Two methods of wedging a pulmonary artery catheter were studied in dogs with experimental pulmonary hypertension secondary to left atrial balloon inflation. In Group 1 (N = 8), the catheter tips were located in a branch of the pulmonary artery so that wedge pressures were obtained with balloon inflation. In Group 2 (N = 8), the catheter tips were positioned 1 to 2 cm beyond the pulmonic valve and readvanced into a branch of the pulmonary artery for each wedge pressure determination. In both groups, wedge pressures were obtained using a balloon inflation volume of 0.8 mL. With left atrial hypertension, the pressure gradient across the inflated balloon (calculated as mean pulmonary artery pressure minus pulmonary artery wedge pressure) was lower than baseline (P < .05). Wedge pressures were determined every five minutes. After two hours, the lungs were removed and studied grossly for hemorrhage. The incidence of pulmonary hemorrhage was 50% in Group 1 dogs, but 0% in Group 2 dogs (P < .03). It is concluded that locating the catheter tip in the proximal pulmonary artery and readvancing it for each wedge pressure determination significantly reduces the risk of catheter-induced pulmonary hemorrhage in this model.

Animals↗

PubMed1987

Predicting the pharmacodynamics of heparin: a clinical evaluation of the Hepcon System 4.

The magnitude of the anticoagulation response to heparin (heparin responsiveness) varies substantially from patient to patient. Identifying extremes of sensitivity and resistance prior to intravenous administration of heparin would facilitate anticoagulation for cardiopulmonary bypass (CPB). The performance of the Hepcon System 4 (HemoTec, Inc, Englewood, CO), an instrument designed for that purpose, was tested. Using nonheparinized blood samples from 157 patients scheduled for surgery requiring CPB, this device performed activated coagulation times (ACT) with three different concentrations of in vitro heparin. After determining each patient's in vitro heparin response, the heparin dose predicted to produce ACT values of 480 seconds (group 1, N = 77) or 600 seconds (group 2, N = 80) was administered. Five minutes later each patient's ACT was determined with the Hemochron method (International Technidyne, Inc, Edison, NJ). Simultaneously, several other variables that might predict heparin responsiveness were investigated. When compared with the observed ACT, the Hepcon System 4 inadequately predicted the response. There was considerable scatter in this comparison, but most frequently the in vitro method substantially underestimated the in vivo heparin dose requirement. Heparin responsiveness decreased significantly with high platelet counts and advanced age, but was unaffected by the initial hematocrit, ACT, partial thromboplastin time, or preoperative heparin therapy. Previous investigations have not identified a relationship between advanced age and reduced heparin responsiveness. Combining the Hepcon heparin dose-response in vitro method with the other parameters evaluated, stepwise regression could only account for 39% of the observed variability in heparin responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

PubMed1987

The influence of periaortic collateral vessels on the intraoperative hemodynamic effects of acute aortic occlusion in patients with aorto-occlusive disease or abdominal aortic aneurysm.

Explore the source record for details and available documents.

Aorta, Abdominal↗

PubMed1987

Influence of balloon inflation and deflation on location of pulmonary artery catheter tip.

Explore the source record for details and available documents.

Adult↗

PubMed1987

Effects of resuscitation from hemorrhagic shock on cerebral hemodynamics in the presence of an intracranial mass.

This study compares intracranial pressure, cerebral blood flow, and cerebral oxygen transport during hemorrhagic shock and following fluid resuscitation with crystalloid or colloid solution in a canine model with an epidural mass lesion. After placement of an epidural balloon, intracranial pressure was increased to 30 mm Hg for 5 minutes and then permitted to vary without further manipulation. Hemorrhagic shock was produced by the rapid removal of blood to achieve a mean arterial pressure of 55 mm Hg for 30 minutes. Resuscitation then was performed with intravenous lactated Ringer's solution, 60 ml/kg, or with 6.0% hetastarch, 20 ml/kg. Following both solutions mean arterial pressure and cardiac output were increased and hemoglobin concentration was reduced. Intracranial pressure was significantly lower immediately after resuscitation in the hetastarch group; it then gradually increased so that the difference was much less 1 hour later. Cerebral blood flow decreased during shock and was not restored by either fluid; cerebral oxygen transport fell further with resuscitation in both groups due to hemodilutional reductions in hemoglobin. Although colloid resuscitation improved systemic hemodynamics and maintained lower intracranial pressure, it failed, as did crystalloid resuscitation, to restore cerebral oxygen transport to prehemorrhagic shock levels.

Animals↗

PubMed1987

Lectin binding to the developing forms of Onchocerca gutturosa microfilariae.

Uterine and skin derived forms of microfilariae (mf) and earlier developing stages of the cattle filarial nematode Onchocerca gutturosa were examined for the lectin binding properties of their external surfaces (ie. egg shell and microfilarial cuticle). Both the uterine and skin derived forms of mf failed to bind any of the lectins tested. Incubation in known microfilaricides did not promote any binding of lectins to these parasites. Peanut agglutinin (PNA) was the only lectin found to bind specifically to earlier developing stages (i.e. the shells of freshly obtained eggs). Diethylcarbamazine (DEC) did not alter the binding pattern from that observed in untreated eggs. Ivermectin eliminated PNA binding but increased Ricinus communis lectin (RCA-1) positivity. Trypsin, collagenase and protease enzymes all affected the binding; chitinase however did not have any effect. These results support the concept that the eggshells of filariae can interact with the host defence responses.

Animals↗

PubMed1987

Effect of total spinal anesthesia on arterial and venous responses to dopamine and dobutamine.

To test whether acute denervation alters the vascular effects of dopamine and dobutamine, we anesthetized 16 greyhounds and placed them on total cardiopulmonary bypass (CPB). Eight dogs received total spinal anesthesia before drug testing; eight dogs were tested in the absence of total spinal anesthesia. During dopamine and dobutamine infusions, venous capacitance [determined by the volume of the CPB venous reservoir (VR)] and mean arterial pressure (MAP) were monitored. The CPB pump flows remained constant throughout our studies. Every dog received six increasing doses of both drugs. In the absence of total spinal anesthesia, both dopamine and dobutamine increased VR (decreased venous capacitance) in a dose-dependent manner. Dobutamine decreased MAP in a dose-related fashion but dopamine had no significant effect on MAP. After total spinal anesthesia, both dopamine and dobutamine produced greater dose-related increases in VR (i.e., decreases in venous capacitance) than in the absence of spinal anesthesia. Dopamine increased MAP but dobutamine had no significant effect. These data demonstrate how dopamine and dobutamine differ in their effects on the arterial circulation in the presence or absence of spinal anesthesia. The acute denervation of spinal anesthesia altered venous and arterial dose-response relationships of both drugs. Finally, our study demonstrates the effectiveness of dobutamine and, perhaps even more so, dopamine as possible alternatives to ephedrine for the pharmacologic correction of the noncardiac circulatory sequelae of spinal anesthesia.

Anesthesia, Spinal↗

PubMed1986

Altered cardiac tissue gene expression during acute hypoxic exposure.

Anoxia has been shown to induce the expression of one or more "stress proteins' in mammalian cells and tissues. A less severe form of oxygen depletion, hypoxic hypoxia, occurs in response to hypobaric decompression which simulates high altitude conditions. Under these conditions mouse hearts accumulate mRNAs for at least two polypeptides at substantially elevated levels. The molecular weights of these proteins, 85 kDa and 95 kDa, are similar to those reported for other mammalian stress proteins or glucose-regulated proteins. Time course experiments suggest that mRNAs for these species increase continuously for up to 16 hours of treatment, while mRNA for 71 kDa and 79 kDa polypeptides are elevated early in the treatment, but later decrease to control values. Total heart mRNA template activity is also increased by the hypobaric treatment. These results demonstrate that mouse cardiac tissue is capable of mounting a cellular stress-like response when exposed to moderately stressful conditions. It also provides a model for studying the direct effects of acute hypoxic stress on cellular gene expression, and its relationship to physiological adaptation.

Animals↗