Biomedical subjects

J Nissinen

Publications and source records attributed to J Nissinen.

At least 19 recordsLinked to original sources

PubMed2004

Electrophysiologic changes in the lateral and basal amygdaloid nuclei in temporal lobe epilepsy: an in vitro study in epileptic rats.

The functional consequences of neuronal loss during epileptogenesis in the lateral and basal amygdaloid nuclei are poorly understood. The present study tested the hypothesis that electrical responsiveness varies in different amygdaloid nuclei in the chronically epileptic amygdala. Further, we examined the amygdaloid region most prone to seizure initiation. Epileptogenesis was triggered in 20 rats by inducing status epilepticus (SE) with electrical stimulation of the lateral nucleus of the amygdala. Electrode-implanted non-stimulated rats served as controls. The occurrence and duration of spontaneous seizures were monitored with video-electroencephalography (EEG) at 8-9 weeks after SE. Thereafter, animals were killed and extracellular recordings were made from slices of both amygdalas. In the lateral nucleus of epileptic animals, the frequency of spontaneous responses was reduced compared with controls (P < 0.05). The amplitudes of evoked field responses were reduced (P < 0.01), whereas paired pulse (PP) facilitation was enhanced (P < or = 0.05). In the basal nucleus of the epileptic animals, PP facilitation was enhanced (P < 0.05) and sensitivity to 4-aminopyridine (4-AP)-induced epileptiform activity was increased compared with controls (P < 0.05). In the epileptic animals, the basal nucleus was also more sensitive than the lateral nucleus to 4-AP-induced epileptiform activity (P < 0.05). Correlation analysis indicated that longer SE duration was associated with longer half widths (P = 0.001) and smaller slopes (P < 0.05) of evoked responses as well as with attenuated PP facilitation (P<0.01). Moreover, a higher frequency of spontaneous seizures was associated with longer half widths (P < 0.05) and smaller slopes (P < 0.05) of evoked responses as well as with enhanced PP facilitation (P < 0.05). These data suggest that there is a reduced release of glutamate and reduced inhibition in the lateral and basal amygdaloid nuclei in epileptic animals. Further, the basal nucleus is more prone to epileptic activity than the lateral nucleus. Finally, the severity of SE and spontaneous seizures in vivo is associated with electrophysiologic alterations in vitro.

4-Aminopyridine↗

PubMed2003

Administration of caspase 3 inhibitor during and after status epilepticus in rat: effect on neuronal damage and epileptogenesis.

Symptomatic temporal lobe epilepsy typically develops in three phases: brain damage --> epileptogenesis --> spontaneous seizures (epilepsy). The challenge is to prevent epileptogenesis after injury. We hypothesized that alleviation of damage by caspase inhibitors will reduce epileptogenesis or at least have disease-modifying effects (less severe epilepsy, milder cognitive decline). Epileptogenesis was triggered by amygdala stimulation-induced status epilepticus (SE) in rats and spontaneous seizures were monitored with video-electroencephalography (EEG). First, we tested the neuroprotective effect of a 1-week treatment with caspase 1, 3 or 9 inhibitors (3 micro g/d/i.c.v., started 3 h after the beginning of SE). The least damage to the hippocampus was observed in animals treated with the caspase 3 inhibitor (z-DEVD-fmk) which reduced the enzyme activity to 6% of that in the vehicle group. Thus, z-DEVD-fmk was chosen for long-term studies, in which the treatment regime remained the same except the dose was doubled (6 micro g/d/i.c.v.). Video-EEG monitoring was performed for 3 to 4 weeks, starting either 8 or 14 weeks after SE. One group of animals was tested in water-maze and fear-conditioning tests, and all animals were perfused for histological analysis. Treatment with the caspase 3 inhibitor neither prevented the development of epilepsy, nor had any disease-modifying effects. Mossy fibre sprouting, however, was reduced. The present data indicate that administration of z-DEVD-fmk monotherapy was not antiepileptogenic despite its short-term neuroprotective effects. These findings challenge the idea that prevention of cell death is the primary target for the development of antiepileptogenic compounds.

Animals↗

PubMed2003

Perioperative stroke in coronary artery bypass patients.

BACKGROUND AND AIMS: Stroke has remained one of the most frustrating complications in coronary artery bypass surgery (CABG). The purpose of this study was to describe the incidence and correlates of stroke in CABG patients operated on in a hospital with low annual volume of open-heart surgery procedures. The aim was moreover to clarify subsequent outcome and self-reported satisfaction-based quality of life of patients who had experienced a stroke. MATERIAL AND METHODS: The material was a cohort of 1318 consecutive CABG patients operated on over a 6-year period. Data was collected prospectively but the final analysis was retrospective. Questionnaires supplemented the estimation of survival and subsequent functional status. RESULTS: The incidence of stroke was 2.6 %. Age > 70 years, chronic obstructive pulmonary disease (COPD), peripheral vascular disease (PVD), cerebral vascular disease (CVD), number of aortic anastomoses and significant atherosclerosis of the ascending aorta were univariate predictors of stroke. Postoperative stroke was experienced in 55.9% of cases delayed appearing from 2nd postoperative day on. Stroke patients had a higher rate of mortality (14.7% vs. 1.0%, p = 0.001) and poorer survival than no-stroke patients (82.4% and 97.4% at one year and 61.2% and 89.7% at six years, p < 0.001). CONCLUSIONS: The incidence of stroke seems to be on the same level in CABG patients from a low volume hospital as in reports from centres with a high volume of annual procedures. Stroke predicts higher mortality, longer intensive care unit (ICU) stay, longer hospitalisation and poorer survival. A relatively high number of stroke patients need permanent institutional care. Satisfaction-based quality of life in CABG patients also remains on a lower level in comparison to patients without neurological complications.

Aged↗

PubMed2002

Peripheral vascular disease as predictor of outcome after coronary artery bypass grafting.

BACKGROUND AND AIMS: Understanding and objective assessment of risks is crucial in cardiac surgery. The aim of this study was to assess the influence of peripheral vascular disease (PVD) on morbidity, mortality and outcome in coronary artery bypass grafting (CABG) patients. MATERIAL AND METHODS: The ankle-brachial pressure index (ABPI) was used as indicator of PVD and was measured in 178 CABG patients. Two groups were established: 1. normal ABPI (0.9-1.3) (n = 136) and 2. lowered ABPI (< 0.9) (n = 35). The mean follow-up was 26 months. RESULTS: The presence of PVD was 20.5 %. Patients with PVD were older (p < 0.05), more often of female sex (p < 0.05), had higher Higgins's risk score (p = 0.001) and more often intermittent claudication (IC) (p < 0.001). PVD significantly predicted atrial fibrillation (FA) (p < 0.05) and relatively postoperative myocardial infarction (MI) (p = 0.058). CONCLUSIONS: The presence of PVD is relatively high in CABG patients and increases with age. PVD predicts some morbidity but seems to have fairly little influence on short-term or middle-term outcome of CABG patients. ABPI may be of only limited value in identifying patients with high operative risk in CABG.

Aged↗

PubMed2001

Is mossy fiber sprouting present at the time of the first spontaneous seizures in rat experimental temporal lobe epilepsy?

The contribution of mossy fiber sprouting to the generation of spontaneous seizures in the epileptic brain is under dispute. The present study addressed this question by examining whether sprouting of mossy fibers is present at the time of appearance of the first spontaneous seizures in rats, and whether all animals with increased sprouting have spontaneous seizures. Epileptogenesis was induced in 16 rats by electrically stimulating the lateral nucleus of the amygdala for 20-30 min until the rats developed self-sustained status epilepticus (SSSE). During and after SSSE, rats were monitored in long-term by continuous video-electroencephalography until they developed a second spontaneous seizure (8-54 days). Thereafter, monitoring was continued for 11 days to follow seizure frequency. The density of mossy fiber sprouting was analyzed from Timm-stained preparations. The density of hilar neurons was assessed from thionin-stained sections. Of 16 rats, 14 developed epilepsy. In epileptic rats, the density of mossy fiber sprouting did not correlate with the severity or duration (115-620 min) of SSSE, delay from SSSE to occurrence of first (8-51 days) or second (8-54 days) spontaneous seizure, or time from SSSE to perfusion (20-63 days). In the temporal end of the hippocampus, the sprouting correlated with the severity of neuronal damage (ipsilateral: r = -0.852, P < 0.01 contralateral: r = -0.748, P < 0.01). The two animals without spontaneous seizures also had sprouting. Increased density of sprouting in animals without seizures, and its association with the severity of neuronal loss was confirmed in another series of 30 stimulated rats that were followed-up with video-EEG monitoring for 60 d. Our data indicate that although mossy fiber sprouting is present in all animals with spontaneous seizures, its presence is not necessarily associated with the occurrence of spontaneous seizures.

Amygdala↗

PubMed2001

Chronic elevation of brain GABA levels beginning two days after status epilepticus does not prevent epileptogenesis in rats.

Vigabatrin (VGB) treatment is neuroprotective in various models of status epilepticus (SE) and delays the development of kindling via mechanisms that are assumed to relate to the elevation of GABA levels in the brain. Here, we tested the hypothesis that a chronic elevation of brain GABA levels obtained by VGB treatment prevents the development of spontaneous seizures (i.e. epilepsy) following SE in rats. Self-sustained SE (SSSE) was induced by stimulating the lateral nucleus of the amygdala. Two days later, chronic VGB (75 mg/kg/day) or saline treatment was started via subcutaneous osmotic minipumps. The development of spontaneous seizures was monitored once a week (24 h at a time) using video-EEG recording. Rats were perfused for histology either at the end of the 10-week drug treatment, or later at the end of an 8-week drug-free follow-up period. Before perfusion for histology, spatial learning and memory perform was tested in the Morris water-maze. Spontaneous seizures were observed in 55% (6/11) of the saline-treated and 73% (8/11) of the VGB-treated rats during the 10-week treatment period. Seizure frequency, severity, and duration were similar in VGB-treated rats and controls during and after the drug-treatment period. VGB treatment did not decrease neuronal damage in various temporal lobe regions or mossy fiber sprouting. VGB treatment also did not attenuate spatial learning or memory impairments. These findings indicate that the augmentation of GABAergic neurotransmission by VGB does not prevent the development of epilepsy when treatment is started 2 days after SE.

Animals↗

PubMed2001

Effect of lamotrigine treatment on status epilepticus-induced neuronal damage and memory impairment in rat.

Status epilepticus causes neuronal damage that is associated with cognitive impairment. The present study examined whether a novel antiepileptic drug, lamotrigine (LTG), alleviates status epilepticus-induced temporal lobe damage and memory impairment, and compared its efficacy with carbamazepine. Status epilepticus was induced by electric stimulation of the perforant pathway (PP) in rats. Treatment with LTG (12.5 mg/kg, twice a day) was started either 3 days before (preLTG group) or 1 h after (postLTG group) a 60 min PP stimulation. Treatment with carbamazepine (CBZ; 30 mg/kg, twice a day) was started 3 days before (CBZ group) a 60 min PP stimulation. All treatments were continued for 2 weeks. Thereafter, the severity of seizures, seizure-induced neuronal damage, quantitative electroencephalogram (EEG), and memory impairment were compared between vehicle-treated unstimulated and stimulated controls, LTG-treated rats, and CBZ-pretreated rats. Both in the preLTG and postLTG groups, damage to hilar somatostatin-immunoreactive neurons, hippocampal CA3b and CA3a pyramidal cells, and the piriform cortex was mild and did not differ from that in unstimulated controls. Furthermore, CA3c damage in the preLTG group did not differ from that in unstimulated controls. Vehicle-treated stimulated controls and CBZ-pretreated rats, however, had significant damage in the hilus, CA3 subregions, and piriform cortex compared with unstimulated controls (P<0.05 for the stimulated side, contralateral side, or both). Treatment with LTG or CBZ had no effect on the number or duration of behavioral seizures during PP stimulation. They did not affect the baseline EEG or status epilepticus-induced slowing of the EEG. Also, the status epilepticus-induced spatial memory impairment in the Morris water-maze was not attenuated by treatment with LTG or CBZ. Our data demonstrate that treatment with LTG has a mild neuroprotective effect on status epilepticus-induced neuronal damage in rats even when administered after the beginning of status epilepticus.

Animals↗

PubMed2000

A new model of chronic temporal lobe epilepsy induced by electrical stimulation of the amygdala in rat.

Spontaneous seizures are the hallmark of human epilepsy but they do not occur in most of the epilepsy models that are used to investigate the mechanisms of epilepsy or to test new antiepileptic compounds. This study was designed to develop a new focal epilepsy model that mimics different aspects of human temporal lobe epilepsy (TLE), including the occurrence of spontaneous seizures. Self-sustained status epilepticus (SSSE) lasting for 6-20 h was induced by a 20-30 min stimulation of the lateral nucleus of the amygdala (100 ms train of 1 ms, 60 Hz bipolar pulses, 400 microA, every 0.5 s). Stimulated rats (n = 16) were monitored with a video-EEG recording system every other day (24 h/day) for 6 months, and every other video-EEG recording was analyzed. Spontaneous epileptic seizures (total number 3698) were detected in 13 of the 15 animals (88%) after a latency period of 6 to 85 days (median 33 days). Four animals (31%) had frequent (697-1317) seizures and 9 animals (69%) had occasional seizures (1-107) during the 6-months follow-up period. Fifty-seven percent of the seizures occurred during daytime (lights on 07:00-19:00 h). At the end of the follow-up period, epileptic animals demonstrated impaired spatial memory in the Morris water-maze. Histologic analysis indicated neuronal loss in the amygdala, hippocampus, and surrounding cortical areas, and mossy fiber sprouting in the dentate gyrus. The present data indicate that focal stimulation of the amygdala initiates a cascade of events that lead to the development of spontaneous seizures in rats. This model provides a new tool to better mimic different aspects of human TLE for investigation of the pathogenesis of TLE or the effects of new antiepileptic compounds on status epilepticus, epileptogenesis, and spontaneous seizures.

Amygdala↗

PubMed2000

Association between the density of mossy fiber sprouting and seizure frequency in experimental and human temporal lobe epilepsy.

PURPOSE: If the sprouting of granule cell axons or mossy fibers in the dentate gyrus is critical for the generation of spontaneous seizures in temporal lobe epilepsy (TLE), one could hypothesize that epileptic animals or humans with increased sprouting would have more frequent seizures. This hypothesis was tested by analyzing the data gathered from experimental and human epilepsy. METHODS: In experiment I (rats with "newly diagnosed" TLE), self-sustained status epilepticus was induced in rats by electrically stimulating the amygdala. Thereafter, the appearance of spontaneous seizures was monitored by continuous video-electroencephalography (EEG) until the animal developed two spontaneous seizures and for 11 d thereafter. Rats were perfused for histology, and mossy fibers were stained using the Timm method. In experiment II (rats with "recently diagnosed" TLE), status epilepticus was induced in rats and the development of seizures was monitored by video-EEG for 24 h/d every other day for 60 days. All animals were then perfused for histology. In experiment III (rats with "chronic" TLE), animals were monitored by video-EEG for 24 h/d every other day for 6 months before histologic analysis. To assess mossy fiber sprouting in human TLE, hippocampal sections from 31 patients who had undergone surgery for drug-refractory TLE were stained with an antibody raised against dynorphin. RESULTS AND CONCLUSIONS: Our data indicate that the density of mossy fiber sprouting is not associated with the total number of lifetime seizures or the seizure frequency in experimental or human TLE.

Amygdala↗

PubMed1999

Effects of vigabatrin treatment on status epilepticus-induced neuronal damage and mossy fiber sprouting in the rat hippocampus.

Selective neuronal damage and mossy fiber sprouting may underlie epileptogenesis and spontaneous seizure generation in the epileptic hippocampus. It may be beneficial to prevent their development after cerebral insults that are known to be associated with a high risk of epilepsy later in life in humans. In the present study, we investigated whether chronic treatment with an anticonvulsant, vigabatrin (gamma-vinyl GABA), would prevent the damage to hilar neurons and the development of mossy fiber sprouting. Vigabatrin treatment was started either 1 h, or 2 or 7 days after the beginning of kainic acid-induced (9 mg/kg, i.p.) status epilepticus and continued via subcutaneous osmotic minipumps for 2 months (75 mg/kg per day). Thereafter, rats were perfused for histological analyses. One series of horizontal sections was stained with thionine to estimate the total number of hilar neurons by unbiased stereology. One series was prepared for somatostatin immunohistochemistry and another for Timm histochemistry to detect mossy fiber sprouting. Our data show that vigabatrin treatment did not prevent the decrease in the total number of hilar cells, nor the decrease in hilar somatostatin-immunoreactive (SOM-ir) neurons when SOM-ir neuronal numbers were averaged from all septotemporal levels. However, when vigabatrin was administered 2 days after the onset of status epilepticus, we found a mild neuroprotective effect on SOM-ir neurons in the septal end of the hippocampus (92% SOM-ir neurons remaining; P < 0.05 compared to the vehicle group). Vigabatrin did not prevent mossy fiber sprouting regardless of when treatment was started. Rather, sprouting actually increased in the septal end of the hippocampus when vigabatrin treatment began 1 h after the onset of status epilepticus (P < 0.05 compared to the vehicle group). Our data show that chronic elevation of brain GABA levels after status epilepticus does not have any substantial effects on neuronal loss or mossy fiber sprouting in the rat hippocampus.

Animals↗

PubMed1999

Neuroprotective effect of remacemide hydrochloride in a perforant pathway stimulation model of status epilepticus in the rat.

Previous studies have demonstrated that remacemide and its desglycinyl metabolite, AR-R 2495AA, reduce neuronal damage in animal models of ischemia, subarachnoid hemorrhage, and traumatic brain injury. The aim of the present study was to investigate whether remacemide hydrochloride also alleviates seizure-induced neuronal damage in a model of status epilepticus induced by the stimulation of the perforant pathway (PP) in the rat. Chronic oral remacemide treatment (3 x 25 mg/kg/day) was started either 2 days before or 2 h after the beginning of PP stimulation (2 mA, 20 Hz, 0.1 ms pulse duration for 60 min). The effects of remacemide treatment on the severity of seizures, electroencephalogram (EEG) parameters, seizure-induced neuronal damage in the temporal lobe regions, and memory impairment were compared to unstimulated and stimulated vehicle-treated controls, and carbamazepine-pre-treated (3 x 40 mg/kg/day) rats. Both remacemide and carbamazepine pretreatments, but not remacemide posttreatment, decreased pyramidal cell damage in the CA3 and CA1 subregions of the hippocampus (P < 0.05). In addition, overall neuronal damage in the extrahippocampal temporal lobe regions (the piriform cortex, entorhinal cortex, and the amygdaloid complex) was milder in remacemide-pretreated rats compared to stimulated control rats (P < 0.01). The neuroprotective effect was most evident on the side contralateral to stimulation. Remacemide or carbamazepine pretreatment had no evident effect on the number or duration of behavioral seizures during PP stimulation. Neither drug altered the spectral parameters of the baseline EEG or prevented status epilepticus-induced EEG slowing observed 2 weeks after PP stimulation. Nor did remacemide or carbamazepine treatment alleviate spatial memory impairment determined in a Morris water-maze task 2 weeks after PP stimulation. Our data provide evidence that pretreatment with remacemide has a moderate neuroprotective effect against status epilepticus-induced neuronal damage.

Acetamides↗

PubMed1998

Computed tomographic evaluation of retrosternal adhesions after pericardial substitution.

BACKGROUND: Reoperative median sternotomy can result in cardiac injury and serious bleeding, with the rate ranging from 2% to 6%. Closure of the native pericardium can maintain a preventing plane of cleavage. In patients in whom primary pericardial closure is not possible, several substitutes have been tried with variable results. We conducted a prospective study to evaluate the clinical feasibility of polytetrafluoroethylene and polyglycolic acid patches as pericardial substitutes, using computed tomography for imaging the postoperative state of the retrosternal space. METHODS: The basic population comprised 540 patients who were scheduled for coronary artery bypass grafting, and 52 of them who met the research criteria were chosen for computed tomographic evaluation after 5 years after the primary operation. RESULTS: As a substitute, polytetrafluoroethylene seemed to be less adhesive to the posterior surface of the sternum. Total adhesion scores were also statistically significant (p < 0.001) to the advantage of polytetrafluoroethylene over polyglycolic acid as a pericardial substitute. CONCLUSIONS: Polytetrafluoroethylene membrane seems to be capable of minimizing retrosternal adhesion formation and thus it may protect the heart during subsequent reoperative sternotomy.

Coronary Artery Bypass↗

PubMed1998

Pericardial closure with polytetrafluoroethylene surgical membrane or biodegradable polyglycolic acid mesh after coronary artery bypass surgery--a baseline report.

BACKGROUND AND AIMS: Complete and tight closure of the native pericardium may kink or even occlude bypass grafts after coronary artery bypass grafting (CABG) and therefore the feasibility of tight closure has been debated. The growing number of reoperations has raised the question how to reduce the risk of damage of the right ventricle and patent grafts. We are performing a prospective randomized trial aiming to evaluate the feasibility of polytetrafluoroethylene (PTFE) surgical membrane and biodegradable polygycolic acid (PGA) mesh as pericardial substitutes for closure purposes in patients undergoing primary isolated CABG surgery. MATERIAL AND METHODS: The series comprises 540 patients who underwent a primary isolated CABG procedure at the Oulu University Hospital from October 1989 to May 1994. RESULTS AND CONCLUSIONS: The baseline results suggest that the PTFE and PGA materials seem to be similar despite the subtle early expression of tamponade related to the PTFE membrane after postoperative bleeding.

Adult↗

PubMed1996

Seizure-induced damage to the hippocampus is prevented by modulation of the GABAergic system.

A variety of cerebral insults induce neuronal damage to the hippocampal formation. The somatostatin-immunoreactive (SOM-ir) neurones in the dentate hilus are particularly vulnerable. In the present study, we demonstrated that augmentation of hippocampal GABAergic inhibition by chronic infusion of gamma-vinyl GABA prevented the delayed seizure-induced damage to hilar SOM-ir neurones. Selective lesions of the cholinergic, serotonergic or noradrenergic pathways to the hippocampus did not attenuate the seizure-induced loss of SOM-ir neurones; rather, the damage was exacerbated by the cholinergic lesion. It is, therefore, the intrahippocampal GABAergic circuitries, rather than the selective subcortical pathways, that are critical for neuroprotection after seizures. Enhanced GABAergic inhibition in the hippocampus prevented damage to hilar SOM-ir neurones, even when started 2 days after status epilepticus. GABAergic agents may thus provide an alternative treatment for delayed neuronal damage caused by cerebral insults.

Animals↗

PubMed1996

Tiagabine prevents seizures, neuronal damage and memory impairment in experimental status epilepticus.

A novel antiepileptic drug, tiagabine ((R)-N-[4,4-di-(3-methylthien-2-yl) but-3-enyl] nipecotic acid hydrochloride), was studied in rats in order to determine its efficacy in preventing seizures, seizure-induced neuronal damage and impairment of spatial memory in the perforant pathway stimulation model of status epilepticus. In pilot experiments, administration of tiagabine (50, 100 or 200 mg/kg/day) with subcutaneously implanted Alzet osmotic pumps led to a dose-dependent increase in tiagabine concentrations in the serum and brain. Two days of tiagabine treatment at a dose range of 50-200 mg/kg/day did not change the levels of gamma-aminobutyric acid (GABA), glutamate or aspartate in cisternal cerebrospinal fluid (CSF) compared to the controls. In the pentylenetetrazol test, the maximal anticonvulsive effect of tiagabine administered via osmotic pumps was achieved already with a dose of 50 mg/kg/day. In the perforant pathway model of status epilepticus, subchronic treatment with tiagabine (Alzet pumps, 50 mg/kg/day) completely prevented the appearance of generalized clonic seizures during stimulation (P < 0.001). In the same rats, tiagabine treatment reduced the loss of pyramidal cells in the CA3c and CA1 fields of the hippocampus (P < 0.05) but not the loss of somatostatin immunoreactive neurons in the hilus. Two weeks after perforant pathway stimulation, the tiagabine-treated rats performed better in the Morris water-maze test than the vehicle-treated rats did (P < 0.001). Our results show that tiagabine treatment reduces the severity of seizures in the perforant pathway stimulation model of status epilepticus. Possibly associated with the reduction in seizure number and severity, tiagabine treatment also reduced seizure-induced damage to pyramidal cells in the hippocampus as well as the impairment of the spatial memory associated with hippocampal damage.

Animals↗

PubMed1995

Normothermic versus mild hypothermic retrograde blood cardioplegia: a prospective, randomized study.

BACKGROUND: Continuous retrograde blood cardioplegia has been introduced as a promising alternative for myocardial protection during cardiac operations, although the optimal conditions for its delivery have been poorly studied. METHODS: We randomized a prospective series of 101 patients to receive either retrograde warm (37 degrees C) or mild hypothermic (28 degrees to 29 degrees C) blood cardioplegia during elective coronary artery bypass grafting. Warm blood cardioplegia was delivered to the aortic root until the heart was arrested, after which the regimen was switched to retrograde and continued either as warm or mild hypothermic cardioplegia. Oxygen consumption and transcardiac pH differences during aortic cross-clamping were determined, and postoperative creatine kinase-MB efflux, hemodynamic recovery, and clinical complications monitored. RESULTS: Clinical characteristics, cardioplegia delivery rates, aortic cross-clamp and cardiopulmonary bypass times, and the number of distal anastomoses were similar in both patient groups. Short intermissions in cardioplegia delivery during construction of distal anastomoses were allowed, the ischemia time in the mild hypothermic group being somewhat longer (8.3% +/- 1.1% versus 5.1% +/- 0.8% of cross-clamp time; p = 0.05). Myocardial oxygen consumption was lower in the mild hypothermic group (2.49 +/- 0.23 versus 3.93 +/- 0.33 mL/min at 30 minutes of cross-clamping; p < 0.01), and the transcardiac pH difference was smaller (0.05 +/- 0.01 versus 0.07 +/- 0.01 at 30 minutes of cross-clamping; p < 0.03). Postoperative creatine kinase-MB levels were higher in the normothermic group. Heart rate was higher and left ventricular stroke work index smaller in the warm group, but otherwise there were no major differences between the groups in hemodynamic recovery. The number of postoperative complications was also similar in both groups. CONCLUSIONS: Although both normothermic (37 degrees C) and mild hypothermic (28 degrees to 29 degrees C) retrograde blood cardioplegia, when delivered in near-continuous fashion, will offer safe myocardial protection during coronary artery bypass grafting, mild hypothermia seemed to provide somewhat better protection under the conditions prevailing here. The effects of different cardioplegia temperatures should perhaps be tested further in patients with recent myocardial infarction, unstable angina, or severely depressed left ventricular function.

Coronary Artery Bypass↗

PubMed1995

Anomalies at the thoracic outlet are frequent in the general population.

BACKGROUND: Abnormal anatomy at the thoracic outlet is frequent in patients operated on for thoracic outlet syndrome (TOS). The present study was designed to find out the rate of thoracic outlet anomalies in the general population. METHODS: Fifty cadavers representing a general population were subjected to a total of 98 meticulously performed cervical dissections to ascertain the frequency of congenital anomalies in the thoracocervicoaxillary region. RESULTS: During the 98 cervical dissections, 62 instances of abnormal anatomy of the thoracic outlet were found, and fully normal anatomy was found in 36 cases. Of the total 69 abnormalies, 66 could be classified according to Roos: 37 were type 3 abnormalities, 15 were type 5, 9 were type 11, and there was 1 each of type 4, type 6, type 7, type 9, and type 10 abnormalities. The remaining 3 abnormalities did not fit into Roos' classification. Only 10% (5/50) of the cadavers had a bilaterally normal anatomy. CONCLUSIONS: The results demonstrate that abnormal structures, such as congenital bands in the thoracic outlet, are more common in the general population than had previously been described. We suggest that fibrous bands confer a predisposition for TOS following a certain degree of stress or injury.

Adolescent↗

PubMed1995

Ultrastructural changes during continuous retrograde warm and mild hypothermic blood cardioplegia for coronary bypass operations.

Ultrastructural changes in myocardial tissue were studied in 21 patients undergoing elective aorta-coronary bypass operation. The patients were randomized into two groups, with 10 of them receiving continuous retrograde warm and 11 continuous retrograde mild hypothermic blood cardioplegia. Biopsy specimens for electron microscopy were taken from the apical part of the left ventricle before and at the end of the aortic crossclamp period and after reperfusion of the myocardium. The ultrastructural changes were analyzed with use of a semiquantitative scoring system and classified as mild, moderate, or severe. Slight ultrastructural changes were found in both groups even before the aortic crossclamp period. At the end of the aortic crossclamp period the most prominent ultrastructural changes were mitochondrial swelling, damage of capillary endothelium, and clearing of the nucleoplasm or margination of chromatin, but some enlargement in intercalated discs was also discernible. Reperfusion of the myocardium for 15 minutes somewhat further increased the overall score of the ultrastructural changes. Two patients in the warm cardioplegia group had a perioperative myocardial infarction, and this may be one reason for the higher postoperative creatine kinase MB efflux in this patient group. Despite this finding, no major differences in the ultrastructural changes between the two cardioplegia groups could be observed. We conclude that only mild to moderate and principally reversible ultrastructural changes occur in myocardium during continuous retrograde warm and mild hypothermic blood cardioplegia for coronary bypass operation.

Aged↗