The purpose of this study was to investigate a resuscitation algorithm that calculates the value of AMSA in real-time to direct the duration of post-shock chest compressions. We hypothesized that such an algorithm would shorten the time to achieve ROSC in swine. Swine were randomized into normal or infarcted myocardia and waveform guided or traditional resuscitation algorithm groups. VF was induced electrically and left untreated for 10minutes. Resuscitation was commenced with 1minute of compressions, resumption of mechanical ventilation, shock and epinephrine. In the traditional group, all shocks were followed by 2minutes of post-shock compressions. In the waveform guided group, AMSA was measured prior to shocks. If AMSA>20mV-Hz, post shock compression duration was shortened to 1minute.This study found that the waveform guided resuscitation algorithm to direct the duration of post-shock chest compressions had no significant effect on time to ROSC or AMSA values when compared to the traditional resuscitation algorithm.

No description available.

Background: Elevated blood glucose in patients undergoing cardiac surgery pose increased risks of sternal incision infections, kidney disease, irregular heartbeats, extended hospital stays, and death. Elevated blood glucose also increases the costs of healthcare from prolonged lengths of stay and increased complications. The Surgical Care Improvement Project (SCIP) #4 performance measure is used to evaluate achievement of a target blood glucose control < 200 milligram/deciliter (mg/dl) post cardiac surgery on postoperative days 1 and 2. In the institution where this study was carried out, blood sugar control in the cardiac surgery patient has presented a challenge. Purpose: The purpose of this practice inquiry was to identify patient characteristics and outcomes in cardiac surgery patients who met the SCIP #4 performance measure versus those patients who did not. Methods: A retrospective nested case-control design was used. Risk factors for postoperative hyperglycemia and in-hospital outcomes were compared between cardiac surgery patients who were SCIP #4 met defined as 6AM BG ≤ 200 mg/dl on postoperative days 1 and 2 and those that were SCIP #4 not met, defined as 6AM BG > 200 mg/dl on postoperative days 1 or 2. Results: Results from this study showed that preoperative hemoglobin AIC and history of diabetes were two major contributors for SCIP #4 not-met status. There was a trend towards a longer length of stay in the SCIP #4 not met group as compared to the met group (9.01 ± 7.33 versus 7.30 ± 4.93 days, respectively; p = . 096). Mortality was 3 times more prevalent in the SCIP #4 not met than the met group (6.2% versus 2.1%, respectively); however, this different did not reach statistical significance (p = .129). Renal failure was four-fold more frequent in patients who were SCIP #4 not-met than who were SCIP #4 met (13.6% vs. 4.1%, respectively; p = 0.003). Conclusions: Results from this study showed that SCIP #4 not met is associated with development of postoperative renal failure in the hospital and a trend towards longer length of stay. History of diabetes and preoperative hemoglobin AIC level should be taken into consideration when evaluating strategies for managing hyperglycemia. Future research is needed to study the relationship between SCIP #4 met status and long-term outcomes. The use of preoperative hemoglobin A1C to identify patients at high risk for uncontrolled postoperative glucose and plan effective glucose control should be studied. Such study may include implementing intravenous insulin on all patients with diabetes and elevated hemoglobin A1C levels and comparing the short and long term outcomes.

No description available.

Scorpion toxins specific for Na+ and K+ channels, have been studied extensively but relatively little has been done on Ca2+ channel toxins. Toxins in the venom of only two South African scorpions P. transvaalicus and P. granulatus have been found to interact with Ca2+ channels. Kurtoxin isolated from the venom of P. transvaalicus inhibits the T and L-type neuronal Ca2+ channels, whereas KLI and KLII (Kurtoxin-like peptide I and II), isolated from P. granulatus, inhibits T-type Ca2+ channel activity in mouse male germ cells. In this study the effects of fractions isolated from the venom of P. granularus on Cca2+ channels in rat ventricular myocytes were investigated by means of the whole-cell patch clamp technique. Fractions of P. granulatus crude venom were isolated with Sephadex G50 columns (fraction I-IV). Fraction III (PgIII) showed a voltage dependent increase of the inward Ca2+ current and influenced the channel kinetics by shifting the voltage dependence of activation towards more hyperpolarizing membrane potentials and decreased the rate of inactivation and deactivation. The time of the current to reach peak was also delayed. PgIII was further separated by HPLC in an attempt to identify the subfraction/s responsible for the agonistic effect. Subfraction I had an agonistic effect similar to PgIII, whereas subfraction II and III, decreased the Ca2+ current. The observed agonistic effect has not been described in the literature. The identification of new peptide structures with unique functions are important in the field of toxin research. Peptides that target Ca2+ channels can be valuable tools to characterize Ca2+ channels. Ca2+ channels in the heart are implicated in a number of pathological disorders like angina, ischemia, some arrhythmias and hypertension. / Thesis (M.Sc. (Physiology))--North-West University, Potchefstroom Campus, 2005.

Left ventricular (LV) filling increases during exercise, but left atrial (LA) phasic function and its contribution to LV filling is poorly understood. Sixteen endurance-trained middle-aged males were studied at rest and during light (LE) and moderate (ME) intensity cycle-ergometry. Atrioventricular-plane displacement (AVPD) increased from rest to LE (from 14±2 mm to 18±2 mm, p<0.01), but did not increase further at ME. LA reservoir volume increased from rest to LE (from 32±8 mL to 40±10 mL, p<0.01). LA passive contribution increased at LE (from 21±5 mL to 27±8 mL, p<0.01), while LA active contribution increased from rest only at ME (from 12±5 mL to 23±9 mL, p<0.01). AVPD, and thus the longitudinal shortening of LV systole, contributes to LA filling primarily during LE, but is a limited mechanism beyond LE. These data suggest that LV filling appears to shift to a reliance on conduit function to increase LV filling at ME.

Recent research indicates the need for a functional balance assessment in cardiac rehabilitation (CR) programs. One assessment technique that may be appropriate is the Community Balance and Mobility Scale (CBMS). The purpose of this study was to investigate psychometric properties of the CBMS when testing patients with cardiovascular disease (CVD). Thirty-one participants from community CR programs were recruited to perform the CBMS and measures of computerized dynamic posturography. Convergent validities between the measures were investigated using correlation coefficients, and floor and ceiling effects of the CBMS were analysed. The results indicated that the CBMS was moderately correlated with all computerized posturography variables, with no floor or ceiling effects present. Analysis of posturography results indicated that CR patients have decreased movement characteristics in the anterior and posterior directions. These findings indicate that the CBMS is a suitable tool to assess and monitor balance in a CR population.

Objective: Heme oxygenase-1 (HO-1) has been well established as a cytoprotective molecule, and has been shown to exert cardioprotective effects in both hypertension and cardiac hypertrophy. However, the precise mechanism of the cardioprotective effect of HO-1 has yet to be fully elucidated. The natriuretic peptide system (NPS) is also a key player in cardiovascular homeostasis and tissue dynamics, and has also been shown to be cardioprotective in a variety of pathologic conditions. This study examined the effect of high dietary salt treatment in genetic models of HO-1, and assessed the expression of the NPS in the left ventricle (LV), in order to gain insight into the relationship between varying levels of HO-1 expression with the development of cardiac hypertrophy and the expression of the NPS. Methods: Age-matched 12-week old male HO-1 knockout (HO-1-/-) and HO-1 cardiomyocyte-specific transgenic overexpressing (HO-1Tg) mice were treated with either normal salt (NS; 0.8%) or high salt (HS; 8.0%) chow for 5 weeks. LV mRNA expression was determined using quantitative real-time RT-PCR. Results: HO-1-/- mice fed HS diet had significantly higher left ventricle-to-body weight ratio (LV/BW) compared to HO-1+/+ mice fed NS diet. HO-1-/- mice had significantly reduced expression of the NPS compared to controls, and these mice did not exhibit a salt-induced increase in ANP expression. HS treatment had no effect on LV/BW in HO-1Tg mice compared to controls. HO-1Tg mice had significantly higher ANP and BNP expression compared to controls. Conclusions: The presence of HO-1 is required for normal salt-induced changes in the local cardiac NPS. HO-1 ablation resulted in significantly lower mRNA expression of the NPS, whereas HO-1 overexpression resulted in higher mRNA expression of the NPS. These data indicate that the detrimental effect of reduced HO-1 expression and the cardioprotective effect of increased HO-1 expression may be due, in part, to altered expression of the NPS. / Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2009-10-20 09:15:20.541

The natriuretic peptide system (NPS) is a hormonal system critical to mammalian cardiovascular homeostasis. The purpose of the present study was to investigate the role of ANP during early postnatal cardiac development by i) monitoring the development of cardiac hypertrophy during early postnatal development of the ANP-/- mice, and ii) comparing morphologic, morphometric and molecular differences in ANP+/+ mice compared to ANP-/- mice during this developmental period. Age matched male ANP+/+ and ANP-/- mice, aged day 1 and weeks 1 to 5, were evaluated. Body weight, organ weights and hematocrit were recorded. RNA was isolated and quantitative real-time RT-PCR was used to monitor cardiac gene expression. An additional cohort of animals was used for morphologic and morphometric analysis. Heart weight to body weight ratio (HW/BW) was dramatically higher in ANP-/- animals at all time points, indicating cardiac hypertrophy is established before the advent of adult blood pressure. Molecular analysis of gene expression revealed a compensatory response of the NPS in the ANP-/- mice. Specifically an up-regulation of BNP expression in ANP-/- mice was noted throughout postnatal development. Similarly, NPR-A and NPR-C demonstrated compensatory action for the lack of ANP, as expressional levels also varied throughout development. Morphological analysis of cardiac vasculature revealed striking structural differences between ANP+/+ and ANP-/- mice. Quantitative stereological analysis of LM images indicated a greater vessel volume in ANP-/- compared to ANP+/+ mice. This study demonstrates that alterations in early molecular events, such as changes in NPS expression, may be responsible for the maintenance and progression of cardiac hypertrophy during early postnatal development in the ANP-/- mice. The absence of ANP during this critical period of development has a profound impact on final cardiac structure leading to future pathological states. / Thesis (Master, Anatomy & Cell Biology) -- Queen's University, 2010-02-05 14:15:33.982

Introduction: Developmental origins of disease refers to the theory that adverse maternal environments influence fetal development and the risk of cardiovascular disease (CVD) in adulthood. To test the hypothesis that gestational hypertension influences the development of CVD in offspring, a novel experimental paradigm was developed using atrial natriuretic peptide gene disrupted mice (ANP-/-). The objective of this thesis was to determine the effect of gestational hypertension on cardio-renal function in offspring. Methods: ANP+/+ females were crossed with ANP-/- males (yielding ANP+/-WT offspring) and ANP-/- females with ANP+/+ males (yielding ANP+/-KO offspring). Previous work has established that ANP-/- dams are hypertensive during pregnancy. Offspring gene expression was measured using qPCR. Offspring arterial blood pressure (BP) was measured with a non-invasive tail cuff system. Offspring left ventricular (LV) function was examined using echocardiography (ECHO). Offspring were treated with normal salt (NS) or high salt (HS) chow for five weeks to assess salt-sensitivity. Daily injections of isoproterenol (ISO) were used to induce cardiac stress in offspring. Collagen deposition was assessed using Masson’s trichrome and picrosirius red staining. Results: Absence of maternal ANP had no effect on either litter size or offspring growth, but caused significant LV hypertrophy in offspring, with no change in LV function. Treatment with ISO resulted in myocardial fibrosis and significant LV diastolic dysfunction with a restrictive filling pattern (increased E/A ratio and E/e’) only in ANP+/-KO offspring. Furthermore, absence of maternal ANP was associated with salt-resistant BP in offspring. Conclusions: Gestational hypertension using the ANP-/- mouse model results in a salt-resistant phenotype in offspring, as well as significant cardiac hypertrophy and an adverse response to activation of the sympathetic nervous system in adult offspring. These data suggest that adverse maternal environments may increase the risk of cardiovascular disease in offspring later in life. / Thesis (Ph.D, Anatomy & Cell Biology) -- Queen's University, 2012-09-18 16:12:01.147