Social support has been associated with reduced mortality and morbidity from a number of causes. To assess possible mechanisms of action relating to cardiovascular (CV) responsiveness, 90 male and female university students delivered a five-minute speech on a controversial topic to a same-sex laboratory confederate. Subjects were randomly assigned to one of three conditions in which the confederate either (a) agreed with the subject, (b) remained impassive (neutral), or (c) disagreed with the subject. Blood pressure (SBP and DBP) and heart rate (HR.) were monitored throughout the experiment. Self-report measures of state self-esteem and affective state were taken pre- and post-task, and reactions to the task were assessed with post-task self-report measures. Subjects reported strong differences in supportiveness of the confederate in the three conditions. Self-report data indicated increase in arousal during the speech (a finding synchronous with CV data), and they reported the Disagree condition to be less pleasant than the Agree condition. CV data were analyzed as a 2 x 3 (sex by experimental condition) repeated measures ANOVA assessing changes from baseline to speech task. Sex differences on CV measures matched patterns generally reported: Men had higher SBP and lower HR than women. All CV measures increased significantly and substantially during the speech task. HR was higher in the Disagree and Neutral conditions than in the Agree condition. SBP and DBP did not differ by condition. There were no sex by condition interactions; however, there was a trend towards men’s HR increasing more in the neutral condition and women’ more in the disagree condition. These data partially support earlier findings in similar experiments while suggesting that subtleties of context, task selection, and content of supportive interaction may have significant impact on the degree to which social support attenuates CV response to social stressors. Unanswered questions for future research are delineated, and implications for designing and implementing interventions that enhance social support are discussed.

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Nesfatin-1 is an eighty two amino acid long peptide cleaved from the N-terminal of its precursor protein, nucleobindin-2 (NUCB2). In addition to its metabolic actions, nesfatin-1 is also involved in modulating cardiovascular functions in rodents. Intracereberoventricular injection of nesfatin-1 increased mean arterial pressure in rats. In rats, nesfatin-1 acts as a post-conditioning agent and elicits cardioprotection against ischemia-reperfusion injury. It also affects the contraction and relaxation of the heart in rats in a dose dependent manner. Nesfatin-1 is emerging as a regulator of cardiovascular functions in rodents. However, whether nesfatin-1 regulates the cardiovascular system of non-mammals remain unknown. We hypothesized that nesfatin-1 is a modulator of cardiovascular functions in zebrafish. Here we characterized endogenous nesfatin-1 in zebrafish heart, and its effects on zebrafish cardiovascular physiology. We found that zebrafish cardiomyocytes express NUCB2 mRNA and nesfatin-1-like immunoreactivity. While NUCB2 mRNA was lower in unfed fish at 1 hour post-regular feeding time compared to the fish at 0 hour time point, it was observed that chronic food deprivation did not alter NUCB2 mRNA expression in zebrafish heart. Ultrasound imaging of zebrafish heart at 15 minutes post-intraperitoneal injection of nesfatin-1 (50 ng/g, 250 ng/g and 500 ng/g body weight) showed a dose-dependent inhibition of end-diastolic volume, but not end-systolic volume, while a significant increase in end-diastolic volume was found at the lowest dosage. However, these combined effects did not alter the stroke volume. A dose dependent decrease in heart rate and cardiac output was observed in zebrafish that received nesfatin-1. Nesfatin-1 caused a significant increase in the expression of Atp2a2a mRNA encoding the calcium-handling pump, SERCA2a, while it has no effects on the expression of calcium handling protein RyR1b encoding mRNA. NUCB2 mRNA and NUCB2/nesfatin-1 like immunoreactivity was detected in the cytoplasm of mouse HL-1 cardiomyocytes. High glucose increased NUCB2 mRNA expression in HL-1 cells. Genes involved in apoptosis, including Akt1, Caspases 1, 2, 3, and TNF were upregulated in the presence of 10 nM nesfatin-1. We also observed that NUCB2 mRNA expression was significantly increased in C57BL/6 mice heart in the presence of high glucose, whereas in diet induced obese C57BL/6 mice, NUCB2 mRNA expression was not altered. Together, our data supports the hypothesis that nesfatin-1 is expressed in the cardiovascular system of mouse and fish, and that nesfatin-1 modulates cardiovascular physiology in zebrafish.

The metabolic syndrome (MS), consequent upon the pandemic of obesity and diabetes, is associated with an increased risk for cardiovascular (CV) disease. Development of sub-clinical cardiac structural and functional changes associated with CV disease risk factors may be detected on echocardiography. The extent to which these structural changes and CV risk factors are dependent on genetic factors is not clearly established. This project was designed to investigate the relationship between CV disease risk factors, cardiac structural and functional changes and underlying genetic abnormalities. Specifically, the risk factor profile and the presence of the MS were determined. This was then correlated with the echocardiographic findings and gene polymorphisms. Method: A randomly selected cohort of 1428 subjects from the Phoenix community was studied. Demographic data was collected using the WHO STEPS instrument. Blood samples for biochemistry and genetic analysis, together with anthropometric measurements, were collected. Blood pressure and echocardiography was performed on all subjects. The metabolic syndrome was classified according to the National Cholesterol Education Panel (NECP) Adult Treatment Panel III (ATP III) and International Diabetes Federation (IDF) criteria. The Lipoprotein Lipase and Human Paraoxonase-1 genes were genotyped on a Light Cycler 480 Real-Time PCR instrument, using allele-specific probes and sequencing. Results: There was a high prevalence of CV risk factors in this sample; particularly increased waist circumference (79%), obesity (64%) insulin resistance (58%) and hypertension (50%) across the age groups. This translated into a high prevalence of MS (38% using NCEP ATPIII and 46% using IDF criteria). There were significant echocardiographic differences between subjects with and without MS for chamber dimensions (p<0.001), left ventricular wall thickness (p<0.001) and mass (p<0.001), diastolic indices (E-wave {p<0.001}, trans-mitral ratio {p=0.017}) and sub-epicardial adipose tissue (SEAT) thickness (p<0.001). Stepwise multivariate analysis identified age (95% CI 0.975; 0.998), gender (95%CI 0.48; 0.9) and hypertension (95% CI 0.53; 0.99) as independent risk factors for diastolic abnormalities. Logistic regression identified age as the most significant contributor to diastolic abnormalities (OR=1.02; 95%CI 1.009; 1.03; Wald=13.4), followed by the waist circumference (OR=1.025; 95%CI 1.014; 1.037) and BMI (OR=1.075; 95% CI 1.035; 1.117). Genetic analysis showed significant associations between the heterozygous variant of Q192R genotype (PON-1 gene) and elevated HDL levels and also between this variant and obese women (p= <0.05). Conclusion: The high prevalence of CV risk factors and MS in this community has reached epidemic proportions. Although the MS was associated with significant remodelling of cardiac structure, alteration of diastolic indices and increased sub-epicardial adipose tissue thickness, BMI and waist circumference were stronger promoters of altered cardiac physiology. This augurs poorly for this population group unless intervention is introduced to address the markedly high prevalence of these culprit drivers. / Thesis (Ph.D.)-University of KwaZulu-Natal, Durban, 2013.

Typescript. / Bibliography: leaves 172-181. / x, 181 leaves ill

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Delayed control of haemorrhage or blood loss has been recognised as a major contributor to preventable trauma deaths, but early detection of internal bleeding is difficult due to unreliability of heart rate (HR) and blood pressure (BP) as markers of volume status. This thesis explores a novel method of early blood loss detection using a noninvasive finger photoplethysmographic (PPG) pulse oximetry waveform that is normally utilised in pulse oximeters for estimating arterial oxygen saturation. Graded head-up tilt (n = 13) and blood donation (n = 43) in human volunteers were selected as experimental models of mild to moderate blood loss. From the tilt study, a novel method for automatically detecting left ventricular ejection time (LVET) from the finger PPG waveform has been developed and verified by comparison with the LVET measured from aortic flow velocity. PPG waveform derived LVET (LVETp) and pulse transit time (PTT) were strongly correlated with aortic LVET and pre-ejection period respectively (median r = 0.954 and 0.964) and with the decrease in central blood volume indicated by the sine of the tilt angle (median r = -0.985 and 0.938), outperforming R-R interval (RRI) and BP in detecting mild central hypovolaemia. In the blood donation study, progressive blood loss was characterised by falling LVETp and rising PTT (p < 0.01). A new way of identifying haemorrhagic phases by monitoring changes and trends in LVETp, PTT and RRI has been proposed based on the results from the two studies. The utility of frequency spectrum analysis of PPG waveform variability (PPGV) in characterising blood loss has also been examined. A new technique of PPGV analysis by computing the coherence-weighted cross-spectrum has been proposed. It has been shown that the spectral measures of finger PPGV exhibited significant changes (p < 0.01) with blood donation and were mildly correlated with systemic vascular resistance in intensive care unit patients (r from 0.53 to 0.59, p < 0.0001), therefore may be useful for identification of different haemorrhagic phases. In conclusion, this thesis has established finger PPG waveform as a potentially useful noninvasive tool for early detection of blood loss.

Dissertation (PhD)--University of Stellenbosch, 2007. / Bibliography. Also available via the Internet.