Outcome and prognostic factors in non-ambulatory Hansen Type I intervertebral disc extrusions: 308 cases.

Thoracolumbar intervertebral disc disease is the most common cause of caudal paresis in dogs. Whilst the pathogenesis of the extrusion has been widely studied, treatment protocols and prognostic factors relating to outcome remain controversial. Recent studies have examined a multitude of factors relating to time to regain ambulation after decompressive surgery. Most intervertebral disc herniations occur in the thoracolumbar region, causing upper motor neuron signs in the rear limbs, which are thought to have a more favourable prognosis compared to the lower motor neuron signs created by herniation of an intervertebral disc in the caudal lumbar region. Due to the potential disruption of the lumbar intumescence, lower motor neuron signs have been reported as having a less favourable prognosis. The purpose of this study was to evaluate the intervertebral disc space as a prognostic factor relating to ambulatory outcome and time to ambulation after decompressive surgery. Hansen Type I intervertebral disc extrusions were studied in 308 non-ambulatory dogs. Preoperative and postoperative neurological status, corticosteroid use, signalment, intervertebral disc space, postoperative physical rehabilitation, previous hemilaminectomy surgery, disc fenestration, return to ambulation, and time to ambulation were reviewed.

A comparison of hemodynamic changes during the transition from mechanical ventilation to T-piece, pressure support, and continuous positive airway pressure in canines.

The immediate transition from positive pressure mechanical ventilation to spontaneous ventilation may generate significant cardiopulmonary hemodynamic alterations based on the mode of weaning selected, particularly in individuals with preexisting cardiac dysfunction. The purpose of this study was to compare hemodynamic responses associated with the initial transition to 3 modes of ventilator weaning (spontaneous ventilation/T-piece, pressure support [PS], and continuous positive airway pressure [CPAP]). Right ventricular hemodynamic responses were evaluated with a thermodilution pulmonary artery catheter; while left ventricular hemodynamic responses were measured by a transducer-tipped Millar catheter and conductance catheter. Two groups of canines were studied. Group 1: normal biventricular function (n = 10) and group 2: propranolol-induced biventricular failure (n = 10). Dependent variables were measured at baseline on controlled mechanical ventilation (MV) and following the initial transition to each of 3 randomized spontaneous ventilatory conditions: T-piece, PS 5 cmH2O, and CPAP 5 cmH2O. Both groups significantly increased cardiac output in response to T-piece. Right ventricular stroke work was also significantly increased with T-piece and CPAP in both groups of subjects. Left ventricular response depended on baseline ventricular function. Baseline ventricular function influenced hemodynamic response to the immediate transition from mechanical to spontaneous ventilation. There were also differential hemodynamic responses based on the ventilatory mode. Consideration of baseline cardiac function may be an important factor in the selection of an appropriate mode of spontaneous ventilation following controlled MV.

Variation in tau, the time constant for isovolumic relaxation, along the left ventricular base-to-apex axis.

Tau (tau), the time constant for isovolumic relaxation, is often used as a measure of cardiac diastolic function. However, several methods of calculating tau have been published which may produce different results and, thereby, different conclusions. The purpose of this study was to determine if the method of tau calculation effects the results when left ventricular pressure (LVP) is measured at different positions along the base-to-apex axis. In 16 dogs, we measured LVP at 6 positions along the base-to-apex axis. We calculated tau using three different methods: 1) a monoexponential model (P(t) = [P0-Pasym]eAt + Pasym, where t = time, P0 = LVP at t = 0, Pasym is asymptotic pressure as t-->infinity, A is -1/tau) with a zero asymptote 2) a monoexponential model with a variable asymptote in which the monoexponential decay equation is differentiated with respect to time and substituted into the original equation so that dP/dt vs. LVP is A (-1/tau), and 3) a monoexponential decay model with variable asymptote in which Pasym and A are varied until the best fit line is reached by minimizing the residual sum of squares. When tau is calculated using method 1, tau measured at the LV base is 98.01% +/- 8.85% of tau at the apex. If calculated using method 2, tau measured at the LV base was 75.46 +/- 39.4% of tau measured at the apex. When method 3 is used for tau calculations, base tau increases to 117.76 +/- 4.91% of the apical tau. We conclude: 1) the method used to calculate tau will effect the results and, thus, conclusions drawn from tau data. 2) When using Method 3, which appears to be the best method for tau calculation, tau increases at the LV base compared to the apex.

Assessment of left-ventricular function.

There are three distinct phases of the cardiac cycle (contraction, active relaxation, and passive relaxation) which should be examined in order to perform a thorough assessment of global left-ventricular function. Accurate measurements of left-ventricular pressure and volume are necessary to assess these phases of the cardiac cycle. The ideal index of contractility is sensitive to the intropic state of the heart, but insensitive to loading conditions, heart rate, and cardiac size. Indices of contractility may be derived from various aspects of the phase of contraction including isovolumic contraction, the end-systolic pressure-volume relationship, the phase of ejection, and the stress-strain relationship. The indices of contractility most commonly employed and arguably closest to 'ideal' are preload recruitable stroke work, an ejection phase index; the dP/dt - end-diastolic volume relationship, an isovolumic contraction phase index; and end-systolic elastance, an index derived from the end-systolic pressure-volume relationship. The active phase of relaxation is most commonly assessed by the time constant (tau) of the exponential ventricular pressure decline that occurs during the isovolumic period of relaxation. The value for tau varies inversely with ventricular function and reflects the active, energy consuming process of relaxation. tau is influenced by many of the same factors which influence contractility. The end-diastolic pressure-volume relationship reflects the passive properties of the left ventricle and may be used to obtain a measure of diastolic stiffness. The end-diastolic pressure-volume relationship is curvilinear (exponential) when end-diastolic pressures are varied over a wide range, but may be approximated by a linear relationship during low filling pressures. Diastolic stiffness is influenced by the viscoelastic properties of the heart, pericardial constraint, the atrioventricular pressure gradient, and ventricular interaction. Knowledge of the indices of the three phases of the cardiac cycle and their interactions are important to the understanding and interpretation of ventricular function in health and disease.

Effects of hypoproteinemia-induced myocardial edema on left ventricular function.

In previous studies, we observed left ventricular (LV) systolic and diastolic dysfunction in association with interstitial myocardial edema (IME) induced by either coronary venous hypertension (CVH) or lymphatic obstruction. In the present study, we examined the effects of myocardial edema induced by acute hypoproteinemia (HP) on LV systolic and diastolic function. We also combined the methods of HP and CVH (HP-CVH) to determine their combined effects on LV function and myocardial water content (MWC). We used a cell-saving device to lower plasma protein concentration in HP and HP-CVH groups. CVH was induced by inflating the balloon in the coronary sinus. Six control dogs were treated to sham HP. Conductance and micromanometer catheters were used to assess LV function. Contractility, as measured by preload recruitable stroke work, did not change in control or HP groups but declined significantly (14.5%) in the HP-CVH group. The time constant of isovolumic LV pressure decline (tau) increased significantly from baseline by 3 h in the HP (24.8%) and HP-CVH (27.1%) groups. The end-diastolic pressure-volume relationship (stiffness) also increased significantly from baseline by 3 h in the HP (78.6%) and HP-CVH (42.6%) groups. Total plasma protein concentration decreased from 5.2 +/- 0.2 g/dl at baseline to 2.5 +/- 0.0 g/dl by 3 h in the HP and HP-CVH groups. MWC of the HP (79.8 +/- 0.25%) and HP-CVH groups (79.8 +/- 0.2%) were significantly greater than that of the control group (77.8 +/- 0.3%) but not different from one another. In conclusion, hypoproteinemia-induced myocardial edema was associated with diastolic LV dysfunction but not systolic dysfunction. The edema caused by hypoproteinemia was more than twice that produced by our previous models, yet it was not associated with systolic dysfunction. CVH had a negative inotropic effect and no significant influence on MWC. IME may not have the inverse causal relationship with LV contractility that has been previously postulated but appears to have a direct causal association with diastolic stiffness as has been previously demonstrated.

Mechanical workload-myocardial water content relationship in isolated rat hearts.

We tested the hypothesis that the mechanical workload of the heart inversely determines the rate of myocardial edema formation in an isolated, perfused rat heart preparation. Heart rate (HR) was varied in three groups by pacing at 125 (HR125), 250 (HR250), or 350 beats/min (HR350). Left ventricular pressure (LVP) was varied in two additional groups by pacing at 250 beats/min and with the addition of either epinephrine (Epi) or propranolol (Pro) to the perfusate. In five otherwise identical groups, variation of coronary vascular resistance was minimized by adenosine. Myocardial water content (MWC) varied significantly and inversely with HR in the HR125, HR250, and HR350 groups. MWC of the HR250 group was significantly less than that of the Pro group but did not differ from the Epi group. However, when adenosine was used, MWC had significant inverse relationships with HR and LVP. We concluded that the mechanical workload of the heart inversely determines the rate and degree of myocardial edema formation in this isolated heart preparation, and both HR and LVP are determinants of this relationship.

Evaluation of a hypertonic saline-dextran solution for treatment of dogs with shock induced by gastric dilatation-volvulus.

OBJECTIVE: To test the hypothesis that small volumes of hypertonic saline-dextran (HSD) solution can be used to effectively resuscitate dogs in shock induced by gastric dilatation-volvulus (GDV), and, compared with administration of large volumes of lactated Ringer's solution (LRS), can be used to limit the overall volume of fluid needed for resuscitation. DESIGN: Prospective, clinical study. ANIMALS: 15 dogs with GDV-induced shock. PROCEDURE: Initially, HSD solution (5 ml/kg of body weight) or LRS (60 to 90 ml/kg) was administered. All dogs then received a maintenance administration (20 ml/kg/h) of LRS. Cardiorespiratory, blood gas, and serum biochemical analyses were performed over a 4-hour period after initiation of treatment. RESULTS: Systolic arterial and central venous pressures and plasma volume increased more rapidly in dogs in the HSD + LRS group. The cumulative dose of fluids administered to dogs in the HSD + LRS group was significantly less than that administered to dogs in the LRS group. Serum sodium and chloride concentrations and osmolality increased significantly in dogs in the HSD + LRS group, but not in dogs in the LRS group. Ventricular arrhythmias were detected in both groups of dogs, but did not appear to be induced by either form of fluid therapy. CLINICAL IMPLICATIONS: Administration of HSD rapidly restored cardiorespiratory function and induced resuscitation equivalent to administration of large volumes of LRS. Use of HSD solutions to treat dogs in GDV-induced shock may be more efficient than use of isotonic fluids. Administration of HSD solution was not associated with noticeable complications.

Impairment of left ventricular function by acute cardiac lymphatic obstruction.

OBJECTIVES: We performed the following study to define the effects of acute cardiac lymphatic obstruction on left ventricular (LV) systolic and diastolic function. METHODS: Cardiac lymphatic obstruction was created in 8 pentobarbital-anesthetized dogs by identifying (Evans blue) and ligating the right and left epicardial lymphatics, the afferent and efferent lymphatics associated with the pretrachael and cardiac lymph nodes, and the thoracic duct. Left ventricular function was assessed by analysis of micromanometer-conductance catheter-derived LV pressure-volume relationships. Contractility was assessed by preload recruitable stroke work (PRSW). The active and passive phases of LV relaxation were assessed by the time constant o isovolumic relaxation (tau) and the end-diastolic pressure-volume relationship (stiffness), respectively. RESULTS: PRSW decreased significantly and tau increased significantly from baseline at 1, 2, and 3 h after cardiac lymphatic obstruction (n = 8), but stiffness did not change. Cardiac lymphatic obstruction had similar effects on LV function in a group of autonomically blocked dogs (n = 5). Left ventricular function did not change in sham treated controls (n = 8). Cardiac lymphatic obstruction induced a significant increase in LV wet/dry weight ratios (3.58 +/- 0.01) when compared to the control group (3.53 +/- 0.02). Histopathology of the myocardium in the lymphatic obstruction groups revealed significant lymphangiectasis and increased interstitial spacing when compared to controls. CONCLUSIONS: Acute cardiac lymphatic obstruction depresses contractility and active relaxation and causes mild LV myocardial edema, but does not alter diastolic stiffness.

Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema.

This study was performed to evaluate the direct and indirect effects of acute coronary sinus hypertension (CSH) on systolic and diastolic left ventricular (LV) function. Coronary sinus pressure was elevated to 25 mmHg for 3 h in eight pentobarbital-anesthetized dogs and then relieved. LV contractility was assessed by preload recruitable stroke work (PRSW) and end-systolic elastance (Ees). Diastolic function was assessed by the time constant of isovolumic relaxation (tau) and the end-diastolic pressure volume relationship (EDPVR). PRSW and Ees decreased progressively, and tau and the slope of the EDPVR increased progressively with CSH. These changes persisted after relief of CSH. beta-Adrenergic and cholinergic receptor blockade, performed in six dogs, did not alter the effects of CSH on systolic or diastolic function. The LV wet-to-dry weight ratios of the groups with CSH were significantly greater than those of a control group without CSH. We conclude that CSH results in changes in the left ventricle that depress contractility, prolong active relaxation, and increase diastolic stiffness. The dysfunction was not the direct effect of CSH or autonomic reflex activation, but may have been induced by fluid accumulation within the interstitium.

Factors associated with perioperative mortality in dogs with surgically managed gastric dilatation-volvulus: 137 cases (1988-1993).

OBJECTIVE: To evaluate factors associated with perioperative mortality in dogs with gastric dilatation-volvulus and to determine the influence of treatment differences between university and private specialty practices on outcome. DESIGN: Retrospective analysis of medical records. ANIMALS: 137 dogs with gastric dilatation-volvulus. PROCEDURE: Signalment; frequency of preoperative and postoperative treatments and complications; intraoperative findings; surgical technique; and hematologic, serum biochemical, and electrocardiographic results were recorded, evaluated for association with mortality, and compared between institutions. RESULTS: Mortality did not differ between institutions, and overall mortality was 18% (24/137). Surgical techniques differed between institutions, but were not associated with mortality. Gastric necrosis was associated with significantly higher mortality (46%; 13/28). When partial gastrectomy or splenectomy was performed, mortality (35 and 32% or 8/23 and 10/31, respectively) was significantly increased. Splenectomy was performed in 11 of 23 dogs requiring partial gastrectomy, and when both procedures were performed, mortality (55%; 6/11) was significantly increased. Preoperative cardiac arrhythmias were associated with significantly higher mortality (38%; 6/16). Mortality in dogs > 10 years old was not significantly greater than that in younger dogs. CLINICAL IMPLICATIONS: Patient management differences between practices did not seem to influence survival in dogs with surgically managed gastric dilatation-volvulus. Signalment, including age, did not influence mortality. Gastric necrosis, gastric resection, splenectomy, and preoperative cardiac arrhythmias were associated with mortality > 30%.

Evaluation of a hypertonic sodium chloride/dextran solution for treatment of traumatic shock in dogs.

OBJECTIVE: To compare the efficacy of 7% NaCl solution (hypertonic saline) in 6% dextran 70 solution (HSD) with that of lactated Ringer's solution (LRS) for treatment of dogs in traumatic shock. DESIGN: Prospective, randomized, clinical study. ANIMALS: 16 traumatized adult dogs with clinical signs of shock. PROCEDURE: Physical, hemodynamic, blood gas, and clinical chemistry measurements were performed prior to treatment. Initial treatment consisted of HSD (n = 8) or LRS (n = 8) administered as a bolus (5 ml/kg of body weight, IV) over a 3-minute period, followed by administration of additional LRS and other treatments to restore hemodynamic and physical criteria to within reference limits. Measurements were repeated for 3 hours after initial treatment. The volumes of LRS and HSD administered were recorded hourly. Degree of injury was scored by using a trauma severity index. RESULTS: Dogs responded similarly to the treatments, and all but 3 dogs survived to be discharged. The amount of fluid administered to dogs in the HSD group over the final 2 hours of the study was significantly less than that administered to the dogs in the LRS group. Serum sodium concentration and osmolality of the dogs in the HSD group were not significantly greater than those values in the LRS group. Bradyarrhythmias were observed in 2 dogs in the HSD group. CLINICAL IMPLICATIONS: Hypertonic sodium chloride/dextran solution is safe and effective for resuscitating dogs in traumatic shock. Seven percent NaCl in 6% dextran 70 may reduce the need for isotonic fluids in the hours after initial resuscitation.

Effects of acid aspiration-induced lung injury on left ventricular function.

BACKGROUND: Acid aspiration-induced acute lung injury (AALI) leads to myocardial leukosequestration and edema in rats and hemodynamic depression in dogs, but the effects of AALI on left ventricular (LV) function have not been carefully studied. METHODS: We examined the effects of 0.1 N HCl administration into the lung on LV function, leukosequestration, and edema in pentobarbital-anesthetized, atropinized (n = 8), or autonomically blocked (n = 7) dogs. Saline solution was administered into the lungs of a control group of autonomically blocked dogs (n = 6). LV contractility was assessed by end-systolic elastance (EES) and preload recruitable stroke work (PRSW). Active relaxation was assessed by the time constant of LV pressure decline (tau). RESULTS: AALI resulted in significant (p < 0.05) decreases in mean arterial pressure and cardiac output and increases in pulmonary artery pressure and systemic vascular resistance in atropinized and autonomically blocked dogs but not in saline control group. In atropinized dogs tau did not change after injury, but EES and PRSW were increased significantly at 2 and 3 hours after injury, despite significant myeloperoxidase activity and extravascular fluid wet-dry weight ratios. EES, PRSW, and tau did not change in the autonomically blocked dogs in response to AALI or in the saline control group. CONCLUSIONS: We concluded that AALI results in a baroreflex mediated enhancement of LV contractility in dogs, despite mild myocardial leukosequestration and edema formation.

Pathogenic aspects of circulatory shock.

Shock has been described and defined by the inciting cause. This method of categorization does little to clarify common pathophysiologic changes known to occur regardless of the etiology. Each type of shock involves different stages that are determined by the inciting cause, its duration, severity of the initial result, susceptibility of the patient, and adequacy of treatment.

Acute lung injury isolated to an in situ lung preparation causes sustained reflex cardiovascular depression in dogs.

We tested the hypothesis that acute lung injury (ALI) isolated to a perfused in situ left lung preparation results in sustained reflex cardiovascular depression. Phorbol myristate acetate (PMA), an agent that activates neutrophils, administered into the isolated lung preparation of chloralose-anesthetized dogs resulted in ALI, as assessed by wet-to-dry weight ratios and histopathology, and significant decreases in heart rate (43%), mean arterial pressure (27%), aortic blood flow (29%) and maximum rate of change in left ventricular pressure (30%). Significant reflex effects occurred by 20 min after PMA administration and were sustained for 40 min (n = 7). Hemodynamic variables recovered when the left lung was denervated 60 min after PMA administration. Indomethacin administered into the isolated circulation before PMA (n = 5) did not significantly influence the ALI or reflex effects. Systemic atropinization (n = 6) prevented only the bradycardia. Left lung denervation before ALI (n = 3) prevented all reflex effects. We conclude that PMA administration into an isolated in situ lung preparation results in ALI and sustained reflex cardiovascular depression that is most likely elicited by pulmonary C-fiber stimulation and mediated by withdrawal of sympathetic efferent nerve activity.

Vagal innervation influences the whole body oxygen consumption-delivery relationship in the dog.

Vagotomy alters regional blood flow distribution by interrupting the tonic central inhibitory effect of cardiopulmonary vagal afferent nerves on sympathetic outflow predominantly to the renal, splanchnic, and cutaneous circulations. We hypothesized that the alteration of blood flow distribution by vagotomy would lead to disruption of the oxygen consumption-oxygen delivery relationship (VO2/DO2), increase critical DO2 (DO2Crit), and decrease whole-body oxygen extraction ratio (O2ER). Nineteen chloralose-anesthetized, paralyzed, splenectomized dogs were submitted to either bilateral vagosympathectomy (n = 7), bilateral vagotomy (n = 6), or sham denervation (n = 6) following baseline cardiorespiratory parameter measurement. VO2 was measured by indirect calorimetry and carotid blood flow by ultrasonic flow probe. Incremental hemorrhages (1-5 mL/kg) were performed to determine the VO2/DO2 relationship. Cardiorespiratory parameters were measured after each hemorrhage at steady-state VO2. DO2Crit was derived from the VO2/DO2 relationship using a best-fit regression analysis technique. The average DO2Crit values of the vagotomy (9.1 +/- .54) and vagosympathectomy (11.5 +/- 1.2 mL/min/kg) groups were significantly greater than the control group (7.72 +/- .43). After hemorrhage had been performed to a point that decreased mean arterial pressure to approximately 70 mmHg from baseline values, carotid blood flow in the vagosympathectomy group was significantly greater than the control group. We conclude that vagotomy disrupts the VO2/DO2 relationship. Vagosympathectomy causes a severe disruption of the VO2/DO2 relationship, probably by the combined effect of vagotomy and interruption of sympathetic nervous system control of blood flow to the head and neck.

Comparative effects of 7% NaCl in 6% dextran 70 and 0.9% NaCl on oxygen transport in endotoxemic dogs.

We compared the effects of 7% NaCl in 6% dextran 70 (HSD) and 0.9% NaCl (IS) resuscitation of endotoxic dogs on hemodynamic and cardiorespiratory parameters and the oxygen consumption-delivery relationship. Escherichia coli endotoxin (3 mg.kg-1, intravenously) was infused over 5 min into 13 paralyzed, chloralose-anesthetized, splenectomized dogs. Six additional dogs received a sham endotoxin infusion (saline) and served as controls. After 30 min, the endotoxic animals were resuscitated to 150% of their baseline cardiac output (CO) and maintained at this CO for 30 min using 7% NaCl in 6% dextran 70 (HSD at 1 ml.kg-1.min-1; n = 7) or 0.9% NaCl (IS at 4 ml.kg-1.min-1; n = 6). Oxygen consumption (VO2), measured by indirect calorimetry, hemodynamic parameters, and oxygen delivery (DO2), improved in similar temporal patterns in both groups during resuscitation and VO2 reached steady-state values. Oxygen delivery, VO2, mean arterial pressure, and cardiac output did not significantly differ between groups at the end of resuscitation, but VO2 increased significantly from baseline values only in the HSD group. The total volume of HSD administered averaged 10.0 +/- 0.2 ml.kg-1 which was significantly less than the volume of IS, which averaged 67.2 +/- 9.3 ml.kg-1. Incremental hemorrhages (2-5 ml.kg-1) were then performed in all dogs to determine the oxygen consumption-delivery relationship and the critical level of oxygen delivery (DO2Crit). The average DO2Crit values of the HSD, IS, and control groups were 9.42, 9.15, and 6.82 ml.min-1.kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous pulmonary C-fiber stimulation produces sustained reflex cardiovascular depression.

We used an isolated perfused in situ left lung preparation to evaluate the hemodynamic response to specific pulmonary C-fiber stimulation with capsaicin in two groups of anesthetized dogs. In one group (n = 6), continuous administration of capsaicin at 5 micrograms.kg-1.min-1 into the isolated pulmonary circulation produced sustained (20 min) reflex decreases in mean arterial pressure, cardiac output, maximal left ventricular rate of pressure over time, and heart rate. These effects were abolished by vagotomy. In a second group (n = 5) of atropinized dogs, a mild hemorrhage was first performed in each dog during control conditions (capsaicin vehicle administration). The hemorrhage was performed by removing 10% of blood volume over 3 min and then replacing this blood 3 min later. After reinfusion and stabilization, the mild hemorrhage was repeated during continuous administration of capsaicin (6.0 +/- 1.0 microgram.kg-1.min-1) into the isolated pulmonary circulation. The decrease of mean arterial pressure in response to hemorrhage was significantly greater during capsaicin administration than during control conditions. Lung denervation prevented the effect of capsaicin administration on the response to hemorrhage. We concluded that continuous pulmonary C-fiber stimulation produces sustained cardiovascular depression and compromises the hemodynamic response to mild hemorrhage in dogs. This latter effect may represent a central alteration of baroreflex gain.

Reflex cardiovascular effects of continuous prostacyclin administration into an isolated in situ lung in the dog.

Bolus administration of prostacyclin (PGI2), an inflammatory product produced by the arachidonic acid cyclooxygenase pathway, into the pulmonary circulation is known to stimulate pulmonary C-fibers and to produce transient reflex cardiovascular depression. We used an isolated perfused in situ left lung preparation to examine the reflex cardiovascular effects of continuous administration of PGI2 into the isolated pulmonary circulation of dogs. PGI2 was infused for 30 min (5 micrograms.kg-1 x min-1) into the innervated isolated left pulmonary circulation in six dogs and into the denervated isolated circulation in seven dogs. Mean arterial pressure and cardiac output were significantly decreased from baseline values during the final 20 min of PGI2 infusion. There were no significant changes in maximum rate of change of left ventricular pressure during systole and in heart rate. All variables returned to baseline levels within 15 min of discontinuation of PGI2 infusion. PGI2 infusion produced no significant measured hemodynamic changes in the denervated group. Control experiments demonstrated that the observed response was not affected by duration of the preparation, lung denervation, or infusion vehicle. These findings suggest that continuous infusion of PGI2 into the isolated pulmonary circulation produces sustained cardiovascular depression via a vagal reflex mechanism that is probably mediated by pulmonary C-fibers.

Comparative effects of 7.5% NaCl in 6% Dextran 70 and 0.9% NaCl on cardiorespiratory parameters after cardiac output-controlled resuscitation from canine hemorrhagic shock.

We resuscitated severely hemorrhaged (mean arterial pressure at 40 mm Hg for 30 min) pentobarbital-anesthetized dogs to 120% of control cardiac output with 7.5% NaCl in 6% Dextran 70 (HSD) or 0.9% NaCl (IS) to compare the effects on hemodynamic and oxygen transport parameters. Hemodynamic parameters and oxygen delivery did not differ between groups. Oxygen consumption and oxygen extraction ratio tended to be higher, and mixed venous oxygen tension lower (P < 0.05) for HSD during the first hour of the postresuscitation period. Resuscitation of the HSD group required significantly less time (10.4 +/- 2.0 vs. 23.6 +/- 1.7 min; P < 0.01) and fluid volume (8.0 +/- 1.1 vs. 47.0 +/- 3.3 ml.kg-1; P < 0.01). We conclude that the resuscitation of hypovolemic dogs with HSD and IS to equivalent cardiac output results in identical improvements in hemodynamics and oxygen delivery but that HSD may provide a better oxygen supply/demand balance during the first hour postresuscitation.