Biomedical subjects

H M Cryer

Publications and source records attributed to H M Cryer.

26 records · Page 2Linked to original sources

PubMed1987

Skeletal microcirculatory responses to hyperdynamic Escherichia coli sepsis in unanesthetized rats.

To determine the microvascular site of vasodilation during hyperdynamic sepsis, we measured arteriolar and venular responses to live Escherichia coli bacteremia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output (by thermodilution) increased, systemic vascular resistance decreased, and a differential arteriolar response occurred, with constriction of large arterioles and dilation of small terminal arterioles. We conclude that dilation of small terminal arterioles in skeletal muscle could contribute to decreased systemic vascular resistance during hyperdynamic sepsis. This may be an appropriate response to increased oxygen demand or decreased tissue utilization of oxygen. Alternatively, small-arteriole dilation may be an inappropriate response and secondary to release of vasoactive inflammatory mediators. If the latter is true, there is a potential therapeutic role for selective manipulation of the tone of small terminal arterioles in hyperdynamic sepsis.

Animals↗

PubMed1985

Effects of tissue acidosis on skeletal muscle microcirculatory responses to hemorrhagic shock in unanesthetized rats.

Arteriolar dilatation, loss of venous tone, and uptake of shed blood characterize decompensated hemorrhagic shock. The loss of compensatory constrictor responses to hemorrhage mainly occurs in the skeletal muscle microcirculation. Tissue acidosis may be an important mediator of this phenomenon. Using a decerebrate in vivo rat cremaster muscle preparation, we observed the microcirculatory responses to hemorrhagic hypotension with cremaster bath conditions of pH 7.4 and pH 7.0. Our data indicate that tissue acidosis attenuates constrictor responses of larger arterioles (100-170 micron) and venules to hemorrhagic hypotension but has no effect on the dilator responses of small arterioles (10-30 micron). We conclude that tissue acidosis contributes significantly to loss of arteriolar resistance and to decreased venous return in the decompensatory phase of hemorrhagic shock.

Acidosis↗

PubMed1985

Liver cirrhosis and biliary surgery: assessment of risk.

Operations on the biliary tract in cirrhotic patients are reported to have a higher than normal risk of operative morbidity and mortality. We reviewed 39 cases from two university-based hospitals over a five-year period. Each patient had biliary tract surgery and biopsy-proven cirrhosis. Eight patients died (21%), and major complications were found in 12 surviving patients (35%). Local and systemic sepsis was the major contributor, accounting for all of the deaths and 17 of the 22 (77%) complications among survivors. Choledochotomy was done in ten patients; three of them died (30%) and nine major complications occurred in the remaining five. Preoperative risk factors found to be predictive of this high morbidity and mortality were ascites (50% mortality, 50% morbidity), prolonged prothrombin time (29% mortality, 38% morbidity), and a serum albumin level of less than 3.5 mg/dl (33% mortality, 40% morbidity). The presence of other major systemic disease was not significantly different between survivors and nonsurvivors. In 12 patients with no ascites and normal preoperative serum chemistry values, no deaths and only one minor complication occurred. We conclude that although biliary surgery in cirrhotic patients carries a high mortality, this risk can be assessed preoperatively. There appears to be a small subgroup of patients with cirrhosis and cholelithiasis who can have a favorable outcome. Operative therapy in these patients should be reserved for the complications of the biliary tract.

Ascitic Fluid↗

PubMed1984

Clarification of risk factors for abdominal operations in patients with hepatic cirrhosis.

Celiotomy in cirrhotic patients is reported to bear a high risk of operative morbidity and mortality. We reviewed 100 consecutive, cirrhotic patients who underwent nonshunt celiotomy. Thirty patients died and major complications occurred in another 30 patients. Hospital mortality rate was 21% in 39 biliary operations, 35% in 26 procedures for peptic ulcer disease, and 55% in nine colectomies . Fifty-two variables were compared between survivors without complication, survivors with complications, and nonsurvivors. A computer-generated, multivariant discriminant analysis yielded an equation predictive of survival. Utilizing coagulation parameters, presence of active infection, and serum albumin, the equation predicted survival with 89% accuracy. In a similar fashion, amount of operative transfusions, absence of postoperative ascites, pulmonary failure, gastrointestinal bleeding, and culture-positive urine predicted survival with 100% accuracy. We conclude that celiotomy in the cirrhotic patient is truly associated with very high morbidity and mortality, and preoperative assessment can predict survival with 89% accuracy.

Abdomen↗

PubMed1984

Approaches to the management of shotgun injuries.

Shotgun wounds present specific challenges for the surgeon. Multiple penetrating wounds frequently involve large anatomic areas with potential multi-system injury. Experience with 121 patients sustaining shotgun wounds over the 5-year period ending 31 December 1981 was reviewed to assess results and evaluate treatment protocols. Sixty-six patients had chest wounds with pleural penetration. Twenty-four wounds were minor and were observed. Each had less than five pellets penetrating the pleura. Twenty-two patients had close-range injuries. Fourteen of these required chest tube drainage alone and eight patients required thoracotomy for control of bleeding. Eleven patients died, six as a direct result of the chest injury. In 55 patients with abdominal-retroperitoneal wounds exploratory operations were done if more than four pellets were thought to be lodged intraperitoneally or if signs of peritonitis were present, while lesser wounds without peritoneal findings were observed. In the 15 patients who did not have exploratory operations, there were no deaths or major complications. Thirty-five patients had exploratory operations. Two patients had five intraperitoneal missiles and no clinical evidence of peritonitis but were found to have significant intestinal perforations. Four patients died. Eighty-three patients with extremity wounds were classified according to location of injury. Forty-five had upper extremity wounds, with nine vascular injuries. Two patients died and one limb was amputated because of soft tissue infection. Thirty-eight patients had lower extremity wounds. Five had major vascular injuries. Preoperative arteriography was obtained in 13 patients with extremity injuries; the results of one of these were falsely negative. There were no deaths or amputations.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdominal Injuries↗

PubMed1984

Microcirculatory norepinephrine constrictor response in hemorrhagic shock.

Hemorrhagic shock is characterized by a phase of compensation that preserves central blood flow and intravascular pressure through an integrated vasoconstrictor response mediated by catecholamines, particularly norepinephrine (NE). The skeletal muscle microcirculation is important in this response. Decompensation occurs when arteriolar vasodilation occurs despite continued hypovolemia and high circulatory levels of NE. Using an isolated decerebrate rat cremaster muscle, we measured constrictor response to NE (10(-7)M tissue concentration) in compensated and decompensated shock. Our data indicate that larger arterioles (143 to 152 microns) show persistent constrictor response with lowered sensitivity to NE. Smaller arterioles (11 to 22 microns) and all venules dilate late in shock but retain constrictor responses to NE. Dilator responses contribute to decompensation in small arterioles and venules but not because of altered NE constrictor response.

Animals↗

PubMed1983

Effects of electrolyte or colloid infusion on the injured lung.

Diffuse lung injury (acid aspiration) and a modest intravascular volume deficit (15% total blood volume) were produced in mongrel dogs. Replacement of lost volume was with shed blood plus an equal volume hydroxy ethyl starch (Group I) or shed blood plus balanced salt solution (3 ml/ml shed blood). Extravascular lung value (EVLW) measurements were used to quantitate edema formation and alveolar arterial oxygen gradient (A-a and O2) was monitored on a reflection of hypoxia. No significant differences were observed in A-a and O2 between groups despite a significantly larger amount of pulmonary edema in Group I (hydroxy ethyl starch).

Animals↗

PubMedDate not supplied

Brain injury causes loss of cardiovascular response to hemorrhagic shock.

The combined cardiovascular effects of hemorrhagic shock and mechanical brain injury were modeled in five groups of pigs. Standard and hypertonic saline resuscitation of hypotension were evaluated. Changes in mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), intracranial pressure (ICP), and brain water were measured. Brain injury (BI) was produced with a fluid percussion device that generated an extradural pressure of 3.5 x 10(5) N/m2 for 400 msec. Shock was caused by bleeding to a MAP of 60 mm Hg for 60 minutes and then resuscitated with shed blood only or shed blood plus 0.9% or 1.8% saline. Brain-injured only and shocked-only pigs served as controls. We found that brain injury alone caused refractory hypotension. Less shed blood was required to produce shock in brain injured animals (p < .05). Shock accompanied by brain injury was not reversed with crystalloid solutions. Volumes of saline required to restore blood pressure were large (> 6 L in 3 hours). 1.8% saline produced less rise in ICP than 0.9% saline but was less effective in restoring blood pressure. Brain edema was not decreased with 1.8% saline. Brain injury altered vascular compensation to hemorrhage and made accepted resuscitative measures ineffective.

Accidents, Traffic↗