Lactation and breast-feeding ability following lateral pedicle mammaplasty.

A retrospective study was undertaken to evaluate the ability of breast-feeding using lateral pedicle reduction mammaplasty. A standard questionnaire was sent to 72 patients who had been operated on at a fertile age. Data was collected regarding the duration and quality of preoperative and postoperative breast-feeding, difficulties while breast-feeding, reasons for discontinuation of breast-feeding or for not attempting to breast-feed, and postoperative subjective sensitivity. Thirteen of the women who replied to the questionnaire had given birth after surgery. The pressure threshold sensitivity of areola-nipple complex was measured in nine of the above cases. To preserve lactation, a technique leaving structures untouched within the pedicle with increased dimensions was used.Breast-feeding was considered successful in this study if it was performed exclusively, without supplementation, for two months. Seven women (54%) breast-fed successfully for between two and 14 months (5.8+/-1.3) following surgery. Two women (16%) were classified as unsuccessful and four women (30%) did not breast-feed at all. The success of breast-feeding was limited by nonsurgical factors including the influence of medical personal. Five of eight women (62%) who had children preoperatively improved their rate of breast-feeding after surgery. No correlation was demonstrated between measured sensitivity and breast-feeding (p=0.65). No significant correlation was found between the resected tissue and breast-feeding (p=0.08). No relation was observed between the duration of breast-feeding and the period between operation and partus.

A retrospective quantitative assessment of breast sensation after lateral pedicle mammaplasty.

Preservation of sensitivity is one of the important objectives in reduction mammaplasty. The lateral or medial pedicle reduction mammaplasty technique aims to maintain superficial innervation of the breast. These superficial nerves are smaller and more variable compared with deep and larger nerve structures, which are excised during this procedure. An assessment of recovery of tactile sensitivity after lateral pedicle mammaplasty was performed retrospectively. One hundred and one women, operated on between the year 1985 and 2000, with a lateral pedicle mammaplasty, were reviewed. Using a standardised questionnaire, women reported on subjective changes in sensation after surgery, including time of recovery and the influence which surgery had on sensual function. Fifty-nine of these women were tested 3-7 years after surgery. Touch sensitivity was measured using a set of 20 Semmes-Weinstein monofilaments. Erectile function was also tested. The mean pressure threshold for the areola region was 19.12 g/mm(2) and for the nipple 16.75 g/mm(2), which is better that in studies on inferior pedicle mammaplasty. In previous studies patients were tested earlier, which may explain this difference.No correlation was found between sensitivity and resected tissue (for the areola p=0.88 and for the nipple p=0.82) or between sensitivity and age of patients (for the areola p=0.73 and for the nipple p=0.80). There were individual differences in the results. It is speculated that variability in anatomy of superficial nerves might explain these differences. Nearly all patients tested regained their erectile function. The majority of patients did not notice any change in their erogenous function. Twelve (12%) reported a post-surgical improvement of sensation. Nipples with partial loss of sensation persisted in 2% of the patients.

Autologous breast reconstruction with a free lumbar artery perforator flap.

Autologous breast reconstruction with a perforator flap has become increasingly popular. This paper presents the free lumbar artery perforator (LAP) flap as an option for breast reconstruction. Flap harvest is easy, no muscle is sacrificed and donor-site morbidity is minimal. Anastomosis of the sensory nerve to the fourth intercostal nerve is possible. The successful use of a LAP flap for breast reconstruction is illustrated with a case report, and the surgical technique is described. This method may be a good alternative for patients with relative contraindications to breast reconstruction with a DIEP flap.

Superior myocardial protection with nicorandil cardioplegia.

OBJECTIVE: The ATP-sensitive potassium channel (K(ATP)) activator nicorandil used as cardioplegic agent may protect the left ventricle during cardiac arrest. Nicorandil in cold blood was compared with standard hyperkalemic blood and crystalloid cardioplegia. METHODS: Twenty-one pigs were randomly assigned to three groups: (1) cold hyperkalemic crystalloid (n=7); (2) cold hyperkalemic blood (n=7); and (3) nicorandil as cardioplegia in cold blood (n=7). Left ventricular mechanical performance, pressure-volume area (PVA) and myocardial oxygen consumption (MVO(2)) were measured before and at 1 and at 2 h after 60 min of cold global ischemia on cardiopulmonary bypass using intraventricular pressure-volume conductance catheters, coronary flow probes and O(2)-content difference. RESULTS: The slope (M(w)) of the stroke work end-diastolic volume relationship, the preload recriutable stroke work relationship, was unchanged after ischemia in the nicorandil group, but was reduced to averaged 62.5% (standard deviation 14) of baseline values in both hyperkalemic perfusions (P<0.05). The slope of the MVO(2)-PVA relationship was unchanged after nicorandil cardioplegia while the slope after hyperkalemic blood and crystalloid cardioplegia increased with 33% (P<0.02) and 52% (P<0.02) of baseline values, respectively. CONCLUSIONS: Nicorandil as sole cardioplegic agent in cold blood given intermittently preserves left ventricular contractility and myocardial energetics significantly better than traditional forms of cardioplegia after cardiac arrest.

Postischemic mechanoenergetic inefficiency is related to contractile dysfunction and not altered metabolism.

Mechanoenergetic inefficiency in postischemic nonnecrotic myocardium may partly be explained by an increased fatty acid (FA) oxidation rate. In the present study, left ventricular (LV) postischemic energy transfer was characterized in 10 intact anesthetized pigs. The LV was stunned by 11 brief left main coronary artery occlusions/reperfusions (20-min accumulated ischemia). Seven pigs served as time controls. The relationship between myocardial oxygen consumption (MVO(2)) and LV pressure-volume area (PVA) was assessed. [(14)C]glucose and [(3)H]oleate markers were used to discriminate between glucose and FA consumption. In stunned hearts, severe postischemic dysfunction was observed, and contractile efficiency was reduced (increased MVO(2)-PVA slope, P = 0.001). Unloaded (nonmechanical) MVO(2) was not affected by ischemia. We observed only a small transient increase in FA preference and conclude that the contribution from increased FA utilization to postischemic mechanoenergetic inefficiency is insignificant. Disrupted postischemic chemical-to-mechanical energy transfer in vivo is, therefore, related to inefficient energy utilization in the contractile apparatus.

N-acetylcysteine increases cerebral perfusion pressure in pigs with fulminant hepatic failure.

OBJECTIVE: Intravenous administration of N-acetylcysteine beyond 15 hrs reduces mortality rates in patients suffering from paracetamol-induced fulminant hepatic failure, although the mechanism of the therapeutic benefit remains unclear. We hypothesized increased survival to be caused by improved hemodynamic performance. The main objective for the study was to explore the effect of N-acetylcysteine on hemodynamics, oxygen transport, and regional blood flow in pigs with fulminant hepatic failure. DESIGN: Prospective, randomized, controlled trial. SETTING: Surgical research laboratory in a university hospital. SUBJECTS: Female Norwegian Landrace pigs. INTERVENTIONS: Fulminant hepatic failure was induced by a total liver devascularization procedure. Five hours later, the pigs were allocated to N-acetylcysteine treatment (150 mg.kg-1 in 100 mL of 0.9% saline over 15 mins, followed by 50 mg.kg-1 in 500 mL of 0.9% saline over a period of 4 hrs) or placebo. MEASUREMENTS AND MAIN RESULTS: Mean arterial pressure stabilized in the N-acetylcysteine group and increased slightly during the last 2 hrs (pGT =.009). Thus, mean arterial pressure was significantly higher compared with placebo after 3 hrs (p =.01). Cerebral perfusion pressure was significantly higher during the last 2 hrs in the N-acetylcysteine group (pGT =.033). Common carotid artery flow also increased and was maintained at a higher level compared with placebo (pG =.027). Systemic vascular resistance index initially decreased but then gradually increased (pGT <.001). Cardiac index increased after 15 mins of N-acetylcysteine infusion, causing a significant interaction (pGT =.038), but did not differ after 3 hrs. No significant differences in hindleg and mesentery hemodynamics were found. A short-lived increase in oxygen delivery caused by a temporary increase in cardiac index was observed but without any corresponding increase in oxygen consumption. CONCLUSIONS: Intravenous N-acetylcysteine infusion increases cerebral perfusion pressure in pigs with fulminant hepatic failure. Earlier reported effects on oxygen transport and uptake could not be confirmed.

Cardiac dysfunction and inefficiency after substrate-enriched warm blood cardioplegia.

OBJECTIVE: The study assessed the outcome after prolonged warm continuous antegrade blood cardioplegia (WCBC) with substrate enrichment, in terms of mechanical performance and mechanoenergetic efficiency. METHODS: WCBC was given for 3 h to three groups of pigs on cardiopulmonary bypass; WCBC alone (n=7), WCBC+glucose and insulin (+GIK, n=7) and WCBC+L-glutamine (+GLN, n=7). Cardiac systolic and diastolic function, pressure-volume area (PVA) and myocardial oxygen consumption (MVO(2)) were assessed before, and twice after WCBC using pressure-conductance catheter, coronary flow-probes and O(2)-content difference. RESULTS: In the WCBC, +GIK and +GLN groups respectively, the following parameters decreased after WCBC compared to baseline: left ventricular developed pressure by 26, 19 and 25% (P<0.001); dP/dt(max) by 36, 37 and 34% (P<0.001); preload recruitable stroke work by 35, 41 and 28% (P<0.001); mechanoenergetic efficiency (PVA/MVO(2)) by 44, 41 and 22% (P<0.001). End-diastolic stiffness increased early after WCBC in the WCBC and +GLN groups, while it was unchanged in the +GIK group (P=0.032). CONCLUSION: Despite continuous aerobic conditions and additional substrates, post-WCBC cardiac contractile function and mechanoenergetic efficiency was severely depressed. The results demonstrate the hazards of sustained normothermic hyperkalemic perfusion.

Myocardial metabolism and efficiency after warm continuous blood cardioplegia.

BACKGROUND: Warm continuous blood cardioplegia (WCBCP) has been recommended during prolonged cardiac arrest to minimize functional deterioration. Myocardial metabolism and efficiency after this cardioplegic modality are not well described. METHODS: Substrate oxidation, blood flow, and myocardial function were measured before, during, and after 3 hours of WCBCP in 7 pigs. RESULTS: Free fatty acid and glucose oxidation decreased by 60% +/- 3.8% and 94% +/- 1.2%, respectively, during cardioplegia (both p < 0.05) and increased to 62% +/- 28% and 122% +/- 62% of baseline during the early recovery phase (p < 0.05 for glucose). One hour after WCBCP oxidation rates were similar to baseline. The transient postcardioplegic increase in substrate oxidation was associated with a 43% +/- 23% elevation of oxygen consumption (MVO2) compared with baseline and a 62% +/- 18% increase in myocardial blood flow. Cardiac output and mean arterial pressure did not change significantly after WCBCP, although myocardial function (stroke work, left ventricular end-systolic pressure, end-diastolic pressure, contractility, and efficiency) was depressed (p < 0.05). End-diastolic pressure and contractility improved from early to late phase of recovery, whereas the other indicators of ventricular function remained depressed. CONCLUSIONS: Myocardial substrate oxidation was preserved after 3 hours of WCBCP, although ventricular function was moderately impaired. Thus, WCBCP with a seemingly normal substrate and oxygen supply was associated with a reduced cardiac efficiency.

Protein S-100beta: a biochemical marker for increased intracranial pressure in pigs with acute hepatic failure.

BACKGROUND: Acute hepatic failure (AHF) may cause encephalopathy. Intracranial pressure (ICP) is frequently monitored to guide therapy, but such monitoring may cause intracerebral haemorrhagic complications. We hypothesize that determination of serum levels of S-100beta, a protein synthesized in astroglial cells, will provide useful clinical information on the presence and extent of intracranial hypertension in AHF. METHODS: Continuous intraparenchymatous ICP monitoring and serial S-100beta measurements in serum were performed in 11 Norwegian Landrace pigs with surgically induced AHF and in 4 sham-operated controls. RESULTS: ICP increased hour by hour in the devascularized pigs in parallel with increased serum levels of protein S-100beta. In the sham-operated controls S-100beta was not detectable at any time point. CONCLUSIONS: Serum levels of S-100beta are increased early in experimental AHF. Determination of protein S-100beta may provide useful information on the presence and extent of intracranial hypertension in AHF.

Myocardial substrate metabolism influences left ventricular energetics in vivo.

The myocardial oxygen consumption (MVO(2)) to left ventricular pressure-volume area (PVA) relationship is assumed unaltered by substrates, despite varying phosphate-to-oxygen ratios and possible excess MVO(2) associated with fatty acid consumption. The validity of this assumption was tested in vivo. Left ventricular volumes and pressures were assessed with a combined conductance-pressure catheter in eight anesthetized pigs. MVO(2) was calculated from coronary flow and arterial-coronary sinus O(2) differences. Metabolism was altered by glucose-insulin-potassium (GIK) or Intralipid-heparin (IH) infusions in random order and monitored with [(14)C]glucose and [(3)H]oleate tracers. Profound shifts in glucose and fatty acid oxidation were observed. Contractility, coronary flow, and slope of the MVO(2)-PVA relationship were unchanged during GIK and IH infusions. MVO(2) at zero PVA (unloaded MVO(2)) was 0.16 +/- 0.13 J x beat(-1) x 100 g(-1) higher during IH compared with GIK infusion (P = 0.001), a 48% increase. The study demonstrates a marked energetic advantage of glucose oxidation in the myocardium, profoundly affecting the MVO(2)-PVA relationship. This may in part explain the "oxygen-wasting" effect of lipid-enhancing interventions such as adrenergic drugs and ischemia.

Oxygen-wasting effect of inotropy in the "virtual work model".

In the "virtual work model," left ventricular total mechanical energy (TME) is linearly related to myocardial oxygen consumption (MVO2). This relationship (MVO2-TME) is supposedly independent of inotropic stimulation, vascular loading, and heart rate variations. We reexamined the effect of inotropic stimulation (dopamine) on the metabolic to mechanical energy transfer in nine open-chest anesthetized pigs. Left ventricular mechanical energy was calculated using TME (mean ejection pressure x end-diastolic volume + stroke work), TMEW (end-diastolic volume reduced by unstressed ventricular volume), and the pressure-volume area (PVA). A highly linear relationship between MVO2 and mechanical energy was found for all three indexes during control and dopamine runs (r = 0.87-0.99). The slopes were unaltered by dopamine. y-Axis intercepts were (control vs. dopamine) as follows (in J. beat-1. 100 mg-1; means +/- SD): TME, 0.36 +/- 0.12 vs. 0.61 +/- 0.30 (P < 0.02); TMEW, 0.43 +/- 0.16 vs. 0.72 +/- 0.32 (P < 0.02); and PVA, 0.34 +/- 0.13 vs. 0.60 +/- 0.30 (P < 0.02). We conclude that the virtual work model is dependent on inotropic stimulation and that new insight into myocardial chemomechanical coupling is not added by this concept.