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Biomedical subjects

G Kvarstein

Publications and source records attributed to G Kvarstein.

8 recordsLinked to original sources
PubMed2003

Detection of organ ischemia during hemorrhagic shock.

BACKGROUND: In a porcine hemorrhagic shock model we aimed to determine: (a) whether blood flow to the intestine and kidney was more reduced than cardiac output; (b) whether parameters of anaerobic metabolism correlated with regional blood flow; and (c) whether metabolic parameters in intestine, kidney and skeletal muscles detected a compromised metabolic state at an earlier stage than did systemic parameters. METHODS: In an animal research laboratory at a university hospital six domestic pigs were subjected to volume-controlled hemorrhage. Every 30 min samples of blood were withdrawn. Systemic and regional hemodynamic parameters and tissue levels of PCO2 were monitored. Whole body and organ-specific oxygen consumption (VO2) and veno-arterial (VA) differences of lactate, glucose, potassium (K+), PCO2, H+ and base excess (BE) were calculated every 30 min. RESULTS: With progressive hemorrhage, intestinal blood flow decreased to the same extent as cardiac output, whereas the reduction in renal blood flow was more pronounced. We found a concomitant reduction in VO2 (onset of supply dependent metabolism) in intestine, kidney and skeletal muscles. In muscular tissue PCO2 increased to levels three times higher than baseline, while renal and intestinal PCO2 increased eightfold. Supply dependency was associated with a concomitant increase in VA CO2 and VA H+. Also, VA lactate increased, mostly in intestine and least in skeletal muscle. Intestinal and renal VA K+ increased, while muscular VA K+ decreased. Arterial lactate and H+ increased considerably, whereas arterial BE decreased. CONCLUSION: With progressive hemorrhage, renal blood flow, but not intestinal and skeletal muscle blood flow, was reduced more than cardiac output. Supply dependent oxygen metabolism (VO2) and organ acidosis occurred simultaneously in the three organs, despite differences in blood flow reductions. Organ ischemia coincided with a pronounced change in arterial lactate and systemic acid base parameters.

Acid-Base Equilibrium↗
PubMed2000

MRI-guided celiac plexus block.

Celiac plexus block is used as a palliative procedure in cases of severe upper abdominal pain caused by pancreatitis or tumors of the pancreas. It can be guided by bony landmarks, fluoroscopy, ultrasound (US), or computed tomography (CT). To avoid severe complications, methods visualizing soft tissue, like CT and magnetic resonance (MR) imaging, are preferable. We describe celiac plexus blocks carried out in an open MR scanner, offering needle guidance with an optical tracking system and near real-time image acquisition. Eight patients with severe chronic abdominal pain were included. In these, 14 celiac blocks were carried out. Good or total pain relief was achieved in 8 of the 14 blocks (57%), a moderate effect in 5 blocks (36%), and no effect in 1 block (7%). The placement of the needle was easily guided with MR in all cases. The MR technique ensures good visualization of soft tissue, direct monitoring of needle movement and avoids exposure to ionizing radiation. Celiac plexus block can safely be carried out in an open MR scanner.

Abdominal Pain↗
PubMed1999

Gas supersaturation in the cecal wall of mice due to bacterial CO2 production.

PCO2 in the lumen and serosa of cecum and jejunum was measured in mice. The anesthetic used was a fentanyl-fluanisone-midazolam mixture. PCO2 was recorded in vivo and postmortem. PCO2 was 409 +/- 32 Torr (55 +/- 4 kPa) in the cecal lumen and 199 +/- 22 Torr (27 +/- 3 kPa) on the serosa in normal mice. Irrigation of the cecum resulted in serosal and luminal PCO2 levels of 65-75 Torr. Cecal PCO2 was significantly lower in germ-free mice (65 +/- 5 Torr). Cecal PCO2 increased significantly after introduction of normal bacterial flora into germ-free mice. Introduction of bacterial monocultures into germ-free mice had no effect. After the deaths of the mice, cecal PCO2 increased rapidly in normal mice. The intestinal bacteria produced the majority of the cecal PCO2, and the use of tonometry in intestinal segments with a high bacterial activity should be interpreted with caution. We propose that serosal PCO2 levels >150-190 Torr (20-25 kPa) in the cecum of mice with a normal circulation may represent a state of gas supersaturation in the cecal wall.

Animals↗
PubMed1997

[CO2 pressure used in the diagnosis of ischemia].

Under ischemic conditions O2 delivery is insufficient, and the cells convert to anaerobic metabolism with production of lactic acid. The protons formed in this process are to a large extent rapidly buffered inside the cell by proteins and HCO3-. Protons buffered by HCO3- form CO2 in the tissue. Since the blood supply during ischemia is minimal, CO2 is not transported away from the tissue and will reach tensions far above pCO2 found under aerobic conditions. Thus, measuring pCO2 can be used to detect ischemia in an organ. Gastrointestinal tonometry is based on the concept of CO2 accumulation during anaerobiosis. It has been customary to calculate so-called interstitial pH (pHi) by incorporating the measured pCO2 in the tonometer and the HCO3- in an arterial blood gas in the Henderson-Hasselbalch equation. However, this method has several weaknesses, and we recommend using the measured pCO2, or rather the difference between gastrointestinal and arterial pCO2. Experimental studies have shown that pCO2 electrodes sensitively detect the onset of ischemia also in solid organs. The accumulation of pCO2 coincides with the shift from supply-independent to supply-dependent oxygen consumption and correlates with other markers of ischemia. pCO2 measurement at organ level is a promising tool in the monitoring of organ ischemia.

Carbon Dioxide↗
PubMed1996

PCO2 electrodes at the surface of the kidney detect ischaemia.

BACKGROUND: Under ischaemic (anaerobic) conditions there will be an accumulation of CO2 in the tissue secondary to a build up of protons that is buffered by HCO3. We reasoned that CO2 could be measured at the surface of the kidney by PCO2 electrodes to detect ischaemic conditions. METHODS: Anaesthetized, mechanically ventilated pigs (25-30 kg) were investigated. Two acute porcine models, one of haemorrhagic shock and one of renal artery stenosis were used. Renal blood flow was gradually decreased, either by successive episodes of bleeding through the arterial cannula or by successive snaring of the renal artery. RESULTS: In both models we found that with decreased blood flow but maintained aerobic metabolism (supply independence) PCO2 both at the surface of the kidney and in the renal vein increased by 2-3 kPa. Thus, the tissue-venous PCO2 difference did not change much. At DO2crit, i.e., at the transition to supply-dependent O2 consumption, the tissue PCO2 started to increase rapidly, as did the tissue-venous PCO2 difference. This is compatible with the notion that a hallmark of ischaemia is decreased ability of the blood to transport away waste products because the contact between large parts of tissue and blood is virtually non-existent. In the renal artery stenosis model kidney surface PCO2 values rose from a baseline of 6.6 +/- 0.6 kPa (mean +/- SEM) to a value near DO2crit of 10.6 +/- 0.8 kPa, reaching a final value of 29.9 +/- 3.5 kPa at no flow. PCO2 in the renal vein, however, reached a maximum of only 8.2 +/- 0.6 kPa. Numbers very similar to these were also found in the haemorrhagic model. The urine production decreased before the onset of ischaemia. When surface PCO2 values increased sharply indicating ischaemia, the urine production was zero. Lactate production by the kidney correlated very well with increasing tissue PCO2 values further corroborating that anaerobic metabolism was detected with the electrodes. CONCLUSION: We conclude that PCO2 electrodes placed at the surface of the kidney detect renal cortical ischaemia.

Animals↗
PubMed1989

The duration of acute respiratory tract infections in children.

In a rural district in Western Norway with 400 children under 16 years, we recorded all children with acute respiratory infections who attended their general practitioner during a period of four months. 90 cases were recorded, giving an incidence of 5.6% per month. Half of the patients contacted the doctor within four days from the initial symptom, every sixth waited more than two weeks. Their symptoms were monitored by the parents. Low fever, nasal discharge and cough were the most long-standing symptoms. After three weeks less than 50% of the patients were completely recovered. The children under one year of age recovered more quickly than the rest. No serious complications or sequelae were recorded.

Acute Disease↗