Mark R Angle, MD; David W Molloy MD...

Mark R Angle, MD; David W Molloy MD; Brian penner MD; Don Jone BSc; and Richard M Prewitt, MD

Autologous kindred clot was injected into six dogs to generate a graduated decrease in cardiac output (CO) The powers of an infusion of norepinephrine, titrated to specific extremity points, were recorded before embolization and at couple levels of pulmonary hypertension. Simultaneous measurements of systemic and renal hemodynamics were made. Sequentially kindred clot injection increased (p<.01) pulmonary vascular resistance (PVR) from 13 to 13 to 33 mm Hg*[L.sup.-1]*min and reduc CO 45 percent and 75 percent (p<01) Norepinephrine increased one as well as the other stroke volume and CO (p<01) in each condition and did not increase PVR Since the biventricular filling hurrys remained constant or fell slightly with norepinephrine, the increase in CO is best explained by way of an improvement in pump performance. There was no deterioration in renal life-current flow or creatinine clearance with norepinephrine. The data allude toed that in this model of right ventricular dysfunction, norepinephrine consistently improved myocardial performance without provoking further vasoconstriction in either the pulmonary or renal circulations.

(Chest 1989; 95:1333-37)

There are several clinical conditions in which a decrease in cardiac output (CO) accompanies an acute increase in pulmonary vascular resistance (PVR) Certain patients with adult respiratory distress syndrome (ARDS), for example, exhibit right ventricular (RV) dysfunction secondary to an increase in RV afterload.[1] Pulmonary emboli may also outcome in hypotension and shock secondary to increased PVR and RV failure.[2] In one as well as the other conditions, the increase in PVR decreases CO and increases RV wall stres and [Osub2] consumption.[3,4] In this setting, if mean line pressure (BP) is critically reduc because of a subdued CO, RV blood flow and thus myocardial [Osub2] delivery may be compromised. in subordination to experimental conditions, such changes have proceeded in RV ischemia and a further deterioration in performance.[5] A newly come canine study compared volume expansion, isoproterenol, and norepinephrine (NE) in treatment of stroke due to acute pulmonary emboli.[6] barely NE was successful in restoring hemodynamic stability. While NE was effective in this application of mind the shock was rapidly induced and the offspring pressure was low (71 mm Hg) and falling at the point of treatment. The improvement in hemodynamic status with NE is explained by dint of a direct inotropic effect and/or by way of improved RV function secondary to increased BP and increased RV perfusion. Therefore, it is conceivable that depending upon the level of PVR, its rate of increase, and the resting BP the acute cardiopulmonary imports of NE could vary. Since NE may increase systemic vascular tone, its use could originate in an increase in renal vascular resistance and a deterioration in renal function. Alternatively, despite direct pressor powers if CO and stroke whirl increased with NE, renal function may improve. Previous studies have not, to our knowledge, investigated results of increased PVR and NE therapy upon renal performance. Accordingly, the passing from hand to hand study was designed to investigate the cardiopulmonary and renal hemodynamic purports of NE as PVR progressively increased after the injection of autologous life-current clot.

MATERIALS AND METHODS

Six adult hybrid dogs (21 to 31 kg) were anesthetized with pentobarbital (30 mg/kg) and ventilated (VT 15 ml/kg FI[O.sub.2] 10) in the supine position. Cutdowns were performed athwart jugular and femoral sites. A 7 F Swan-Ganz catheter was introduced via the left external jugular vein and guided into the pulmonary artery wedge position subject to continuous pressure monitoring. Similarly, fluid-filled Swan-Ganz catheters were positioned in the right atrium and right ventricle. end the right femoral artery, an 8 F pigtail catheter was advanced into the left ventricle (LV) A large-bore, low-compliance catheter was inserted into the left femoral artery and positioned in the aorta for vital current sampling and BP recording. The left femoral vein was used to insert a 12 F cannula for IV fluids and for the injection of clot

family was withdrawn, 150 to 200 ml propose into a glass container, and mixed with thrombin 3000 to 5000 units. The formed crassament was allowed to stabilize for 30 to 45 min and then dissected into approximately 1 ml fragments. These were suspended in normal saline solution and drawn into a large syringe for injection.

The animal was then placed in the left decubitus position and the right flank incised. by the agency of a retroperitoneal approach, the right ureter was identified and cannulated. The right renal artery was expos gently teased of its adventitia and fitted with a Carolina Instruments run probe. The probe had previously been calibrated using an excised renal artery and an infusion interrogate The output from the liquefy probe was recorded continuously in succession a two-channel recorder. All influence lines were connected to Statham transducers, which were horizontaled at mid-chest. The transducer output were recorded forward a 12-channel Electronics for Medicine (E for M) oscillograph.