Dependence of Intramyocardial Pressure and Coronary Flow on Ventricular Loading and Contractility: A Model Study

The phasic coronary arterial inflow during the normal cardiac cycle has been explained with simple (waterfall, intramyocardial pump) models, emphasizing the role of ventricular pressure. To explain changes in isovolumic and low afterload beats, these models were extended with the effect of three-dimensional wall stress, nonlinear characteristics of the coronary bed, and extravascular fluid exchange. With the associated increase in the number of model parameters, a detailed parameter sensitivity analysis has become difficult. Therefore we investigated the primary relations between ventricular pressure and volume, wall stress, intramyocardial pressure and coronary blood flow, with a mathematical model with a limited number of parameters. The model replicates several experimental observations: the phasic character of coronary inflow is virtually independent of maximum ventricular pressure, the amplitude of the coronary flow signal varies about proportionally with cardiac contractility, and intramyocardial pressure in the ventricular wall may exceed ventricular pressure. A parameter sensitivity analysis shows that the normalized amplitude of coronary inflow is mainly determined by contractility, reflected in ventricular pressure and, at low ventricular volumes, radial wall stress. Normalized flow amplitude is less sensitive to myocardial coronary compliance and resistance, and to the relation between active fiber stress, time, and sarcomere shortening velocity

Cannulation and continuous cross-sectional area measurement of small blood vessels

Techniques have been developed for the study of isolated small arteries. To pressurize and perfuse segments of these vessels, a cannula with a low resistance to flow was developed. This cannula consisted of two concentric micropipettes. The end of a vessel segment was sucked into the inner pipette and clamped by applying subatmospheric pressure on the outer pipette. Subsequently, the vessel was pressurized via the inner pipette. To enable perfusion, the segment was cannulated at both ends. Mean cross-sectional area (CSA) of the cannulated segments was continuously measured using a fluorescence technique. The emission of light by fluorescein isothiocyanate (FITC) labeled dextran in the vessel lumen was measured using a photomultiplier tube (PMT). PMT current was linearly related to the vessel CSA. Twenty-nine rat mesenteric vessels with inside diameters ranging from 110 to 350 microns (mean 226 microns) when maximally dilated at 80 mm Hg were cannulated. CSA was monitored during variations in perfusion pressure and addition of vasoactive agent

Influence of pressure alterations on tone and vasomotion of isolated mesenteric small arteries of the rat.

1. Myogenic responses may account for control of organ blood flow. The study of these responses without interference from the organ requires an isolation technique for vessels which contribute significantly to flow resistance. This study reports on experiments on isolated small mesenteric arteries. 2. Distal rat mesenteric arcade arteries and first-order branches (diameter range 145-365 microns, mean 293 microns) were manually dissected and cannulated using a double-barrelled micro-cannula. Luminal cross-sectional area of these vessels was continuously monitored by means of a fluorescence technique. 3. Nine out of eighteen vessels developed basal tone at 80 mmHg distending pressure, resulting in a 45.2 +/- 5.1% (mean +/- S.E.M) decrease of cross-sectional area. Tone was induced in the other vessels by 0.3-1 microM-noradrenaline, resulting in a 59.5 +/- 7.1% decrease in cross-sectional area. 4. In vessels with either spontaneous or induced tone, stepwise changes of pressure resulted in passive effects, followed by myogenic responses. 5. Steady-state pressure-cross-sectional area relations of vessels with basal tone showed a significant negative slope (-0.5% mmHg-1), while pressure-cross-sectional area relations of vessels with induced tone were essentially flat between 40 and 120 mmHg. 6. Five vessels with basal tone and eight vessels with induced tone developed vasomotion at 80 mmHg. Frequencies of spontaneous and induced vasomotion were 14 (range 4-31) and 21 (9-25) cycles min-1 respectively. Amplitudes were 5 (1-10) and 8 (3-17)% of the passive cross-sectional area. In both groups, frequency was positively, and amplitude negatively correlated with pressure. 7. These data show that myogenic responses are induced by wall stress, rather than by distension of the vascular wall. Basal tone is not a prerequisite for the appearance of myogenic responses

Heterogeneous NADH fluorescence during post-anoxic reactive hyperemia in saline perfused rat heart

In the present study epicardial NADH fluorescence photographs were taken of rat hearts during dynamic transitions of oxygen content of the myocardium. Hearts were perfused in a Langendorff set-up where it was possible to switch between low and high-pO2 perfusates. NADH fluorescence photographs were taken with a suitable fluorescence set-up and photo negatives digitized and analyzed by use of a computer. Restoration of perfusion with a high-pO2 solution resulted in a reactive hyperemic flow being established. Prior to the occlusion being lifted high NADH fluorescence was observed. Reactive hyperemic flow was associated with heterogenic NADH fluorescence patterns which diminished as control flow was restored. The patterns observed during reactive hyperemia were identical to those observed when tissue oxygen was restored by high-pO2 perfusion following high flow hypoxia achieved by low-pO2 perfusion. This study shows that heterogenic epicardial flow patterns are associated with reactive hyperemi

Influence of comorbid heart disease on dyspnea and health status in patients with COPD – a cohort study

Maaike Giezeman,1,2 Mikael Hasselgren,1 Karin Lisspers,3 Björn Ställberg,3 Scott Montgomery,4–6 Christer Janson,7 Josefin Sundh8 1School of Medical Sciences, Örebro University, Örebro, Sweden; 2Centre for Clinical Research, County Council of Värmland, Karlstad, Sweden; 3Department of Public Health and Caring Sciences, Family Medicine and Preventive Medicine, Uppsala University, Uppsala, Sweden; 4Clinical Epidemiology and Biostatistics, Örebro University, Örebro, Sweden; 5Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden; 6Department of Epidemiology and Public Health, University College, London, UK; 7Department of Medical Sciences, Respiratory, Allergy and Sleep Research, Uppsala University, Uppsala, Sweden; 8Department of Respiratory Medicine, School of Medical Sciences, Örebro University, Örebro, Sweden Purpose: The aim of this study was to examine the changing influence over time of comorbid heart disease on symptoms and health status in patients with COPD. Patients and methods: This is a prospective cohort study of 495 COPD patients with a baseline in 2005 and follow-up in 2012. The study population was divided into three groups: patients without heart disease (no-HD), those diagnosed with heart disease during the study period (new-HD) and those with heart disease at baseline (HD). Symptoms were measured using the mMRC. Health status was measured using the Clinical COPD Questionnaire (CCQ) and the COPD Assessment Test (CAT; only available in 2012). Logistic regression with mMRC ≥2 and linear regression with CCQ and CAT scores in 2012 as dependent variables were performed unadjusted, adjusted for potential confounders, and additionally adjusted for baseline mMRC, respectively, CCQ scores. Results: Mean mMRC worsened from 2005 to 2012 as follows: for the no-HD group from 1.8 (±1.3) to 2.0 (±1.4), (P=0.003), for new-HD from 2.2 (±1.3) to 2.4 (±1.4), (P=0.16), and for HD from 2.2 (±1.3) to 2.5 (±1.4), (P=0.03). In logistic regression adjusted for potential confounding factors, HD (OR 1.71; 95% CI: 1.03–2.86) was associated with mMRC ≥2. Health status worsened from mean CCQ as follows: for no-HD from 1.9 (±1.2) to 2.1 (±1.3) with (P=0.01), for new-HD from 2.3 (±1.5) to 2.6 (±1.6) with (P=0.07), and for HD from 2.4 (±1.1) to 2.5 (±1.2) with (P=0.57). In linear regression adjusted for potential confounders, HD (regression coefficient 0.12; 95% CI: 0.04–5.91) and new-HD (0.15; 0.89–5.92) were associated with higher CAT scores. In CCQ functional state domain, new-HD (0.14; 0.18–1.16) and HD (0.12; 0.04–0.92) were associated with higher scores. After additional correction for baseline mMRC and CCQ, no statistically significant associations were found. Conclusion: Heart disease contributes to lower health status and higher symptom burden in COPD but does not accelerate the worsening over time. Keywords: COPD Assessment Test, CAT, Clinical COPD Questionnaire, CCQ, modified Medical Research Council dyspnea score, mMRC, ischemic heart disease, heart failur

Interrater reliability of diagnosing complex regional pain syndrome type I

Background: Diagnosis of complex regional pain syndrome type I (CRPS I) is based on clinical observation of symptoms. As little information is available on the reliability of CRPS I diagnosis, we evaluated the agreement between therapists with regard to the presence and severity of CRPS I and its symptoms. Methods: The interrater reliability was evaluated in 37 presumed CRPS I patients by three observers; one consultant anesthesiologist and two resident anesthesiologists. Patients were assessed on the basis of Veldman's CRPS criteria. Results: The interrater reliability for diagnosing CRPS I was good for the majority of observer combinations. The percentage of agreement for the absence or presence of CRPS I was good (88%-100%). Cohen's Kappa's ranged from 0.60 to 0.86. The agreement for the mean symptom score ranged from 70.2% to 88.6%; Kappa's were lower and showed more variation. Interrater reliability for assessment of the severity of CRPS I and its symptoms was poor. Factors influencing the interrater reliability were symptom type, individual observers and sample population. Conclusion: Diagnosing CRPS I can be performed on the basis of clinical observation. Further assessment of severity of CRPS I and its symptoms should be performed with reliable and valid measurement instruments