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Biomedical subjects

R N Garrison

Publications and source records attributed to R N Garrison.

At least 109 records · Page 6Linked to original sources

Terminal loop cutaneous ureterostomy in cadaveric kidney transplantation.

The presence of a nonfunctional bladder is a common finding in some patients with end-stage renal disease in whom transplantation is a proposed option. Over the last 20 years, we have performed six terminal loop cutaneous ureterostomies for urinary drainage during kidney transplantation. Neurogenic bladder in five patients and exstrophy in one patient prohibited use of the bladder. Four long-term graft survivors (19 months and 4, 10, and 20 years) experienced no short-term problems with the procedure, but two episodes of pyelonephritis have occurred. In our patients no graft dysfunction or loss could be attributed to infection, and no stomal stenosis or revision has occurred. We conclude that terminal loop cutaneous ureterostomy is feasible using normal-caliber ureters, and is a safe, effective means of urinary drainage during kidney transplantation when the bladder is not available. It also eliminates the necessity of preparatory bowel surgery that has its attendant risk of contamination in an immunocompromised patient.

Adult↗

Great expectations: stress and the medical family. 1987 Committee on Issues, Association for Academic Surgery.

The high divorce rate and significant stress experienced by families of academic surgeons stimulated the Committee on Issues of the Association of Academic Surgery to choose medical family stress as the topic for the 1987 Committee presentation at the annual meeting. The Committee hoped to provide insight into the cause of this stress and new strategies for coping with this pervasive problem. Forty-three percent of the 505 surgeons who entered the Association from 1981 through 1984 and 38% of their spouses responded to a questionnaire covering issues of time management, response to stress, child rearing, financial security, and spouse career. A panel consisting of Shirley P. Levine, M.D., Hiram C. Polk, Jr., M.D., and Lane A. Gerber, Ph.D., after discussing the questionnaire results, recommended realistic goal setting, specific prioritization of activities, recognition of the considerable contributions of the spouse, and insight into personal limitations as mechanisms for improving family function.

Female↗

Hypertension alters microvascular responses in skeletal muscle to hyperdynamic bacteremia and hypodynamic Escherichia coli sepsis.

Altered vascular reactivity to numerous vasoactive substances in hypertension formed the basis for studying the in vivo microcirculation of skeletal muscle tissue during high cardiac output bacteremia and low cardiac output sepsis. Large and small arteriole and venule diameters of the cremaster muscle were measured via videomicroscopy in normotensive and 1K-1C-renovascular hypertensive rats before and after the infusion of live Escherichia coli bacteria. During hyperdynamic bacteremia and during hypodynamic sepsis, large arterioles constricted and small arterioles dilated in normotensive animals. During hyperdynamic bacteremia, this differential arteriolar response was blunted in hypertension. In hypodynamic sepsis, large arterioles did constrict in the hypertensive animals, but small arteriolar dilation was still blunted. Sodium-nitroprusside, a postreceptor acting agent applied locally, maximally dilated small arterioles to the same level in all groups to indicate that the ability of vascular smooth muscle to relax is intact in hypertension. We conclude that the failure of the small arterioles to dilate during sepsis in hypertension is not due to a loss of vascular smooth muscle function, but that hypertension may functionally alter arteriolar reactivity at the receptor and/or endothelial level to interfere with E. coli-mediated responses in the skeletal muscle microvasculature.

Animals↗

Fractional change in blood volume following normal saline infusion in high-risk patients before noncardiac surgery.

Patients with multiple-system disease were considered to be at high-risk to develop cardiac complications when undergoing an elective noncardiac surgical procedure. Their operative risk was prospectively assessed by a protocol that included recording the presence of established clinical risk factors and measuring the hemodynamic response to an intravenous infusion of up to 2 L of normal saline given over a two-hour period. The day prior to their operations, 126 patients were admitted to the Surgical Intensive Care Unit, where pulmonary artery catheters were inserted without serious complications. One hundred and eleven patients tolerated the entire 2-L infusion. The hemoglobin concentration of blood was measured before and after the infusion. The fractional change in blood volume (BV after/BV before) calculated with hemoglobin data was 1.06 +/- 0.06 (mean +/- SD). A multivarient discriminant analysis showed that the fractional change in blood volume was a covariant with a higher correlation rank than the hemodynamic data in identifying patients at risk for an adverse outcome.

Aged↗

Hypoperfusion of the intestinal microcirculation without decreased cardiac output during live Escherichia coli sepsis in rats.

In order to determine the intestinal microvascular responses to normotensive, high cardiac output (CO) bacteremia, we measured vascular diameters and blood flow at different levels of the intestinal microcirculation during live E. coli bacteremia in male Sprague-Dawley rats (n = 16). Precollicular brainstem transection was used to allow study free of drug anesthesia. The microcirculation of a loop of small intestine (with intact neurovascular connections) was observed by in vivo video microscopy and optical Doppler velocimetry at a magnification of x1,500. Intraluminal microvessel diameters and red cell velocity were measured in successive branches until the vessel entered a villus. CO was measured by transpulmonary thermodilution. Intravenous infusion of 1 x 10(9) live E. coli caused a 20% increase in CO at 50 min and a 14% decrease in systemic vascular resistance. However, microvascular blood flow to the small intestine decreased by 27% at 1 hr and by 56% at 2 hr. Progressive arteriolar constriction (25-50%, P less than .05) occurred at all levels of the intestinal microcirculation. These data indicate that intestinal hypoperfusion caused by arteriolar constriction occurs during high CO bacteremia. This hypoperfusion could contribute to mucosal injury and intestinal mucosal barrier dysfunction during sepsis.

Animals↗

Role of the microcirculation to skeletal muscle during shock.

Our laboratory has performed a number of experiments to outline the role of the skeletal muscle microcirculation during hemorrhage and sepsis. We have suggested that the transition from the compensated to decompensated state in hemorrhagic shock could be attributed to the loss of vascular smooth muscle tone in small precapillary arterioles. This loss of tone is not due to a decrease in vascular smooth muscle reactivity to norepinephrine. However, tissue acidosis which is a uniform finding in the shock state contributes to this loss of vascular smooth muscle tone in large arterioles but not in small arterioles. The skeletal muscle responses to hyperdynamic sepsis were a mild constriction of large arterioles with a marked dilation of small vessels. It is this latter dilation which contributes to decreased systemic vascular resistance in sepsis. The microvessels reacted similarly in the hypodynamic septic state and do not appear to be responsible for the transition from the hyper- to the hypodynamic state in sepsis. The marked constrictor influence of large vessels seen in hemorrhage were not present in sepsis, indicating a possible vasodilator influence or loss of vasoconstrictor reactivity during sepsis but not hemorrhage. Similar findings were noted in both hyper- and hypodynamic endotoxemia suggesting that the energy metabolism effect of high dose endotoxin does not play a major role in skeletal muscle microvascular responses. Overall skeletal muscle vascular tone is due to a balance of vasoconstrictor influences that predominate in large arterioles which appear to be mediated by adrenergic nerve activity and vasodilator influences in small arterioles which are due to an escape from adrenergic nerve activity along with activation of local control factors by mediators of the inflammatory process, such as complement. The initial vasodilator response appears to be mediated by release of EDRF from the endothelial cell. Prostaglandins but not histamine or serotonin appear to be important in the initiation of vasodilation in small arterioles and in the modulation of existing vasoconstricting influences.

Acidosis↗

Differential response of the microvasculature in the liver during bacteremia.

To determine the initial hepatic microvascular responses to bacteremia, male Sprague-Dawley rats (n = 19) were decerebrated and the left liver lobe from each animal exteriorized and suffused with environmentally controlled Krebs solution. Direct in vivo videomicroscopy was used to measure diameter changes in at least four portal venules (PV) and four proximal periportal sinusoids (PS) at the inlet of hepatic lobules in each of seven livers or four terminal centrilobular sinusoids (CS) and four collecting central venules (CV) at the outlet in each of 12 livers during a baseline period and for 2 hr after intravenous (i.v.) infusion of 1 X 10(9) live Escherichia coli or saline (control). Cardiac output, systemic arterial blood pressure, and body temperature were monitored continuously during the experiments. These data indicate that E. coli bacteremia causes a redistribution of hepatic microvascular blood flow within the liver lobule at both the inlet and outlet regions with increased perfusion of certain microvascular segments and decreased perfusion of others. In the areas observed, a 2:1 dilated/constricted microvessel ratio suggests an initial increased overall liver blood flow within the first 2 hr of experimentally induced bacteremia.

Animals↗

Role of muscle microvasculature during hyperdynamic and hypodynamic phases of endotoxin shock in decerebrate rats.

Microcirculatory derangements in skeletal muscle could act to change cardiac output during endotoxemia. To explore this idea, we measured arteriole and venule responses to low-dose and high-dose endotoxemia in the rat cremaster muscle by direct in vivo videomicroscopy. Our data indicate that cardiac output increased in the low-dose group and decreased in the high-dose group. In both animal groups, a differential arteriolar response occurred to give small arteriole dilation and large arteriole constriction while venous diameters did not change. We conclude that: 1) changes in cardiac output during endotoxemia are not related to microvascular responses in skeletal muscle, and 2) the microvascular responses in skeletal muscle could be responsible for the decreased systemic vascular resistance during high cardiac output endotoxemia, but not for the elevated systemic vascular resistance during low cardiac output endotoxemia.

Animals↗

Prostaglandins maintain renal microvascular blood flow during hyperdynamic bacteremia.

Any beneficial effects of prostaglandin synthesis inhibitors on systemic hemodynamic derangements during sepsis may be offset by the effect of these inhibitors to reduce renal blood flow. To determine the specific role of prostaglandins in maintaining renal perfusion during hyperdynamic live Escherichia coli bacteremia in rats, we used in vivo video-microscopy and optical doppler velocimetry to quantitate changes in renal microvascular blood flow, and to determine if endogenous prostaglandins participate in these responses. E. coli infusions constricted preglomerular arterioles and decreased renal microvascular blood flow in decerebrate animals without drug anesthesia but dilated pre- and postglomerular arterioles in urethane-anesthetized rats. Local inhibition of renal prostaglandin production with mefenamate after E. coli infusion caused renal arteriolar constriction in both groups and decreased renal blood flow to indicate that renal prostaglandin production is an important mechanism for maintenance of renal microvascular blood flow during high cardiac output sepsis.

Animals↗

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↗

Emergency right colon resection.

Controversy exists over the management of the stoma following emergency right colonic resection. To define the stoma management following colon resection, 70 patients who underwent an emergency right colectomy were studied retrospectively. Thirty-six underwent a primary anastomosis and 34 received a diversion with an ileostomy. Indications for resection were as follows: penetrating injury, 28 patients; blunt injury, five patients; obstruction, 13 patients; perforation, 15 patients; vascular injury, seven patients; and hemorrhage, two patients. The mortality was equal in both groups (21%). Severe morbidity directly related to the ileostomy was noted in six patients (18%), and three leaks (8%) were noted in the anastomotic group. High mortality continues to be associated with emergency right colon resection, regardless of the indication for the procedure. This high death rate is not lowered by diversion in deference to an anastomosis.

Adult↗

Mechanisms of malignant ascites production.

The accumulation of malignant ascites is determined primarily by the obstruction of diaphragmatic lymphatics with tumor inhibiting the outflow of peritoneal fluid. An abnormal increase in peritoneal fluid production has been shown to contribute to ascites formation by a marked neovascularization of the parietal peritoneum. Cell-free malignant ascitic fluid obtained from rats with intra-abdominal Walker 256 carcinoma when infused into the peritoneal cavities of normal animals causes an increase in edema formation and an increase in the permeability of protein from normal omental vessels. Protamine sulfate, a known inhibitor of angiogenesis when infused into the peritoneal cavity along with cell free malignant ascitic fluid, significantly reduces the leak of protein from the intravascular space when compared to ascites alone. Persistent permeability changes continue to exist even after the inhibition of vessel proliferation. These results indicate that angiogenesis is responsible for a major portion of the increase in permeability caused by malignant ascitic fluids. Other tumor-induced factors may be present which alter vascular permeability by other mechanisms which remain to be elucidated.

Animals↗

Malignant ascites. Clinical and experimental observations.

Malignant ascites formation is a grave prognostic sign, but palliative efforts seem justified in some patients. Lack of knowledge concerning the natural history of this process hinders the choice of therapeutic options. Over 5 years, 107 patients with untreated malignant ascites were reviewed to define their survival. Pancreas (20), ovary (18), and colon (18) were the most frequent tumors, with 52% of patients presenting with ascites at the time of the initial cancer diagnosis. Cytology evaluation of the ascitic fluid was positive for tumor cells in 57% of cases and a high protein content was noted in 65%. Mean survival of the entire series was only 20 weeks from the time of diagnosis of ascites, with tumors of ovarian and lymphatic origin having better mean survivals of 32 and 58 weeks, respectively. Patients with high ascitic protein levels fared better than those with low levels. In an effort to explain this correlation of elevated protein levels and a favorable survival rate, a hypothesis was proposed that certain tumors secrete a factor, which alters vascular permeability and causes fluid accumulation in the absence of lymphatic obstruction. In an experimental rat model of malignant ascites, the intraperitoneal infusion of cell-free malignant ascitic fluid caused an increase in edema formation and a significant increase in capillary permeability to protein in the omentum. This demonstrated change in the leak of protein explains the formation of ascites by some tumors in the absence of tumor obstruction of the draining lymphatics of the peritoneal cavity and suggests another important mechanism in the genesis of malignant ascites.

Adult↗

Experimental bacteremia and hepatic nutrient blood flow.

To study altered hepatic nutrient blood flow during the early phases of bacteremia, Sprague-Dawley rats (250-350 gm) underwent carotid cannulation; 24 hr later, they received an intravascular infusion of 2.5 X 10(8) Escherichia coli (LD70) over 45 min. Controls were anesthetized and cannulated only. Experimental and control animals then received a flow-dependent dose of indocyanine green (5 mg/kg) via the cannula, and arterial blood was sampled at 3, 4, 5, 6, 7, and 8 min after. Separate groups of animals were studied at 3 and 6 hr after bacteremia. The half-life (t1/2) of indocyanine green clearance was then determined at each time period, with t1/2 representing an estimation of total hepatic nutrient blood flow. Results indicated a prolonged t1/2 at both time periods in the bacteremic rats. Hepatic histology from plastic-embedded sections appeared to reveal fibrin, platelets, and leukocyte fragments within the sinusoids. From these data, we conclude that reduced nutrient blood flow occurs during experimental bacteremia prior to systemic changes of arterial pressure.

Animals↗

Candida sepsis. Implications of polymicrobial blood-borne infection.

Eighty-three patients with 117 episodes of candidemia were reviewed to examine the clinically significant variables and the results of treatment for this problem. Mortality was 52%. Patients who had bacteremia either synchronously or metachronously in association with Candida species had poorer survival rates. Staphylococcal and enterococcal species were the most frequently associated bacteria. Patients with Candida parapsilosis had better survival rates than patients with other species. Portals of entry for fungemia were catheters, wounds, the urinary tract, and the peritoneal cavity, but were undefined in 54% of patients. Antifungal chemotherapy could not be identified as affecting the outcome in these patients. It is suggested that candidemia in most patients represents a failure of host defense, and that septicemia of either bacteria or fungi may arise from the gastrointestinal tract in critically ill, immunocompromised patients.

Adolescent↗

Bacterial synergism between the enterococcus and Escherichia coli.

The pathogenicity of the enterococcus in surgical infections remains unclear. To examine this issue, rats received an intravascular infusion of 10(9) enterococcus. No rats died. Rats that received a sublethal inoculum of Escherichia coli with 5 X 10(8) enterococcus had a 40% mortality (P less than 0.05). Cutaneous infections in rabbits with E. coli, Bacteroides fragilis, and enterococcus were examined singly and in combination. Infections with E. coli measured 21 +/- 1 mm, with enterococcus were 15 +/- 1 mm, and with B. fragilis were 9 +/- 1 mm in diameter. When E. coli and enterococcus were combined together, significantly larger cutaneous infections were noted (P less than 0.05). No apparent synergism existed between the enterococcus and B. fragilis. These data indicate a synergistic relationship between the enterococcus and E. coli.

Animals↗

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↗