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Biomedical subjects

M R Pinsky

Publications and source records attributed to M R Pinsky.

At least 91 records · Page 5Linked to original sources
PubMed1996

Dynamic right and left ventricular interactions in the rabbit: simultaneous measurement of ventricular pressure-volume loops.

PURPOSE: This study was performed to characterize the dynamic factors determining ventricular interdependence in an open-pericardium intact animal model. MATERIALS AND METHODS: Simultaneous measures of right ventricular (RV) and left ventricular (LV) pressures and volumes in 6 urethane-anesthetized open-chested, open-pericardium rabbits. RV and LV V were calculated every 2 milliseconds. Measurements were made at initial baseline blood volume, and again after two infusions of 20 mL/kg isoconductive colloid solution. At each blood volume level, partial aortic (AO), pulmonary artery (PAO), and inferior vena caval (IVC) occlusions were performed. Biventricular diastolic compliance and end-systolic elastance were calculated from these data. RESULTS: Baseline end-diastolic (ED) and end-systolic (ES) V were 3.29 +/- 0.55 and 2.43 +/- 0.33 mL (mean +/- SD) for the LV, and 3.38 +/- 1.56 and 2.84 +/- 1.36 mL for the RV, respectively. AO increased all LV pressure and volume (P < .05) but did not alter RV ED volume (2.85 +/- 1.20 mL) or ED pressure (3.3 +/- 2.0 to 3.6 +/- 2.1 mm Hg). PAO increased RV ES pressure (P < .05) but did not alter RV ED volume, ED pressure, or ES volume, although it decreased LV ED volume (2.82 +/- 0.59, P < .05). AO also immediately increased end-systolic RV elastance to a value greater than that defined by IVC (7.9 +/- 4.4 to 10.9 +/- 6.6 mm Hg/mL, P < .05). Intravascular volume expansion though increasing baseline pressure and volume, did not alter qualitatively biventricular responses to AO, PA, or IVC. CONCLUSION: Ventricular interdependence has both systolic and diastolic components that have differing directional effects. In the pericardectomized rabbit, increases in RV ED volume decrease LV ED volume by decreasing LV diastolic compliance, but do not alter LV systolic function. Whereas, increases in LV ED volume decrease RV ES volume resulting in an increase in RV maximal elastance, but minimally alter RV diastolic function.

Animals↗
PubMed1996

Organ-specific therapy in critical illness: interfacing molecular mechanisms with physiological interventions.

Sepsis and SIRS is the outward manifestation of a generalized uncontrolled inflammatory response, which, if sustained, induces widespread endothelial damage and MODS. Immunomodulating therapies, at present, have proven ineffective in reducing morbidity and mortality, presumably because of the heterogeneous nature of sepsis and septic shock and the reciprocating and redundant nature of this inflammatory cascade. Organ-specific therapies can support life but impair both organ-specific function and remote organ function. Novel therapies aimed at minimizing further organ dysfunction may improve outcome in a cost-effective fashion by preventing both further primary organ dysfunction or remote organ dysfunction secondary to the subsequent activation of the inflammatory response.

Animals↗
PubMed1996

Increases in peripheral oxygen demand affect blood flow distribution in hemorrhaged dogs.

Blood flow redistribution away from the gastrointestinal tract and kidney occurs during progressive hemorrhage and stress. However, the effects of remote increases in oxygen demand on a circulation with limited ability to respond have not been described. Thus, we observed the effect of remote increases in oxygen demand on splanchnic and renal blood flow in hemorrhaged dogs. Nine alpha-chloralose-anesthetized, splenectomized dogs were subjected to hemorrhage of 10 ml/kg followed by an additional 5 ml/kg. At each of these two stages, bilateral femoral nerve stimulation was used to increase lower extremity oxygen demand while lower extremity, splanchnic, renal blood flows and arteriovenous oxygen content differences were monitored. Hemorrhage was associated with redistribution of blood flow away from the lower extremities and kidneys and increasing the oxygen extraction ratio of the splanchnic bed. Lower extremity stimulation increased whole-body oxygen consumption (7.3 +/- 2.7 to 11.4 +/- 4.5 ml O2/min/kg, p < 0.01). If arterial pressure remained stable during stimulation (> 90% of baseline value, n = 9), visceral organ blood flow did not change. However, when blood pressure decreased (< 70% of baseline, n = 8), splanchnic (226.3 +/- 143.5 to 140.9 +/- 126.4 ml/min, p < 0.01) and renal (59.6 +/- 30.2 to 28.5 +/- 26.0 ml/min, p < 0.01) blood flow also decreased. Thus, in the anesthetized, hemorrhaged dog, increased peripheral oxygen demand results in further redistribution of blood flow away from the gastrointestinal tract and kidneys only when there is a concurrent decrease in blood pressure.

Animals↗
PubMed1996

Transvisceral lactate fluxes during early endotoxemia.

The pathogenesis of hyperlacticemia during sepsis is poorly understood. We investigated the role of lung, kidney, gut, liver, and muscle in endogenous lactate uptake and release during early endotoxemia in an intact, pentobarbital-anesthetized dog model (n = 14). Ultrasonic flow probes were placed around the portal vein and hepatic, renal, and femoral arteries. After splenectomy, catheters were inserted into the pulmonary artery, aorta, and hepatic, left renal, and femoral veins. Whole blood lactate and blood gases from all catheters, organ flows, and cardiac output were measured before and 30 to 45 min after a bolus infusion of Eacherichia coli endotoxin (1 mg/kg). After endotoxin infusion, mean arterial blood lactate level increased from 0.92 +/- 0.11 to 1.60 +/- 0.15 mmol/L (p < 0.0001). Lung lactate flux changed from uptake to release of lactate adding a mean of 9.97 +/- 16.23 mmol/h (p < 0.05) to the systemic circulation. Liver and muscle lactate fluxes remained neutral at all times, while kidney and gut took up lactate from the circulation both before and after endotoxin infusion (mean renal uptake, 2.73 +/- 3.85 mmol/L; p < 0.001; mean gut uptake, 2.46 +/- 2.31 mmol/h; p < 0.002). Except for the kidney, where a decrease in blood flow correlated with diminished uptake, there was no correlation between changes in transvisceral lactate fluxes and organ or systemic oxygen delivery during endotoxemia. A positive correlation between lactate uptake and oxygen consumption during endotoxemia was seen for both gut (p < 0.0001) and kidney (p < 0.002). We conclude that, in the dog, the pathogenesis of endotoxin-induced hyperlacticemia is complex. The lung may be responsible for significant lactate release, and other viscera that normally take up lactate are unable to adequately clear this increased lactate.

Animals↗
PubMed1995

Changes in electrocardiographic morphology reflect instantaneous changes in left ventricular volume and output in cardiac surgery patients.

We examined the relation between changes in R-to-T wave amplitude ratios (R:T) and left ventricular (LV) performance as cardiac output was rapidly varied by inferior vena caval occlusion in 6 subjects prior to cardiopulmonary bypass. To assess the influence of contractility, paired studies before and after bypass were performed in 4 subjects. Stroke volume and cardiac output were assessed by aortic flow probe, and transesophageal echocardiographic LV area measures using the automated border-detection method were used to give LV stroke area, stroke force, maximal LV area, fractional area change, end-systolic elastance, and preload recruitable stroke force. Data were collected on computer and analyzed by linear regression. Significant changes in R:T and measured LV variables during the inferior vena caval occlusion were stroke volume (r = 0.81), LV stroke area (r = 0.77), LV stroke force (r = 0.81), maximal LV area (r = 0.78), and cardiac output (r = 0.80). However, R:T varied inconsistently in relation to fractional area change. After cardiopulmonary bypass, the linear relation between R:T with LV stroke force, LV stroke volume, and maximal LV area persisted, but at a lesser slope. Although absolute pre-inferior vena caval occlusion R:T did not correlate with end-systolic elastance or preload recruitable stroke force, the change in the slope of these linear relations correlated well with the change in end-systolic elastance after surgery (r = 0.92). Instantaneous changes in electrocardiographic morphology reflect changes in LV preload-dependent variables, whereas long-term changes in electrocardiographic morphology may also reflect changes in contractile state.

Aged↗
PubMed1995

Leukocyte activation in the peripheral blood of patients with cirrhosis of the liver and SIRS. Correlation with serum interleukin-6 levels and organ dysfunction.

OBJECTIVE: Leukocyte adhesion plays an important role in inflammation. Adhesion molecules such as CD11b on polymorphonuclear neutrophil leukocytes (PMNs) up-regulate in response to tumor necrosis factor-alpha, interleukin-8 (IL-8), and other mediators that are involved in systemic inflammatory response syndrome (SIRS). This study examined the behavior of CD11b and other membrane molecules in SIRS in relation to serum cytokines and the severity of illness. DESIGN: Survey study. SETTING: Liver transplantation intensive care unit at a tertiary care center. PATIENTS: A consecutive sample of 22 patients admitted to the liver transplantation intensive care unit for complications related to cirrhosis of the liver in the absence of other disease. Sixteen of the patients developed SIRS and multiple organ dysfunction syndrome with suspected bacterial infections. Seven control subjects were also studied. MAIN OUTCOME MEASURES: Modified Goris organ failure score and Acute Physiology and Chronic Health Evaluation II score. RESULTS: Mean serum IL-6 levels, but not IL-1 beta or tumor necrosis factor-alpha levels, correlated with organ failure (r = 0.79, P < .001). Leukocyte cell-surface markers fluctuated from day to day. The mean of several values was more stable. Mean CD11b and CD35 on PMNs correlated with serum IL-6 level (r = 0.75, P < .001, and r = 0.77, P < .005, respectively). Up-regulation of both CD11b and CD35 display on PMNs correlated with organ failure (r = 0.74, P < .001, and r = 0.71, P < .01, respectively). Polymorphonuclear neutrophil leukocyte L-selectin, CD31, and CD16 were simultaneously decreased, consistent with PMN activation. Monocytes appeared to be activated, but the pattern of surface molecule display was different. CONCLUSIONS: In human SIRS, the circulating monocyte and PMN pools undergo alterations suggestive of leukocyte activation, including up-regulation of PMN CD11b in correlation with the serum IL-6 level and severity of organ dysfunction.

Adult↗
PubMed1995

Strong ion gap: a methodology for exploring unexplained anions.

PURPOSE: This paper describes the calculation of the strong ion gap (SIG), a physical chemical methodology similar to the anion gap (AG), as a measure of the anion/cation balance exclusive of sodium, potassium, chloride, and bicarbonate. We compared the SIG and AG methodologies in three groups of subjects with and without unexplained anions. These groups were (1) healthy volunteers with hyperlacticemia during exercise; (2) intensive care unit (ICU) patients with sepsis; and (3) ICU patients with severe liver disease. METHODS: The SIG, AG, and corrected AG (AGc) were calculated for each group from data available in the original reports (groups 1 and 2) and by retrospective chart review (group 3). RESULTS: The SIG correlated poorly with the AG in group 2, whereas no correlation was seen in groups 1 and 3. The AGc correlated with SIG in all three groups (r = .99, .93, and .91 respectively; P < .01 for each group). Although the AG was similar, the SIG differed for each group. Group 1 had levels of SIG near zero, and groups 2 and 3 had mean SIG's of 4.80 +/- 4.67 mEq/L and 9.60 +/- 6.43 mEq/L respectively. The composition of the anion gap differed markedly among subject types. CONCLUSIONS: The SIG correlates with the AG once corrected for all known anions. The SIG technique can detect unknown anions in a patient population known to have them and does not detect unknown anions in healthy volunteers during exercise. This test detects large amounts of unknown anions in some patients with sepsis or liver disease. Therefore, the test is both sensitive and specific in characterizing metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1995

Hepatic anion flux during acute endotoxemia.

We sought to determine the role the liver might play in the regulation of anion-cation balance during both stable baseline conditions and acute endotoxemia. Ten pentobarbital sodium-anesthetized dogs were instrumented at laparotomy with ultrasonic flow probes around the left renal artery, portal vein, and hepatic artery, and catheters were inserted into the hepatic vein, portal vein, pulmonary artery, left renal vein, and abdominal aorta. Measurements were obtained from each site at baseline and 30-45 min after the intravenous infusion of endotoxin. The total anion flux across the liver was calculated from the strong-ion difference. At baseline, the liver removed anions from the circulation (-0.34 meq/min). With early endotoxemia, however, the liver switched to the release of anions (0.12 meq/min; P = 0.0046). After endotoxin administration, the gut, which was neutral at baseline, began to take up anions (-0.47 meq/min; P = 0.008). Anion flux across the lung and kidney was unchanged. We conclude that in the dog the liver, which removes anions at baseline, switches to release anions during early endotoxemia and may be a major site of acid production in early sepsis.

Acid-Base Equilibrium↗
PubMed1995

Cardiopulmonary effects of positive pressure ventilation during acute lung injury.

STUDY OBJECTIVES: To assess the gas exchange and hemodynamic effects of pressure-limited ventilation (PLV) strategies in acute lung injury (ALI). We hypothesized that in ALI, the reduction of plateau airway pressure (Paw) would be associated with less alveolar overdistention and thus have better hemodynamic and gas exchange characteristics than larger tidal volume (Vr) ventilation. SETTING: Laboratory. DESIGN: Prospective time-controlled sequential animal study. MEASUREMENTS: Right atrial, pulmonary artery, left atrial, arterial, lateral pleural (Ppl), and pericardial (Ppc) pressures, Paw, ventricular stroke volume, mean expired CO2, and arterial and mixed venous oxygen contents. Airway resistance and static lung compliance were also measured. INTERVENTIONS: Intermittent positive pressure ventilation (IPPV) given before (control) and after induction of ALI by oleic acid infusion (0.1 mL/kg). IPPV at FIO2 of 1, VT of 12 mL/kg, and frequency adjusted to maintain normocarbia. ALI PLV was given during ALI and defined as that VT which gave a similar plateau Paw to that of control IPPV. High-frequency jet ventilation (HFJV) and ALI HFJV were also given and defined as frequency within 10% of heart rate and mean Paw similar to that during control IPPV. RESULTS: After ALI, static lung compliance, PaO2, and pH decreased, whereas airway resistance and PaCO2 increased. For a constant lung volume, Ppl and Ppc were not different between control and ALI. Both absolute dead space (VD) and intrapulmonary shunt fraction increased after ALI, but absolute VD was lower with ALI PLV and ALI HFJV when compared with ALI IPPV. Ventilation did not alter hemodynamics during ALI. CONCLUSIONS: Changes in lung volume determine Ppc and Ppl. PLV strategies do not alter hemodynamics but result in less of an increase in VD/VT than would be predicted from the obligatory decrease in VT.

Animals↗
PubMed1994

A system for the on-line acquisition, visualization, and analysis of pressure-area loops.

Transesophageal echocardiography is a widely accepted technique for the assessment of left ventricular (LV) function in the operating room, intensive care unit, and cardiac catheterization suite. Not only do the images generated by these systems provide the observer with dynamic views of currently ongoing cardiac mechanics, but the computed LV area values obtained by the automated border detection system can be converted to an analog signal and then used to generate pressure-area loops if LV pressure is measured simultaneously. The intraventricular area has been shown to correlate closely with intraventricular volume and to vary proportionately. Therefore, it can be substituted for volume to generate pressure-area loops that display equivalent behavior to external perturbations as pressure-volume loops. Visualization of these waveforms and the values extracted from them, along with the associated hemodynamic values, provide valuable insight into ventricular function and heart-lung interactions. This paper describes a system that was designed and developed to acquire, display, store, and analyze pressure-area loops in addition to other associated hemodynamic signals of interest.

Computer Systems↗
PubMed1994

Assessment of left ventricular performance by on-line pressure-area relations using echocardiographic automated border detection.

OBJECTIVES: The purpose of this study was to evaluate left ventricular performance by on-line pressure-area relations using echocardiographic automated border detection in the in situ canine heart in a manner similar to pressure-volume analyses. BACKGROUND: Echocardiographic automated border detection can measure ventricular cavity area as an index of volume and may be interfaced with pressure to construct pressure-area loops on-line. METHODS: Eight anesthetized open chest dogs had simultaneous measurement of ventricular pressure, aortic flow and midventricular short-axis area. Pressure-area loops were constructed by a computer workstation interfaced with the ultrasound system. Stroke area (Maximal area--Minimal area) and stroke force (integral of P dA [P = pressure; A = area]) values during inferior vena cava (n = 8) and aortic (n = 4) occlusions were compared with stroke volume and estimates of stroke work, respectively. Inotropic modulation was induced with dobutamine infusion (2 to 5 micrograms/kg body weight per min), followed by propranolol infusion (2 to 5 mg). End-systolic and maximal elastance and preload recruitable stroke force (stroke force versus end-diastolic area) were derived for each period. RESULTS: Changes in stroke area and stroke force were significantly correlated with changes in stroke volume and estimates of stroke work during caval occlusion (n = 8) (r = 0.87 +/- 0.02, SEE = 8 +/- 1% and r = 0.90 +/- 0.03, SEE = 8 +/- 2%, respectively). In dogs with aortic occlusion (n = 4), changes in stroke area significantly correlated with changes in stroke volume for pooled data (r = 0.84, SEE = 8%, y = 1.0x + 3). Ventricular performance increased with dobutamine infusion (n = 7): end-systolic elastance 30 +/- 11 to 67 +/- 24 mm Hg/cm2 (p < 0.02 vs. control values); maximal elastance 37 +/- 11 to 82 +/- 26 mm Hg/cm2 (p < 0.02 vs. control values); preload recruitable stroke force 81 +/- 24 to 197 +/- 92 mm Hg (p < 0.02 vs. control values). Decreases occurred with propranolol infusion (n = 5) end-systolic elastance 20 +/- 4 to 13 +/- 4 mm Hg/cm2 (p < 0.002 vs. control values); maximal elastance 29 +/- 8 to 15 +/- 5 mm Hg/cm2 (p < 0.002 vs. control values); preload recruitable stroke force 66 +/- 14 to 40 +/- 9 mm Hg (p < 0.002 vs. control values). CONCLUSIONS: On-line pressure-area relations are a potentially useful means to assess left ventricular performance in a manner that is quantitatively similar to the predicted responses of pressure-volume relations.

Animals↗
PubMed1994

Rapid estimation of left ventricular contractility from end-systolic relations by echocardiographic automated border detection and femoral arterial pressure.

BACKGROUND: Automated echocardiographic measures of left ventricular (LV) cavity area are closely correlated with changes in volume and can be coupled with LV pressure to construct pressure-area loops in real time. The objective was to rapidly estimate LV contractility from the end-systolic relations of cavity area (as a surrogate for LV volume) and femoral arterial pressure (as a surrogate for LV pressure) in patients undergoing cardiac surgery. METHODS: Studies were attempted on 18 consecutive patients with recordings of LV pressure, LV area, and femoral arterial pressure on a computer workstation interfaced with the ultrasound system. End-systolic pressure-area relations (in terms of pressure-area elastance [E'es]) from pressure-area loops during inferior vena caval occlusions were determined before and immediately after cardiopulmonary bypass using both LV and arterial pressure by semiautomated and automated iterative linear regression methods. RESULTS: Data sets were available for 13 patients before and 8 patients after bypass (21 studies in 14 patients). E'es by arterial pressure was closely correlated with E'es by LV pressure: r = 0.96, standard error of the estimate = 2 mmHg/cm2, y = 1.01 x -0.7 by the semiautomated method and r = 0.94, standard error of the estimate = 3 mmHg/cm2, y = 1.02 x -0.5 by the automated method. Analysis of semiautomated and automated estimates of E'es from arterial pressure and E'es using LV pressure by the Bland-Altman method showed no systematic measurement bias and calculated limits of agreement of 8 and 9 mmHg/cm2, respectively. Similar decreases in E'es by arterial and LV pressure occurred from before to after bypass in 7 patients with paired data sets: 32 +/- 12 to 15 +/- 6 mmHg/cm2 and 32 +/- 15 to 15 +/- 7 mmHg/cm2, respectively (P < 0.05 for both). CONCLUSIONS: On-line femoral arterial pressure and LV area data by echocardiographic automated border detection may be used to rapidly calculate E'es as a means to estimate LV contractility in selected patients.

Adult↗
PubMed1994

Inhaled nitric oxide partially reverses hypoxic pulmonary vasoconstriction in the dog.

Nitric oxide (NO) inhaled during a hypoxia-induced increase in pulmonary vasomotor tone decreases pulmonary arterial pressure (Ppa). We conducted this study to better characterize the hemodynamic effects induced by NO inhalation during hypoxic pulmonary vasoconstriction in 11 anesthetized ventilated dogs. Arterial and venous systemic and pulmonary pressures and aortic flow probe-derived cardiac output were recorded, and nitrosylhemoglobin (NO-Hb) and methemoglobin (MetHb) were measured. The effects of 5 min of NO inhalation at 0, 17, 28, 47, and 0 ppm during hyperoxia (inspiratory fraction of O2 = 0.5) and hypoxia (inspiratory fraction of O2 = 0.16) were observed. NO inhalation has no measurable effects during hyperoxia. Hypoxia induced an increase in Ppa that reached plateau levels after 5 min. Exposure to 28 and 47 ppm NO induced an immediate (< 30 s) decrease in Ppa and calculated pulmonary vascular resistance (P < 0.05 each) but did not return either to baseline hyperoxic values. Increasing the concentration of NO to 74 and 145 ppm in two dogs during hypoxia did not induce any further decreases in Ppa. Reversing hypoxia while NO remained at 47 ppm further decreased Ppa and pulmonary vascular resistance to baseline values. NO inhalation did not induce decreases in systemic arterial pressure. MetHb remained low, and NO-Hb was unmeasurable. We concluded that NO inhalation only partially reversed hypoxia-induced increases in pulmonary vasomotor tone in this canine model. These effects are immediate and selective to the pulmonary circulation.

Administration, Inhalation↗