Richard C. Schaeffer

Some pharmacological properties of the venom of the scorpionfish Scorpaena guttata—II☆

Abstract Labile components of California scorpionfish venom produce marked respiratory and hemodynamic changes in cats, rabbits and dogs. The venom affects respiratory rate, causes bronchoconstriction and pulmonary edema; large doses cause respiratory arrest. The venom produces arterial hypotension within 15 sec, followed by a period of increased pressure. The hypotension represents a major distributive defect of blood volume in the peripheral circuit due to a defect in arterial resistance most likely due to the release of endogenous acetylcholine. This effect can be inhibited by pretreatment with atropine. Other prominent alterations include pulmonary artery hypertension, elevation of left ventricular end-diastolic pressure, portal venous hpertension, ECG changes, elevation of the packed cell volume and initial augmentation of systemic venous return. It is most likely that the venom acts through a combination of direct actions, neurogenic reflex mechanisms and effects induced by the liberation of autopharmacological substances.

Cardiovascular failure produced by a peptide from the venom of the Southern Pacific rattlesnake, Crotalus viridis helleri

Abstract R. C. Schaeffer, Jr. , T. R. Pattabhiraman , R. W. Carlson , F. E. Russell and M. H. Weil . Cardiovascular failure produced by a peptide from the venom of the Southern Pacific rattlesnake, Crotalus viridis helleri . Toxicon 17 , 447–453, 1979.—Hemodynamic, metabolic and respiratory effects of a 30 min i.v. infusion of crude venom (1·4 mg/kg) and three venom components (Peptide I, 0·5 mg/kg; Protein I, 1·2 mg/kg, Protein II, 3·4 mg/kg) were studied in 24 sedated rats (270–309 g). Venom shock, characterized by hypotension, lactacidemia, hemoconcentration, hypoproteinemia and death was observed in animals given the crude venom or Peptide I. Just prior to death, respiratory distress was observed in most animals that died. Hemolysis and hematuria were observed in the animals given Protein I or Protein II. These data suggest that the increase in vascular permeability to protein and red blood cells induced by the crude venom can, for the most part, be attributed to the peptide. In addition, Protein I and Protein II appear to account for the hemolytic activity. The toxic effects of the venom components appear to be synergistic.

Effects of colloid or crystalloid solutions on edemagenesis in normal and thrombomicroembolized lungs.

We studied the effects of crystalloid (75 ml/kg of Ringers lactate) or colloid (6% dextran-70, 6% hydroxyethyl starch, or 25 ml/kg of 5% human serum albumin) fluid infusions or no treatment (control) on the calculated lung capillary (Pc)-plasma oncotic pressure (pi c) gradient and pulmonary edema. Two sets of mongrel dogs were studied: uninjured (n = 25; 14 to 22 kg) and pulmonary fibrin-microembolized (n = 25; 15 to 23 kg). In both sets of experiments, left atrial pressure was controlled (15 mm Hg) throughout the 4-h plus experimental period. In the uninjured set, the Pc-pi c gradient averaged +1.0 and -0.2 mm Hg in the hydroxyethyl starch and dextran groups, +0.7 and +2.3 mm Hg in the human serum albumin and control groups, and +6.2 mm Hg in the Ringers lactate group. In the fibrin-microembolized group, this gradient averaged 2.6, 2.4, 3.0, 5.3, and 9.5, respectively. The extravascular lung water to bloodless dry lung wet weight ratios in the no-fluid treatment group of the uninjured and microembolism groups with increased pressure (3.8 +/- 0.3 to 4.1 +/- 0.4 [SEM]; NS) are consistent with interstitial or perivascular edema. There were, however, no significant differences noted between the respective control groups or any fluid treatment group in either set of experiments. These data support the view that infusion of either colloid or crystalloid solutions in normal or pulmonary fibrin-microembolized lungs does not produce sufficient change in the Pc-pi c gradient to elevate edemagenesis when pulmonary capillary pressure is limited to 22 mm Hg in dogs.

Shock due to profound hypothermia and alcohol ingestion: Report of two cases

Cardiovascular failure (shock) associated with acute alcohol ingestion and severe hypothermia (core temperature 23 and 21°C) was studied in 2 patients. In each case, perfusion failure was associated with lactacidemia, severe bradycardia, and agonal respirations. Infusion of fluids and mechanical ventilation reversed shock and prevented a fatal outcome. One case, complicated by renal failure and volume overload with pulmonary edema, was managed with peritoneal dialysis. These findings suggest that perfusion failure associated with severe accidental hypothermia after acute alcohol ingestion is due to a combination of hypovolemia, bradycardia, and respiratory depression.

Cardiorespiratory effects of volume overload with colloidal fluids in dogs.

Mongrel dogs (n = 31, 17–28 kg) were rapidly given (iv, 30 min) an infusion (75 ml/kg) of 6% dextran-70 (DEX, n = 9), 6% hydroxyethyl starch (HES, n = 7), or 5% human serum albumin (ALB, n = 6) to elevate pulmonary artery wedge pressure (WP) in an effort to simulate left ventricular failure as a method for study of pulmonary edema and the cardiopulmonary effects of these fluids. A control group (CON, n = 9) received only 50 ml/h of 0.9% NaCI over the 2-h experiment. Colloidal fluids produced marked increases (p < 0.05) in cardiac index (CI), WP and plasma oncotic pressure (COP) with hemodilution. Although the increase in CI was less marked after DEX, no significant differences in CI were observed between the DEX, HES and ALB groups. DEX led to a significantly (p < 0.01) higher WP than HES or ALB throughout the study. Immediately after infusion of DEX, COP was greater (p < 0.05) than after HES or ALB. Subsequently, there was no difference in COP among the fluid groups. DEX and HES led to comparable plasma volume expansion that was greater (p < 0.05) than ALB. Mean arterial pressure (MAP) and heart rate (HR) were little affected for any of the groups. The lung wet/dry weight ratios for HES and ALB were slightly (p = ns) higher than CON, although the ratio for DEX was significantly greater than all other groups. These data suggest that rapid volume overload with DEX leads to higher pulmonary pressures and a high lung wet/dry weight ratio. An increase in permeability to macromolecules after DEX is suggested in some animals. HES produces a similar plasma volume expansion as DEX, but pulmonary vascular pressures after HES parallel those of ALB and the amount of lung edema after this volume of HES or ALB is small.

Acute Respiratory Failure in the Critically Ill: “Shock Lung”

Pulmonary failure has emerged as the single most lethal complication in the practice of critical care medicine. “Shock lung” or “adult respiratory distress syndrome” (ARDS) represents a clinical constellation often referred to as “shock lung.” The purpose of this chapter is to review some of the current concepts of the pathophysiology and principles of management of acute respiratory failure (ARF) following shock or complicating a critical medical or surgical illness. Our own studies have been with special emphasis on fluid accumulation in the lung.