Search PubMed⌕ Search

Biomedical subjects

C L Sprung

Publications and source records attributed to C L Sprung.

At least 109 records · Page 6Linked to original sources
PubMed1985

Effects of histamine on bronchial artery blood flow and bronchomotor tone.

The effects of aerosolized 5% histamine (10 breaths) on bronchial artery blood flow (Qbr), airflow resistance (RL), and pulmonary and systemic hemodynamics were studied in mechanically ventilated sheep anesthetized with pentobarbital sodium. Histamine increased mean Qbr and RL to 252 +/- 45 and 337 +/- 53% of base line, respectively. This effect was significantly different from base line for 30 min after challenge. The histamine-induced increase in RL was blocked by pretreatment with the histamine H1 receptor antagonist, chlorpheniramine, whereas the histamine-induced elevation in Qbr was prevented by the H2 antagonist, metiamide. Both responses were blocked only when both antagonists were present. Changes in Qbr were not directly associated with alterations in systemic and pulmonary hemodynamics or arterial blood gas composition. In vitro histamine caused a dose-dependent contraction of ovine bronchial artery strips that was prevented by H1 antagonist. The H2 agonist, impromidine, caused relaxation of precontracted arterial strips and was more potent and efficacious than histamine, whereas H1 agonists failed to elicit a relaxant response. Thus these findings indicate that histamine aerosol induces a vasodilation in the bronchial vascular bed; histamine has a direct effect on Qbr that is independent of alterations in RL, systemic and pulmonary hemodynamics, or arterial blood gas composition; and, histamine-induced bronchoconstriction is mediated predominantly by H1-receptors, whereas increased Qbr is controlled predominantly by H2-receptors, probably located in resistance vessels. This local effect of histamine on Qbr may have important implications in the pathophysiology of bronchial asthma and pulmonary edema.

Animals↗
PubMed1984

The effects of high-dose corticosteroids in patients with septic shock. A prospective, controlled study.

To determine whether corticosteroids are efficacious in severe septic shock, we conducted a prospective study of 59 patients randomly assigned to a methylprednisolone, dexamethasone, or control group. Patients were treated 17.5 +/- 5.4 hours (mean +/- S.E.M.) after the onset of shock, and 55 patients required vasopressor agents. Early in the hospital course, reversal of shock was more likely in patients who received corticosteroids than in those who did not. Four (19 per cent) of 21 methylprednisolone-treated, 7 (32 per cent) of 22 dexamethasone-treated, and none of 16 control patients had reversal of shock 24 hours after drug administration (corticosteroid groups vs. control group, P less than 0.05). Patients treated with corticosteroids within four hours after the onset of shock had a higher incidence of shock reversal (P less than 0.05). At 133 hours after drug administration, 17 (40 per cent) of 43 corticosteroid-treated patients had died, and 11 (69 per cent) of 16 control patients had died (P less than 0.05). However, these differences in reversal of shock and survival disappeared later in the course. Overall, 16 (76 per cent) of 21 patients receiving methylprednisolone, 17 (77 per cent) of 22 patients receiving dexamethasone, and 11 (69 per cent) of 16 controls in the hospital died. We conclude that corticosteroids do not improve the overall survival of patients with severe, late septic shock but may be helpful early in the course and in certain subgroups of patients.

Adolescent↗
PubMed1984

Secondary bacterial peritonitis in cirrhotic patients with ascites.

Bacterial peritonitis in patients with cirrhosis has a wide variety of clinical presentations. We report a group of 21 cirrhotic patients with secondary peritonitis from intra-abdominal sources. Seven had infected ascites. All of them had unrecognized secondary peritonitis which was diagnosed and treated as spontaneous (primary) bacterial peritonitis (SBP). Ascitic fluid analysis yielded a mean white blood cell count of 23,750 +/- 10,935/cu mm with 91.5% polymorphonuclear leukocytes, significantly higher than patients surveyed with SBP, 1,757 +/- 2,154/cu mm (P less than .001). Ascitic fluid protein levels were also higher than those typically seen in SBP: 4.4 +/- 1.5 gm/dl vs 0.8 +/- 0.4 gm/dl (P less than .001). The ascites: serum protein ratio was consistent with an exudate in those patients with secondary peritonitis (0.7 +/- 0.2) in contrast to typically infected transudate in patients with SBP (0.15 +/- 0.05) (P less than .001). Bacteriologic determination was similar: single organisms with Escherichia coli the most common. Often the clinical features and ascitic fluid analysis will not differentiate spontaneous from secondary peritonitis. It is, therefore, clinically prudent to consider secondary bacterial peritonitis in cirrhotic patients, especially with ascitic fluid WBC counts in excess of 5,000/cu mm and protein levels of greater than or equal to 2.5 gm/dl. Noninvasive diagnostic procedures should be included to search for sources of intra-abdominal infection.

Anti-Bacterial Agents↗
PubMed1984

A calcified adenocarcinoma of the lung with very high CT numbers.

A case is reported of a man with a solitary pulmonary nodule that had an average CT number of 366 HU. Biopsy of the lesion demonstrated a primary adenocarcinoma of the lung with diffuse calcification. It is concluded that high CT numbers of solitary nodules do not ensure a benign lesion.

Adenocarcinoma↗
PubMed1983

Prophylactic use of lidocaine to prevent advanced ventricular arrhythmias during pulmonary artery catheterization. Prospective double-blind study.

To determine whether prophylactic lidocaine could decrease the incidence of advanced ventricular arrhythmias, 62 patients undergoing 67 pulmonary artery catheterizations were given lidocaine or placebo before and during catheterization. Advanced ventricular arrhythmias occurred in 42 of the 67 catheterizations (63 percent). In 18 of 31 patients receiving lidocaine (58 percent) arrhythmias developed, whereas 24 of 36 patients who received placebo (67 percent) had evidence of arrhythmias. These differences were not significant. However, patients with catheterization times of less than 20 minutes who were treated with lidocaine had less ectopy (25 percent) than patients treated with placebo (68 percent) (p less than 0.05). Two patients has sustained ventricular tachycardia and both were receiving placebo. No complications of lidocaine prophylaxis were noted. Prophylactic lidocaine appears to decrease the incidence of mechanically induced arrhythmias in critically ill patients undergoing catheterization that is not prolonged.

Adult↗
PubMed1983

The adult respiratory distress syndrome.

The adult respiratory distress syndrome (ARDS) is an extreme form of noncardiogenic pulmonary edema associated with alveolar-capillary damage. Clinical features include acute respiratory distress, dyspnea and tachypnea, severe hypoxemia refractory to oxygen therapy, and diffuse bilateral pulmonary infiltrates. Any number of serious disorders can cause ARDS, but the processes leading to the alveolar permeability defect are not understood. Therefore, therapy remains nonspecific and supportive. Treatment includes positive end-expiratory pressure, careful fluid management, steroid therapy, and adequate nutrition. Unfortunately, even with the most sophisticated intensive care, the mortality of ARDS is still greater than 50%.

Adult↗
PubMed1982

Advanced ventricular arrhythmias during bedside pulmonary artery catheterization.

To determine the incidence of advanced arrhythmias and acute right bundle branch block during beside pulmonary artery catheterization, 119 critically ill patients undergoing 150 pulmonary artery catheterizations were prospectively studied using continuous electrocardiographic monitoring with permanent recordings. Ventricular arrhythmias other than isolated premature ventricular contractions, couplets or bigeminy occurred during 80 of the 150 catheterizations (53 percent). These included ventricular salvos (three to five consecutive premature ventricular contractions) in 30 percent, nonsustained ventricular tachycardia (five to 30 premature ventricular contractions) in 20 percent and sustained ventricular tachycardia (more than 30 consecutive premature ventricular contractions) in 3 percent. In two patients, ventricular fibrillation developed; in another three patients, lidocaine or precordial thump was required to terminate the episodes of ventricular tachycardia. The incidence of advanced ventricular arrhythmias was statistically correlated with either the presence of predisposing risk factors for ventricular ectopy (p less than 0.05) or prolonged catheterization time (p less than 0.01). A new right bundle branch block developed in seven patients (5 percent) and persisted for a mean of 9.5 hours.

Adult↗
PubMed1982

Relation of colloid osmotic pressure to arterial hypoxemia and cerebral edema during crystalloid volume loading of patients with diabetic ketoacidosis.

The effect of crystalloid volume loading on serum colloid osmotic pressure, arterial oxygen (Po2), alveolar-arterial oxygen gradient (A-aDo2), and cerebral lateral ventricle dimensions was prospectively studied in 18 patients with diabetic ketoacidosis. Serial measurements showed concomitant decreases in colloid osmotic pressure, hematocrit, arterial Po2 (p less than 0.001), and significant increases in A-aDo2 (p less than 0.001) during treatment. Serial echoencephalograms were taken of 11 of the 18 patients; each patient served as his or her own control. Nine of these 11 patients showed significant decreases in lateral ventricle width during treatment; seven patients showed the echoencephalographic "hash" marks characteristic of cerebral edema. Follow up studies showed resolution of these abnormalities. Volume loading with large amounts of crystalloid solution seems to produce an acute hypooncotic state that may cause the development of both subclinical pulmonary and cerebral edema.

Adolescent↗
PubMed1981

Evidence for increased permeability in reexpansion pulmonary edema.

Concurrent analyses of the colloid osmotic pressure of pulmonary edema fluid and serum were performed in two patients with reexpansion pulmonary edema. In addition, pulmonary artery wedge pressure was measured during pulmonary edema in one patient. The colloid osmotic pressure of the pulmonary edema fluid was 73 and 81 percent of the serum value. The pulmonary arterial wedge pressure in one patient was within normal limits (8 mm Hg). Reexpansion pulmonary edema appears to be due to increased pulmonary capillary permeability rather than to hemodynamic mechanisms.

Adult↗
PubMed1981

The spectrum of pulmonary edema: differentiation of cardiogenic, intermediate, and noncardiogenic forms of pulmonary edema.

Pulmonary edema fluid and serum samples were obtained from 20 patients with cardiac and noncardiac pulmonary edema, and total protein, albumin, and globulin concentrations were measured. The mean edema fluid to serum protein ratio in patients with pure cardiogenic pulmonary edema was 0.37 +/- 0.09. In contrast, the patients with pure noncardiogenic pulmonary edema had protein ratios of 0.84 +/- 0.12 (p less than 0.001). Another group of patients with both cardiac and noncardiac causes for edema demonstrated edema fluid to serum protein ratios that were significantly higher than those found in the cardiogenic patients and lower than the protein ratios in the noncardiogenic patients (0.60 +/- 0.07) (p less than 0.01) A cardiac or noncardiac causes of pulmonary edema could be determined in all patients, using edema fluid to serum total protein ratios in conjunction with globulin ratios. Cardiogenic and noncardiogenic pulmonary edema represent the extremes in the spectrum of pulmonary edema. A combination of increased permeability and hydrostatic pressure may account for an intermediate form of pulmonary edema.

Adult↗