Health Effects of 12 Weeks of Team-Sport Training and Fitness Training in a Community Health Centre for Sedentary Men with Lifestyle Diseases.

This study compares the effects of team-sport training, for sedentary men with lifestyle diseases, with fitness training in a pragmatic set-up in a community health centre (CHC). Thirty-two men in the fitness group (FiG) and 36 men in the team-sport group (TsG) completed the training and trained for 60-90 min, two times/week for 12-16 weeks. In FiG and TsG, mean heart rate (HR) during training was 73.2% and 74.5% of HRmax, respectively. Percentage of training time above 90%HRmax was 6 ± 9% and 10 ± 15% and the percentage of participants who spent > 10% of total training time with HR > 90%HRmax was 20% and 41%, in FiG and TsG, respectively. In FiG, total fat mass was reduced by 3.5% (P < 0.01), while performance in the 6 min walking test (6MWT) increased by 11% (P < 0.001). In TsG, total fat mass was reduced by 2.2% (P < 0.01), while 6MWT performance improved by 5% (P < 0.05). Between-group differences were observed for systolic BP (P = 0.041) and mean arterial pressure (P = 0.050) in favour of TsG and for sit-to-stand test (P = 0.031) in favour of FiG. In conclusion, small-sided team sport is a worthy alternative to fitness training since the overall health effects are comparable, for example, improved balance and reduced fat mass. Team sport elicits high heart rates and improves cardiovascular health by reducing blood pressure, while fitness training improves sit-to-stand test performance related to activity of daily living.

Psychiatric and cognitive symptoms in Huntington's disease are modified by polymorphisms in catecholamine regulating enzyme genes.

Huntington's disease (HD) is an autosomal dominantly inherited neurodegenerative disorder characterized by motor, psychiatric, and cognitive manifestations. HD is caused by a CAG repeat expansion in the Huntingtin (HTT) gene but the exact pathogenesis remains unknown. Dopamine imbalance has previously been shown in HD, and furthermore dopamine is thought to be implicated in cognition, behavioral and motor disturbances. A substantiated inverse correlation between motor onset and the elongated CAG repeat in the HTT has been established. This relation does not account for the full variability of the motor onset, and efforts have been put into finding genetic modifiers of motor onset, however, mostly with unsuccessful outcome. In this study, we took an alternative approach focusing on symptom complexes and searched for modifiers of cognitive impairment and psychiatric symptoms in a well-described cohort of Danish HD gene-expansion carriers. We show that cognitive impairment and psychiatric symptoms in HD are modified by polymorphisms in the monoamine oxidase A (MAOA) and catechol-O-methyltransferase (COMT) genes and by the 4p16.3 B haplotype. These results support the theory of dopamine imbalance in HD, and point toward more personalized treatment modalities of HD in the future.

Hereditary spastic paraplegia is not associated with C9ORF72 repeat expansions in a Danish cohort.

OBJECTIVES: Hereditary spastic paraplegia (HSP) is a heterogeneous group of neurodegenerative disorders characterized by a progressive gait disorder, lower limb spasticity, hyper-reflexia, weakness and extensor plantar responses. Recently, large intronic hexanucleotide repeat expansions (GGGGCC) in C9ORF72 have been found to cause frontotemporal dementia (FTD), amyotrophic lateral sclerosis and FTD with motor neuron disease. Owing to the overlapping phenotypes among HSP, amyotrophic lateral sclerosis and FTD with motor neuron disease along with shared pathological findings, we hypothesized that C9ORF72 expansions might be a genetic risk factor or modifier of HSP. METHODS: Clinically characterized HSP patients were investigated for elongations in the hexanucleotide repeat of C9ORF72. RESULTS: Upon analyses of the repeat lengths in the C9ORF72 gene in a Danish cohort of HSP patients, we found no expansions. CONCLUSION: We conclude that HSP is most likely not associated with repeat expansions in C9ORF72.

Remote ischemic perconditioning in thrombolysed stroke patients: randomized study of activating endogenous neuroprotection - design and MRI measurements.

BACKGROUND: Intravenous administration of alteplase is the only approved treatment for acute ischemic stroke. Despite the effectiveness of this treatment, 50% of patients suffer chronic neurological disability, which may in part be caused by ischemia-reperfusion injury. Remote ischemic perconditioning, performed as a transient ischemic stimulus by blood-pressure cuff inflation to an extremity, has proven effective in attenuating ischemia-reperfusion injury in animal models of stroke. Remote ischemic perconditioning increases myocardial salvage in patients undergoing acute revascularization for acute myocardial infarction. To clarify whether a similar benefit can be obtained in patients undergoing thrombolysis for acute stroke, we included patients from June 2009 to January 2011. AIM AND DESIGN: The aims of the study are: to estimate the effect of remote ischemic perconditioning as adjunctive therapy to intravenous alteplase of acute ischemic stroke within the 4-h time window and to investigate the feasibility of remote ischemic perconditioning performed during transport to hospital in patients displaying symptoms of acute stroke. Patients are randomized to remote ischemic perconditioning in a single-blinded fashion during transportation to hospital. Only patients with magnetic resonance imaging-proven ischemic stroke, who subsequently are treated with intravenous alteplase, and in selected cases additional endovascular treatment, are finally included in the study. STUDY OUTCOMES: Primary end-point is penumbral salvage. Penumbra is defined as hypoperfused yet viable tissue identified as the mismatch between perfusion-weighted imaging and diffusion-weighted imaging lesion on magnetic resonance imaging scans. Primary outcome is a mismatch volume not progressing to infarction on one-month follow-up T2 fluid attenuated inversion recovery. Secondary end-points include: infarct growth (expansion of the diffusion-weighted imaging lesion) from baseline to the 24-h and one-month follow-up examination. Infarct growth inside and outside the acute perfusion-weighted imaging-diffusion-weighted imaging mismatch zone is quantified by use of coregistration. Clinical outcome after three-months. The influence of physical activity (Physical Activity Scale for the Elderly score) on effect of remote ischemic perconditioning. Feasibility of remote ischemic perconditioning in acute stroke patients. SUMMARY: This phase 3 trial is the first study in patients with acute ischemic stroke to evaluate the effect size of remote ischemic perconditioning as a pretreatment to intravenous alteplase, measured as penumbral salvage on multimodal magnetic resonance imaging and clinical outcome after three-months follow-up.

Comparison of two sulfonylureas with high and low myocardial K(ATP) channel affinity on myocardial infarct size and metabolism in a rat model of type 2 diabetes.

AIMS/HYPOTHESIS: Sulfonylureas (SUs) may impair outcome in patients with acute coronary syndrome. Most experimental studies of the myocardial effects of SU treatment are performed in non-diabetic models. We compared the effect of two widely used SUs, glibenclamide (gb) and gliclazide (gc), with high and low myocardial K(ATP) channel affinity, respectively, at therapeutic concentrations on infarct size, left ventricular (LV) function and myocardial glycogen, lactate and alanine content before and after ischaemia/reperfusion (I/R). METHODS: Non-diabetic Wistar and diabetic Goto-Kakizaki rat hearts were investigated in a Langendorff preparation. Gb (0.1 µmol/l) and gc (1.0 µmol/l) were administrated throughout the study. Infarct size was evaluated after 120 min of reperfusion. Myocardial metabolite content was measured before and after ischaemia. RESULTS: Infarct size was smaller in diabetic hearts than in non-diabetic hearts (0.33 ± 0.03 vs 0.51 ± 0.05, p < 0.05). Gb increased infarct size (0.54 ± 0.04 vs 0.33 ± 0.03, p < 0.05) and reduced post-ischaemic LV developed pressure (60 ± 3 vs 76 ± 3 mmHg, p < 0.05) and coronary flow (4.9 ± 0.5 vs 7.1 ± 0.4 ml min(-1) g(-1), p < 0.05) in gb-treated diabetic rats compared with untreated diabetic rats. On comparing gb-treated diabetic rats with untreated diabetic rats, glycogen content was reduced before (9.1 ± 0.6 vs 13.6 ± 1.0 nmol/mg wet weight, p < 0.01) and after ischaemia (0.9 ± 0.2 vs 1.8 ± 0.2 nmol/mg wet weight, p < 0.05), and lactate (4.8 ± 0.4 vs 3.2 ± 0.3 nmol/mg wet weight, p < 0.01) and alanine (1.38 ± 0.12 vs 0.96 ± 0.09 nmol/mg wet weight, p < 0.05) contents were increased during reperfusion. Gc-treatment of diabetic and non-diabetic rats did not affect any of the measured variables. CONCLUSIONS/INTERPRETATIONS: Gb, but not gc, exacerbates I/R injury and deteriorates LV function in diabetic hearts. These effects of gb on diabetic hearts may be due to detrimental effects on myocardial carbohydrate metabolism.

Post-conditioning with cyclosporine A fails to reduce the infarct size in an in vivo porcine model.

BACKGROUND: Cyclosporine A has generated intense interest in the field of cardioprotection due to its ability to protect the mitochondria at reperfusion by blocking the opening of the mitochondrial permeability transition pore. The aim of our study was to examine the cardioprotective effect of Sandimmun, a clinically available formulation of cyclosporine A, in an in vivo large mammal model. METHODS: Forty-eight pigs were randomly allocated to one of three groups: (i) Control group (Con, n=19), (ii) Cyclosporine group, (Cyclo, n=19) Sandimmun 10 mg/kg i.v. bolus 5 min before reperfusion and (iii) Pre-conditioning group (Precon, n=10) two cycles of 10 min ischemia interspersed with 30-min reperfusion. The study was further sub-divided into a metabolic protocol, evaluating myocardial metabolism by measuring changes in the interstitial lactate concentration, and a coronary flow protocol. All animals were subjected to 40 min of left anterior descending coronary artery occlusion, followed by 180 min of reperfusion before histochemical staining and assessment of infarct size by planimetry. RESULTS: Infarct sizes were measured as: Con 51.4 +/- 16.5%, Cyclo 47.3 +/- 15.7% and Precon 2.4 +/- 3.6%, with no significant difference between the Con and Cyclo groups but a highly significant difference between the Precon and Cyclo and Con groups (P<0.0001 for both comparisons). In the Cyclo group, the interstitial lactate concentration was significantly increased compared with the Con group at 6-min reperfusion, although significantly lower at 14 min presumably due to accelerated washout. CONCLUSION: In this large animal model, a 10 mg/kg bolus administration of Sandimmun 5 min before reperfusion did not reduce the infarct size.

Huntington's disease does not appear to increase the risk of diabetes mellitus.

Huntington's disease (HD) is an autosomal, dominantly inherited, neurodegenerative disorder characterised by neurological, cognitive and psychiatric symptoms. HD has been associated with diabetes mellitus, which is, to some extent, supported by studies in transgenic HD mice. In transgenic mice, the severity of the diabetic phenotype appears to correlate with the length of a polyglutamine expansion in the protein huntingtin. In the present study, we investigated the association between diabetes mellitus and HD by performing an oral glucose-tolerance test (OGTT) to evaluate the glucose-tolerance status and OGTT-related insulin release in 14 HD patients. Furthermore, we expressed N-terminal huntingtin fragments with different polyglutamine lengths in an insulinoma-cell line (INS-1E) to investigate how mutant huntingtin influences glucose-stimulated insulin release in vitro. We found no difference between a group of early- and middle-stage HD patients and a large group of control individuals in any of the assessed variables. However, the glucose-stimulated induction of insulin release was significantly reduced in the insulinoma-cell line expressing highly expanded huntingtin compared to cells expressing huntingtin with modestly elongated polyglutamine stretches. These data indicate that insulin release from beta-cells expressing mutant huntingtin appears to be polyglutamine length-dependent, and that polyglutamine lengths within the range normally found in adult onset HD do not influence insulin release. This challenges the assumption of an increased risk of diabetes among HD patients, although our results do not exclude a changed glucose tolerance in end-stage HD patients or in patients with juvenile onset HD. It also raises the question of which extent transgenic mice models reflect the pathology of human HD in this regard.

Cardioprotective effect of L-glutamate in obese type 2 diabetic Zucker fatty rats.

1. Because diabetic hearts have an increased threshold for cardioprotection by ischaemic preconditioning (IPC), we hypothesized that protection by L-glutamate during reperfusion is restricted in Type 2 diabetic hearts. Previously, we found that L-glutamate-mediated postischaemic cardioprotection mimics IPC. 2. Rat hearts were studied in a Langendorff preparation perfused with Krebs'-Henseleit solution and subjected to 40 min global no-flow ischaemia, followed by 120 min reperfusion. L-Glutamate (0, 15 and 30 mmol/L) was added to the perfusate during reperfusion of hearts from non-diabetic (Wistar-Kyoto) and diabetic (Zucker diabetic fatty (ZDF)) rats, studied at 16 weeks of age. The infarct size (IS)/area-at-risk (AAR) ratio was the primary end-point. Expression of L-glutamate excitatory amino acid transporter (EAAT) 1 (mitochondrial) and EAAT3 (sarcolemmal) was determined by quantitative polymerase chain reaction and immunoblotting. 3. The ISS/AAR ratio did not differ between control hearts from Wistar-Kyoto and ZDF rats (0.52 ± 0.03 and 0.51 ± 0.04, respectively; P = 0.90). L-Glutamate (15 mmol/L) significantly reduced the IS/AAR ratio in non-diabetic hearts, but not in diabetic hearts, compared with their respective controls. The higher concentration of L-glutamate (30 mmol/L) reduced infarct size in diabetic hearts to the same degree as in non-diabetic hearts (IS/AAR 0.35 ± 0.03 (P = 0.002) and 0.34 ± 0.03 (P = 0.004), respectively). The mitochondrial L-glutamate transporter EAAT1 was downregulated in hearts from ZDF rats at both the mRNA and protein levels (P < 0.0005 and P < 0.0001, respectively). However, there was no change in EAAT3 expression at the protein level. Myocardial L-glutamate content was increased by 43% in diabetic hearts (P < 0.0001). 4. Hearts from obese diabetic rats have an elevated threshold for metabolic postischaemic cardioprotection by L-glutamate. These findings may reflect underlying mechanisms of inherent resistance against additional cardioprotection in the diabetic heart.

Primary PCI as the preferred reperfusion therapy in STEMI: it is a matter of time.

There is a continuing controversy about the acceptable time-window for primary percutaneous coronary intervention (PPCI) in patients with ST-elevation myocardial infarction (STEMI). Recent American and European guidelines recommend PPCI if the delay in performing PPCI instead of administering fibrinolysis (PCI-related delay) is <60 min and the presentation delay is more than 3 h. Based on a review of the literature, this viewpoint recommends a revision of the guidelines. The evidence supports an acceptable PCI-related delay of 80-120 min and PPCI as the better reperfusion strategy also in the early incomers. Furthermore, the previous assumption that PPCI is less time-dependent than fibrinolysis is questioned. To maximise the number of patients with STEMI eligible for PPCI the optimal logistic may be to establish the diagnosis in the prehospital phase, to bypass local hospitals and re-route patients directly to catheterisation laboratories running 24/7.

Post-conditioning reduces infarct size in an open-chest porcine acute ischemia-reperfusion model.

BACKGROUND: Timely reperfusion is a prerequisite for myocardial salvage; however, re-oxygenation of the ischemic myocardium initiates reperfusion injury. Post-conditioning diminishes the detrimental aftermath of an acute myocardial infarction through alleviation of reperfusion injury. Ischemic post-conditioning consists of a series of brief interruptions in the coronary blood supply that has to be applied within the first minutes after re-establishing the coronary flow. METHODS: Sixteen female mixed Danish Landrace and Yorkshire pigs weighing 20 kg were included. The heart was exposed through a midline sternotomy. A snare was positioned around the left anterior descending coronary artery downstream of the second diagonal branch. After randomization to either no treatment (control group) or treatment by ischemic post-conditioning (post-conditioning group), the pigs underwent 45 min of ischemia and 180 min of reperfusion. The post-conditioning group had a post-conditioning algorithm applied consisting of 15 s of reperfusion alternating with 15 s of re-occlusion repeated 10 times. RESULTS: The groups were comparable with regard to body weight, hemodynamics and the size of the area at risk. The post-conditioning group had an absolute reduction in infarct size of 18.1% [confidence interval (CI): 6.2: 30.0%] compared with the control group (P=0.0056). In the post-conditioning group, infarction developed in 39.6+/-12.0% (1 SD) of the area at risk compared with 57.8+/-10.2% (1 SD) in the control group. CONCLUSION: When ischemic post-conditioning was applied at reperfusion, we found an absolute reduction in infarct size of 18.1% presumably attributable to a diminished reperfusion injury. The model we have developed is suitable for further studies of this promising intervention.

A study of police operated dispatch to acute coronary syndrome cases arising from 112 emergency calls in Aarhus county, Denmark.

BACKGROUND: The accuracy of the Danish police operated "112" emergency call system was studied. Dispatch of the anaesthesiologist staffed mobile emergency care unit (MECU) to acute coronary syndrome (ACS) cases was used as an indicator of accuracy of dispatch to life threatening emergencies. METHODS: This was an observational cohort study of patients given a 112 system report of heart attack and patients with a provisional diagnosis of ACS made on scene by the MECU. Sensitivity, specificity, and positive predictive value with 95% confidence intervals (CI) were calculated. RESULTS: There were 341 reports of "heart attack" and 205 patients with ACS. Sensitivity was 75% (95% CI 68% to 80%) specificity 90% (89% to 92%) and positive predictive value 45% (40% to 50%). CONCLUSION: The accuracy of 112 dispatch of the MECU was found to be moderate. We suggest more training of dispatch staff and medical supervision.

Effect of the oral hypoglycaemic sulphonylurea glibenclamide, a blocker of ATP-sensitive potassium channels, on walking distance in patients with intermittent claudication.

AIMS: The oral hypoglycaemic sulphonylurea glibenclamide stimulates endogenous insulin secretion through blockade of ATP-sensitive potassium (KATP) channels on pancreatic beta cells, but also blocks cardiovascular KATP channels, leading to increased peripheral vascular resistance and reduced peripheral blood flow in non-diabetic subjects. Therefore, this study examined whether a single oral dose of glibenclamide adversely affected the pain-free or maximal walking distance in patients with intermittent claudication. METHODS: In a double-blind, randomized crossover study, 12 non-diabetic patients with intermittent claudication were given a single oral dose of glibenclamide (5.25 mg) or placebo separated by a washout period of 1 week. A treadmill test was carried out 180 min after glibenclamide/placebo intake for determination of pain-free and maximal walking distance. Plasma glucose concentrations were kept constant by an euglycemic clamp. Changes in ankle/brachial blood pressure index (ABI), serum insulin, and serum glibenclamide were also assessed. RESULTS: The pain-free walking distance was 62.8 +/- 9.8 metres (mean +/- sem) after glibenclamide and 52.6 +/- 5.9 metres after placebo (P = 0.52). The maximal walking distance was 142.7 +/- 18.7 metres after glibenclamide and 132.6 +/- 16.6 metres after placebo (P = 0.23). The ABI was not significantly changed by glibenclamide compared with placebo. Serum glibenclamide was 0.51 +/- 0.08 microm 180 min after administration of the drug. Glibenclamide produced an 8-fold increase in circulating insulin compared with placebo (P < 0.001). CONCLUSIONS: Glibenclamide given as a single oral dose commonly used in glucose-lowering drug therapy does not reduce pain-free or maximal walking distance in non-diabetic patients with intermittent claudication.

Survival trends among Danish patients undergoing coronary angiography for known or suspected ischaemic heart disease: a population based follow up study, 1992-2000.

OBJECTIVE: To determine, from population based clinical data, changes in the survival of Danish patients examined by coronary angiography for known or suspected ischaemic heart disease (IHD) during the 1990s. DESIGN: Follow up study. SETTING: The departments of cardiology at Rigshospitalet, Copenhagen University Hospital, and Skejby Hospital, Aarhus University Hospital, Denmark. PATIENTS: Patients with IHD (n = 7021) who underwent first time coronary angiography in 1992, 1996, or 2000. MAIN OUTCOMES MEASURES: Three year survival was compared between cohorts and with that of the general population. Cox proportional hazards regression was used to estimate mortality ratios adjusted for differences in patient characteristics. RESULTS: Survival improved substantially--for example, adjusted mortality ratio was 0.69 (95% confidence interval (CI) 0.55 to 0.87) when comparing patients from 2000 with patients from 1992. The absolute standardised survival rates after three years of follow up were 87.1% (95% CI 85.4% to 88.8%), 89.9% (95% CI 88.5% to 91.3%), and 91.2% (95% CI 90.3% to 92.1%) among patients examined in 1992, 1996, and 2000, respectively. The improvement was not explained by the improvement in overall survival in the general population during the study period. CONCLUSIONS: The survival of Danish patients with known or suspected IHD appears to have improved substantially during the 1990s.

Percutaneous coronary intervention in diabetic patients: a problem?

Pharmacological and technological advances in surgical and interventional coronary treatment modalities have shown reduced cardiovascular mortality in non-diabetic patients, but diabetic patients have not gained the same benefit of invasive treatment as non-diabetics. Although early studies suggest a poorer outcome after angioplasty than after coronary by-pass grafting (CABG) in diabetic patients, more recent studies including improved pharmacological therapy and stent implantation seem to justify increased use of revascularization by percutaneous coronary intervention (PCI) in diabetics with stable and unstable coronary syndromes as the relative benefit in long-term survival, non-fatal myocardial infarction and cerebrovascular accidents is similar. However, diabetic patients are still subject to higher morbidity and mortality after revascularization with CABG and PCI. This is related to increased co-morbidity, metabolic dysregulation, difficulties in obtaining complete revascularization, and more frequent appearance of new lesions as well as restenosis and hemostatic abnormalities. Drug-eluting stents appear to reduce the risk of restenosis, and aggressive antithrombotics also tend to improve the outcome. Unsolved problems are the significance of incomplete revascularization and whether a PCI strategy is associated with a procedure induced progression of the native diabetic vascular disease in treated or untreated vessels. Trials addressing adjunctive treatment and long-term clinical outcome specifically in diabetic patients should clarify these questions.

Myocardial infarction centres: the way forward.

In the era of primary PCI, a strategy of admitting patients to the nearest hospital should be obsolete. Instead, a prehospital diagnostic strategy should be implemented in order to: (1) refer patients directly to interventional centres, thereby eliminating delay at local hospitals; (2) alert the interventional centre, thereby reducing door to balloon times; (3) initiate adjunctive medication in the prehospital phase.

Ischaemic preconditioning does not protect the heart in obese and lean animal models of type 2 diabetes.

AIMS/HYPOTHESIS: The prevalence of type 2 diabetes mellitus is increasing worldwide with obese diabetic patients constituting the majority of this population. Type 2 diabetes is associated with increased morbidity and mortality after acute myocardial infarction. Previous experimental studies of ischaemia-reperfusion tolerance in diabetes have only been performed in animal models of type 1 diabetes mellitus, yielding conflicting data. The aim of the present study was to characterise and compare the tolerance to ischaemia and effects of ischaemic preconditioning (IPC) in hearts from obese Zucker diabetic fatty (ZDF) and lean Goto-Kakizaki (GK) type 2 diabetic rats, using non-obese Zucker and Wistar rats as respective controls. METHODS: The two rat strains were divided into 8 groups. The ZDF study (n=47) consisted of: Control -IPC, Control +IPC, ZDF -IPC and ZDF +IPC. The GK study (n=38) consisted of: Control -IPC, Control +IPC, GK -IPC and GK +IPC. Hearts, which were studied in a Langendorff preparation perfused with Krebs-Henseleit buffer, were subjected or not to IPC (+IPC, -IPC) before 50 minutes of regional ischaemia and 120 minutes reperfusion. RESULTS: Ischaemic reperfusion injury was smaller in obese (p<0.05) and lean (p<0.05) type 2 diabetic animals than in their respective control animals. IPC reduced ischaemic reperfusion injury during reperfusion in non-diabetic control rats (p<0.01), but failed to protect hearts from both diabetic animal models. Post-ischaemic haemodynamic recovery was impaired in the ZDF rats compared to both control and GK rats (p<0.05). CONCLUSIONS/INTERPRETATION: Ischaemic preconditioning does not protect hearts from obese or lean type 2 diabetic animals. However, the susceptibility of the type 2 diabetic myocardium to ischaemic damage is lower than in non-diabetic hearts. The method described here could be used as a tool to study the pathogenesis of increased cardiovascular morbidity and mortality in type 2 diabetes.

Are we underestimating the full potential of early thrombolytic treatment in patients with acute myocardial infarction?

Use of the Boersma curve in order to describe the beneficial effect of thrombolytic treatment at different treatment delays seems questionable, because the curve may underestimate the favourable prognostic effects of early thrombolysis in patients with acute myocardial infarction

The effect of litter size and day of lactation on amino acid uptake by the porcine mammary glands.

Twelve multiparous sows (PIC Camborough 15; parity >2) were used to investigate the relationship between litter size and day of lactation, and plasma amino acid (AA) arteriovenous differences (A-VD), AA uptake, and plasma flow across the mammary glands. Sows were assigned randomly to one of the following litter sizes: 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, or 14 pigs per litter by cross fostering on d 2 postpartum. All sows were surgically fitted with catheters in the carotid artery and the main mammary vein. Matched arteriovenous blood samples were obtained on d 9, 12, 15, 18, 21, and 24 postpartum. Daily mammary uptake of AA was based on the product of plasma A-VD and daily mammary plasma flow (MPF). Daily MPF was estimated using the Fick method based on lysine conservation across the gland, and daily milk production. For the majority of AA, as litter size increased, A-VD did not increase, except for alanine (P < 0.05, linear and quadratic) and valine (P < 0.1; trend; linear and quadratic). As day of lactation increased, A-VD for the majority of AA increased (P < 0.05, linear and quadratic) except for arginine, lysine, and phenylalanine. As litter size increased, net daily mammary AA uptake increased for all indispensable AA (P = 0.001 to P < 0.05, linear and quadratic), excepting arginine. Milk production increased with increasing litter size (P < 0.001, linear) and with increasing day of lactation (P < 0.05, quadratic). Daily MPF increased (P < 0.05, linear) with increasing litter size, but did not change during the period measured from d 9 to 24. In conclusion, litter size appears to be a major determinant of net mammary AA uptake with daily mammary plasma flow a driving variable, whereas AA A-VD is a function of day of lactation and a major variable in determining net AA uptake with advancement of lactation.

Telemedicine used for remote prehospital diagnosing in patients suspected of acute myocardial infarction.

INTRODUCTION: In patients with acute myocardial infarction (AMI), considerable time elapses from symptom onset until initiation of thrombolytic therapy or primary percutaneous coronary intervention. Prehospital diagnosing can reduce time delays, and remote diagnosing using telemedicine may be appropriate in areas and countries where ambulances are not staffed with physicians. OBJECTIVES: To evaluate whether it was technically feasible for physicians at a remote university hospital to diagnose ST-segment-elevation-AMI (AMI(STelev)) in patients suspected of AMI, who were transported by ambulances to a local hospital. To determine associated prehospital delays and in-hospital treatment delays. METHODS: Patients carried in telemetry equipped ambulances had 12-lead electrocardiograms (ECGs) acquired as soon as possible. En route to the local hospital the ECGs were transmitted to a remote university hospital, by use of the GSM-system. The physician on call at the university hospital interviewed the patients, who were provided with cellular phone headsets, and alerted the local hospital if signs of AMI(STelev), bundle-branch-block-AMI or malignant arrhythmia were detected. Patients transported by traditional ambulances were included in a prospective control group. RESULTS: In 214 (86%) of 250 patients prehospital diagnosing was successful. Geographically related transmission problems were the primary reason for failure. Ninety-eight per cent of transmitted electrocardiograms and obtained history takings were technically acceptable for diagnostic purposes. Door-to-needle times were shorter amongst patients with AMI(STelev) who were subjected to prehospital diagnosing (n = 13) as compared with patients transported by traditional ambulances (n = 14) (38 vs. 81 min) (P = 0.004). CONCLUSIONS: It was technically feasible to use telemedicine for remote prehospital diagnosing of patients suspected of AMI. Patients subjected to prehospital diagnosing had shorter door-to-needle times compared with a prospective control group.