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Cor J Kalkman

Publications and source records attributed to Cor J Kalkman.

29 records · Page 2Linked to original sources
PubMed2003

A new miniature fiber oxygenator for small animal cardiopulmonary bypass.

Neurocognitive decline following cardiac surgery is an increasing problem, particularly affecting older patients. The use of cardiopulmonary bypass is a suspected cause. Research into pathophysiology and possible preventive measures requires the use of an animal model. Commercial oxygenators are too large and expensive for use in small animals. We describe a fiber oxygenator scaled for use in the rat. In vitro and in vivo testing show that it is able to support full gas exchange in this size of animal, and causes no allergic or toxic reactions.

Animals↗
PubMed2003

Cognitive self-assessment one year after on-pump and off-pump coronary artery bypass grafting.

BACKGROUND: Coronary artery bypass grafting (CABG) is associated with significant cerebral morbidity. This is usually manifested as cognitive decline and may be caused by cardiopulmonary bypass. The primary objective of this study was to explore whether patients report more cognitive failures 1 year after CABG than preoperatively. Secondary objectives were to evaluate whether there is a difference in reported cognitive failures between patients undergoing on-pump and off-pump CABG and whether a difference between CABG patients and healthy control subjects exists. Finally the relation between objective and subjective cognitive functioning was quantified. METHODS: In this prospective study, the Cognitive Failures Questionnaire (CFQ) was assigned preoperatively and 1 year postoperatively to 81 patients who were randomly assigned to undergo off-pump (n = 45) or on-pump (n = 36) CABG. A control sample of 112 age-matched healthy subjects was included who were administered the CFQ once. RESULTS: No difference was found in the total CFQ score (p = 0.222) and CFQ worry score (p = 0.207) between 1 year after CABG and before CABG. There was no difference between on-pump and off-pump CABG (total score, p = 0.458; worry score, p = 0.563). A significant difference was found in CFQ total score between CABG patients and control subjects (p < 0.001), with control subjects reporting more cognitive failures than CABG patients. Finally, patients who showed cognitive decline in the Octopus trial did not have a higher CFQ total score (p = 0.671) and CFQ worry score (p = 0.772) than patients without cognitive decline 1 year after CABG. CONCLUSIONS: The present findings suggest that CABG does not result in a substantial proportion of patients with subjectively experienced cognitive decline 1 year after the procedure, irrespective of the type of surgical technique (on-pump versus off-pump).

Activities of Daily Living↗
PubMed2003

Interaction between the spinal melanocortin and opioid systems in a rat model of neuropathic pain.

BACKGROUND: The authors recently demonstrated that administration of the melanocortin-4 receptor antagonist SHU9119 decreased neuropathic pain symptoms in rats with a sciatic chronic constriction injury. The authors hypothesised that there is a balance between tonic pronociceptive effects of the spinal melanocortin system and tonic antinociceptive effects of the spinal opioid system. Therefore, they investigated a possible interaction between these two systems and tested whether opioid effectiveness could be increased through modulation of the spinal melanocortin system activity. METHODS: In chronic constriction injury rats, melanocortin and opioid receptor ligands were administered through a lumbar spinal catheter, and their effects on mechanical allodynia were assessed by von Frey probing. RESULTS: Naloxone (10-100 microg) dose-dependently increased allodynia (percent of maximum possible effect of -67 +/- 9%), which is in agreement with a tonic antinociceptive effect of the opioid system. SHU9119 decreased allodynia (percent of maximum possible effect of 60 +/- 13%), and this effect could be blocked by a low dose of naloxone (0.1 microg), which by itself had no effect on withdrawal thresholds. Morphine (1-10 microg) dose-dependently decreased allodynia (percent of maximum possible effect of 73 +/- 14% with the highest dose tested). When 0.5 microg SHU9119 (percent of maximum possible effect of 47 +/- 14%) was given 15 min before morphine, there was an additive antiallodynic effect of both compounds. CONCLUSIONS: Together, these data confirm that there is an interaction between the spinal melanocortin and opioid systems and that combined treatment with melanocortin-4 receptor antagonists and opioids might possibly contribute to the treatment of neuropathic pain.

Analgesics, Opioid↗
PubMed2002

Cognitive outcome after off-pump and on-pump coronary artery bypass graft surgery: a randomized trial.

CONTEXT: Coronary artery bypass graft (CABG) surgery is associated with a decline in cognitive function, which has largely been attributed to the use of cardiopulmonary bypass (on-pump procedures). Cardiac stabilizers facilitate CABG surgery without use of cardiopulmonary bypass (off-pump procedures) and should reduce the cognitive decline associated with on-pump procedures. OBJECTIVE: To compare the effect of CABG surgery with (on-pump) and without (off-pump) cardiopulmonary bypass on cognitive outcome. DESIGN AND SETTING: Randomized controlled trial conducted in the Netherlands of CABG surgery patients enrolled from March 1998 through August 2000, with 3- and 12-month follow-up. PARTICIPANTS AND INTERVENTION: Patients scheduled for their first CABG surgery (mean age, 61 years; n = 281) were randomly assigned to off-pump surgery (n = 142) or on-pump surgery (n = 139). MAIN OUTCOME MEASURES: Cognitive outcome at 3 and 12 months, which was determined by psychologists (blinded for randomization) who administered 10 neuropsychological tests before and after surgery. Quality of life, stroke rate, and all-cause mortality at 3 and 12 months were secondary outcome measures. RESULTS: Cognitive outcome could be determined at 3 months in 248 patients. Cognitive decline occurred in 21% in the off-pump group and 29% in the on-pump group (relative risk [RR], 0.65; 95% confidence interval [CI], 0.36-1.16; P =.15). The overall standardized change score (ie, improvement of cognitive performance) was 0.19 in the off-pump vs 0.13 in the on-pump group (P =.03). At 12 months, cognitive decline occurred in 30.8% in the off-pump group and 33.6% in the on-pump group (RR, 0.88; 95% CI, 0.52-1.49; P =.69). The overall standardized change score was 0.19 in the off-pump vs 0.12 in the on-pump group (P =.09). No statistically significant differences were observed between the on-pump and off-pump groups in quality of life, stroke rate, or all-cause mortality at 3 and 12 months. CONCLUSION: Patients who received their first CABG surgery without cardiopulmonary bypass had improved cognitive outcomes 3 months after the procedure, but the effects were limited and became negligible at 12 months.

Cardiopulmonary Bypass↗
PubMed2002

Delayed detection of motor pathway dysfunction after selective reduction of thoracic spinal cord blood flow in pigs.

OBJECTIVE: Clinical monitoring of myogenic motor evoked potentials to transcranial stimulation provides rapid evaluation of motor-pathway function during surgical procedures in which spinal cord ischemia can occur. However, a severe reduction of spinal cord blood flow that remains confined to the thoracic spinal cord might render ischemic only the descending axons of the corticospinal pathway. In this situation lower-limb motor evoked potentials could respond relatively late compared with a similar spinal cord blood flow reduction of the lumbar spinal cord that renders predominantly motoneurons ischemic. METHODS: Selective thoracic and lumbar spinal cord ischemia was induced by sequential clamping of segmental arteries during continuous assessment of laser-Doppler spinal cord blood flow at the thoracic and lumbar spinal cord. Myogenic motor evoked potentials were recorded from the upper and lower limbs. The time to loss of motor evoked potentials was compared (n = 11) during reduction of laser-Doppler spinal cord blood flow below 25% of baseline (ischemic segment), and flow was maintained at greater than 75% of baseline in the nonischemic segment, both during thoracic and lumbar spinal cord ischemia. RESULTS: Average laser-Doppler spinal cord blood flow in the ischemic segment was similar during thoracic (26% +/- 15% [+/- SD]) and lumbar (26% +/- 16%) ischemia, whereas normal flow was maintained in the nonischemic segment. The time to motor evoked potentials loss was considerably longer after thoracic spinal cord ischemia (15 +/- 11 minutes) than after lumbar spinal cord ischemia (3 +/- 2 minutes, P <.005). CONCLUSION: In this experimental model of selective spinal cord ischemia, a severe reduction of lumbar spinal cord blood flow results in rapid loss of myogenic motor evoked potentials, whereas a similar blood flow reduction in the thoracic spinal cord results in relatively slow loss of motor evoked potentials. The effectiveness of motor evoked potentials to rapidly assess spinal cord integrity might be limited when spinal cord ischemia is confined to the thoracic segments.

Animals↗
PubMed2002

Spinal cord blood supply in patients with thoracoabdominal aortic aneurysms.

OBJECTIVE: In patients with thoracoabdominal aortic aneurysms (TAAAs), the blood supply to the spinal cord is highly variable and unpredictable because of obstructed intercostal and lumbar arteries. This study was performed for the prospective documentation of patent segmental arteries during TAAA repair and the assessment of their functional contribution to the spinal cord blood supply. METHODS: TAAA repair was performed in 184 consecutive patients (68 with type I aneurysm, 91 with type II, and 25 with type III) according to a protocol that included left heart bypass grafting, cerebrospinal fluid drainage, and the monitoring of motor-evoked potentials (MEPs). Patent intercostal and lumbar arteries were documented, and all reattached, selectively grafted, and oversewn segmental arteries were noted. MEP amplitude that decreased to less than 25% of baseline was considered an indication of critical spinal cord ischemia and prompted spinal cord revascularization. RESULTS: Adequate MEP levels were encountered in 183 of 184 patients. One patient had early paraplegia (absent MEPs), two patients had delayed paraplegia develop, and two patients had temporary paraparesis, which accounted for an overall neurologic deficit of 2.7%. The median total number of patent intercostal and lumbar arteries in type I, II, and III aneurysms was three, five, and five, respectively. In eight of 68 type I cases, no segmental arteries were seen between the fifth thoracic vertebrae (T5) and the first lumbar vertebrae (L1) and MEP levels remained adequate because of distal aortic perfusion. In 18 of 91 type II cases, the aortic segment T5 to L1 did not contain patent arteries, and in six of these patients, the segment L1 to L5 did not have lumbar arteries either. In the latter patients, MEP levels depended on the pelvic circulation provided with the left heart bypass graft. In the other 12 of 91 type II cases, the only patent arteries were the lumbar arteries between L3 and L5. The loss of MEPs could be corrected with the reattachment of these arteries. In seven of 25 type III cases, the MEP levels also depended on lumbar arteries L3 to L5 and in three of 25 cases, no segmental arteries were available and MEP levels recovered after the reperfusion of the pelvic circulation. With the combination of the findings of type II and III cases, spinal cord perfusion was directed by lower lumbar arteries in 16% of the cases (19 of 116) and pelvic circulation in 8% of the cases (nine of 116). CONCLUSION: In patients with TAAA, most intercostal and lumbar arteries are occluded and spinal cord perfusion depends on an eminent collateral network, which includes lumbar arteries and pelvic circulation. The monitoring of MEPs is a sensitive technique for the assessment of spinal cord ischemia and the identification of segmental arteries that critically contribute to spinal cord perfusion. Surgical strategies on the basis of this technique reduced the incidence rate of neurologic deficit to less than 3%.

Adult↗
PubMed2002

The effects of low-pressure carbon dioxide pneumoperitoneum on cerebral oxygenation and cerebral blood volume in children.

UNLABELLED: We examined the effects of low-pressure carbon dioxide pneumoperitoneum on regional cerebral oxygen saturation (ScO(2)) and cerebral blood volume (CBV) in children. Fifteen children, ASA I--III, scheduled for laparoscopic fundoplication, were investigated in the head-up position (10) and ventilated to a baseline end-tidal CO(2) (PETCO(2)) between 25 and 33 mm Hg. Ventilatory settings remained unchanged during the operation. ScO(2) and CBV were assessed with near-infrared spectroscopy and recorded together with end-tidal and arterial carbon dioxide (PaCO(2)) at 5 time points: before insufflation, 30, 60, and 90 min after the start of CO(2) insufflation, and 10 min after desufflation. The intraabdominal pressure was kept between 5 and 8 mm Hg. During insufflation, PETCO(2) increased from 30.0 plus minus 2.8 to 38.3 plus minus 5.1 mm Hg (P < 0.001) and PaCO(2) increased from 32.0 plus minus 4.7 to 40.4 plus minus 5.9 mm Hg (P < 0.001). ScO(2) increased by 15.7% plus minus 8.8% (from 61 plus minus 9 to 70 plus minus 9 arbitrary units ) (P < 0.001). CBV increased by 4.6% plus minus 8.8% (from 123 plus minus 66 to 128 plus minus 66 arbitrary units [P = 0.048]). After desufflation, PETCO(2) and PaCO(2) decreased, but did not return to preinsufflation values. ScO(2) and CBV also decreased after desufflation. In conclusion, hyperventilation and the head-up position before CO(2) insufflation are not sufficient to prevent the CO(2)-mediated cerebral hemodynamic effects of low-pressure pneumoperitoneum (5--8 mm Hg) in children. IMPLICATIONS: Peritoneal CO(2) absorption during laparoscopic surgery causes hypercapnia and CO(2)-mediated cerebral hemodynamic effects. Hyperventilation and the head-up position before CO(2) insufflation is not sufficient to counteract these effects of low-pressure pneumoperitoneum (5--8 mm Hg) in children.

Blood Volume↗
PubMed2002

The role of transcranial motor evoked potentials in predicting neurologic and histopathologic outcome after experimental spinal cord ischemia.

BACKGROUND: Monitoring of myogenic motor evoked potentials to transcranial stimulation (tcMEPs) is clinically used to assess motor pathway function during aortic and spinal procedures that carry a risk of spinal cord ischemia (SCI). Although tcMEPs presumably detect SCI before irreversible neuronal deficit occurs, and prolonged reduction of tcMEP signals is thought to be associated with impending spinal cord damage, experimental evidence to support this concept has not been provided. In this study, histopathologic and neurologic outcome was examined in a porcine model of SCI after different durations of intraoperative loss of tcMEP signals. METHODS: In 15 ketamine-sufentanil-anesthetized pigs (weight, 35-45 kg) the spinal cord feeding lumbar arteries were exposed. tcMEP were recorded from the upper and lower limbs. Under normothermic conditions, animals were randomly allocated to undergo short-term tcMEP reduction (group A, < 10 min, n = 5) or prolonged tcMEP reduction (group B, 60 min, n = 10), resulting from temporary or permanent clamping of lumbar segmental arteries. Neurologic function was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated 72 h after induction of SCI. RESULTS: In all animals except one, segmental artery clamping reduced tcMEP to below 25% of baseline. All but one animal in group A had reduced tcMEP for less than 10 min and had normal motor function and no infarction at 72 h after the initial tcMEP reduction. Seven animals in group B (70%) had reduced tcMEP signals for more than 60 min and were paraplegic with massive spinal cord infarction at 72 h. Two animals (one in both groups) had tcMEP loss for 40 min, with moderate infarction and normal function. In general, histopathologic damage and neurologic dysfunction did not occur when tcMEP amplitude recovered within 10 and 40 min after the initial decline, respectively. CONCLUSION: Prolonged reduction of intraoperative tcMEP amplitude is predictive for postoperative neurologic dysfunction, while recovery of the tcMEP signal within 10 min after the initial decline corresponds with normal histopathology and motor function in this experimental model. This finding confirms that intraoperative tcMEPs have a good prognostic value for neurologic outcome during procedures in which the spinal cord is at risk for ischemia.

Animals↗
PubMed2002

Peri-ischemic aminoguanidine fails to ameliorate neurologic and histopathologic outcome after transient spinal cord ischemia.

Inhibition of neurotoxic events that lead to delayed cellular damage may prevent motor function loss after transient spinal cord ischemia. An important effect of the neuroprotective substance aminoguanidine (AG) is the inhibition of inducible nitric oxide synthase (iNOS), a perpetrator of focal ischemic damage. The authors studied the protective effects of AG on hind limb motor function and histopathologic outcome in an experimental model for spinal cord ischemia, and related these findings to the protein content of iNOS in the spinal cord. Temporary spinal cord ischemia was induced by 28 minutes of infrarenal balloon occlusion of the aorta in 40 anesthetized New Zealand White rabbits. Animals were assigned randomly to two treatments: saline (n = 20) or AG (n = 20; 100 mg/kg intravenously before occlusion). Postoperatively, treatment was continued with subcutaneous injections twice daily (saline or 100 mg/kg AG). Normothermia (38 degrees C) was maintained during ischemia, and rectal temperature was assessed before and after subcutaneous injections. Animals were observed for 96 hours for neurologic evaluation (Tarlov score), and the lumbosacral spinal cord was examined for ischemic damage after perfusion and fixation. Lastly, iNOS protein content was determined using Western blot analysis 48 hours after ischemia in five animals from each group. Neurologic outcome at 96 hours after reperfusion was the same in both groups. The incidence of paraplegia was 67% in the saline-treated group versus 53% in the AG-treated group. No differences in infarction volume, total number of viable motoneurons, or total number of eosinophilic neurons were present between the groups. At 48 hours after reperfusion, iNOS protein content in the spinal cord was increased in one animal in the AG-treated group and in three animals in the control group. The data indicate that peri-ischemic treatment with high-dose AG in rabbits offers no protection against a period of normothermic spinal cord ischemia. There was no conclusive evidence of spinal cord iNOS inhibition after treatment with AG.

Animals↗