased skin reactivity to primary irritants was not demonstrated in the ‘eczematous subjects’. The value of testing with irritants in pre-employment evaluation could not be confirmed.     

Cerebral blood flow and metabolism during adenosine–induced hypotension in patients undergoing cerebral aneurysm surgery

The effects of adenosine-induced hypotension on cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and cerebral lactate production, together with systemic haemodynamics, were studied in 10 patients undergoing cerebral aneurysm surgery in neurolept anaesthesia with controlled hyperventilation. CBF changes were determined in six of the patients with a retrograde thermodilution technique in the jugular vein. Hypotension was induced with a continuous infusion of adenosine in the superior vena cava. The dose range was 0.06-0.35 mg/kg/min, and this caused a 42% reduction in mean arterial blood pressure (MABP) from 79 +/- 4 to 46 +/- 1 mmHg (10.5 +/- 0.5 to 6.1 +/- 0.1 kPa) through a profound reduction in systemic vascular resistance (SVR), which amounted to 61%. No significant change occurred in CBF. Whole body AV-difference of oxygen was decreased by 37%, and cerebral AV-difference by 28%, corresponding to reductions in whole body oxygen uptake and CMRO2 of 16 and 17%, respectively. Cerebral AV-difference of lactate did not change. In the posthypotensive period MABP was increased by 10%, together with a minor increase in CBF (15%). It is concluded, that adenosine-induced hypotension at MABP levels between 40-50 mmHg (5.3-6.7 kPa) does not affect cerebral oxygenation unfavourably, and may even offer a protective effect by reducing cerebral oxygen demand. The slight CBF increase in the posthypotensive period was probably secondary to an increase in MABP together with a blunted autoregulation, but in no case was this effect considered to be harmful for the patient.     

TOWARDS A BETTER UNDERSTANDING OF LOW-BACK PAIN: A REVIEW OF THE MECHANICS OF THE LUMBAR DISC

By measurement of intradiscal pressure in vitro, the hydrostaticproperties of the nucleus pulposus of normal lumbar intervertebraldisc was established. The stress distribution within normaldiscs subjected to vertical load was also explained, demonstratingthe high tangential strains occurring in the posterior partof the annulus fibrosus. Intravitally performed measure- mentsof disc pressure have demonstrated how the load on the lumbardisc varies according to the position of the subjectl's body.Compared to the pressure or load in the upright standing position,reclining reduces the pressure by 70%, while unsupported sittingincreases the load by 40% and forward leaning and weight liftingby more than 100%. Similar relatively large augmentations ofthe load were observed in subjects performing various commonlyused muscle-strengthening exercises. Measurement of intradiscalpressure is instrumental in explaining, from a mechanical point,the occurrence of posterior ruptures in the lumbar discs, andprovides a basis for the rational treatment of patients withlow-back pain in so far as these exhibit increase of pain onincreased mechanical loads. For the majority of patients with low-back pain, the cause isunknown, although most evidence so far presented links the lumbarintervertebral disc to the pain syndromes. Results of recentstudies have shown that both chemical and mechanical factorsare probably of importance. So far we cannot successfully treatthe chemical part of the disc syndrome. Since all our patientsexhibit more pain when the spine is mechanically loaded, knowledgegained from intravital disc-pressure measurements provides abasis for successfully treating the mechanical part of the condition.Since none of the frequently prescribed and more spectacularremedies has ever been proved statistically superior to anyof the others, it is most fair to our patients and to ourselvesto use simpler, less expensive, and less dangerous programmes,such as bed-rest, administration of salicylates, and properergonomic advice. Based on a scientific approach, the low-back-painschool is intended to help the patient to be able to cope withthese back troubles, to avoid excess therapy, and to decreasethe cost both for the individual and for Society. ^*Based on the Annual Lecture delivered to the Society for BackPain Research at Guy’s Hospital, London, on November 221974.     

Global cerebral blood flow during infusion of adenosine in humans: assessment by magnetic resonance imaging and positron emission tomography

Adenosine, an endogenous vasodilator, induces a cerebral vasodilation at hypotensive infusion rates in anaesthetized humans. At lower doses (< 100 μg kg^?1 min^?1), adenosine has shown to have an analgesic effect. This study was undertaken to investigate whether a low dose, causing tolerable symptoms of peripheral vasodilation affects the global cerebral blood flow (CBF). In nine healthy volunteers CBF measurements were made using axial magnetic resonance (MR) phase images of the internal carotid and vertebral arteries at the level of C2–3. Quantitative assessment of CBF was also obtained with positron emission tomography (PET) technique, using intravenous bolus []> ¹⁵O]butanol as tracer in four of the subject at another occasion. During normoventilation (5.4 ± 0.2 kPa, mean ± s.e.m.), the cerebral blood flow measured by magnetic resonance imaging technique, as the sum of the flows in both carotid and vertebral arteries, was 863 ± 66 mL min^?1, equivalent to about 64 ± 5 mL 100 g^?1 min^?1. The cerebral blood flow measured by positron emmission tomography technique, was 59 ± 4 mL 100 g^?1 min^?1. All subjects had a normal CO₂ reactivity. When adenosine was infused (84 ± 7 μg kg^?1 min^?1) the cerebral blood flow, measured by magnetic resonance imaging was 60 ± 5 mL 100 g^?1 min^?1. The end tidal CO₂ level was slightly lower (0.2 ± 0.1 kPa) during adenosine infusion than during normoventilation. In the subgroup there was no difference in cerebral blood flow as measured by magnetic resonance imaging or positron emission tomography. In conclusion, adenosine infusion at tolerable doses in healthy volunteers does not affect global cerebral blood flow in unanaesthetized humans.