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Biomedical subjects

P O Park

Publications and source records attributed to P O Park.

9 recordsLinked to original sources
PubMed1997

Surgical outcome and cost-minimisation-analyses of laparoscopic and open hernia repair: a randomised prospective trial with one year follow up.

OBJECTIVE: To compare outcome and costs between laparoscopic and open hernia repair. DESIGN: Prospective randomised study. SETTING: One university and two district hospitals in Sweden. SUBJECTS: 200 men aged 25-75 years. MAIN OUTCOME MEASURES: Operating time, hospital stay, complications, and time to recovery. A cost-minimisation-analysis was used in which the total costs were calculated for a defined period of time for each option. RESULT: The one year follow-up rate was 98%. Mean (SD) operation times in the laparoscopic and open groups were 72 (30) and 62 (25) minutes, respectively (p = 0.009). Hospital stay and complication rates did not differ between the groups. Among employees the mean (SD) periods off work in the laparoscopic and open groups were 10 (8) and 23 (21) days, respectively (p = 0.0001). The mean direct costs of the laparoscopic operation were increased by SEK 4037 (US$ 483) but the savings in indirect costs resulting from earlier return to work were SEK 11392 (US$ 1364). CONCLUSIONS: Laparoscopic hernia repair gave the employed patients faster recovery and return to work, and was the most cost-effective strategy provided that both direct and indirect costs were included.

Adult↗
PubMed1994

Effects of a novel 21-aminosteroid or methylprednisolone in experimental total intestinal ischemia.

OBJECTIVE: To investigate whether tirilazad mesylate, a 21-aminosteroid, protects the small intestinal mucosa from injury following total warm or cold ischemia and reperfusion. DESIGN: Randomized vehicle-controlled experimental study. SETTING: A university department of surgery. ANIMALS: Wistar rats. The warm ischemia series preceded the cold ischemia series. Animals were randomized within each series. Microscopic evaluation was performed on coded tissue slides. INTERVENTIONS: Warm ischemia was induced by a hydrostatic pressure cuff inflated to 10 mm Hg above the systolic arterial pressure for 60 minutes. Cold ischemia was studied after small intestinal transplantation. The transplant was stored for 5 hours in University of Wisconsin solution at 8 degrees C. Ischemia was followed by 60 minutes of reperfusion. In both series, tirilazad mesylate (3 mg/kg) or methylprednisolone sodium succinate (30 mg/kg) was given. Controls were given tirilazad vehicle or saline solution. MAIN OUTCOME MEASURE: Microscopic grade of small intestinal mucosal injury. RESULTS: Mucosal injury was evident in all groups of animals that were subjected to warm or cold ischemia. Reperfusion following cold ischemia induced a significant reperfusion injury. Neither tirilazad nor methylprednisolone protected the small intestinal mucosa during ischemia or reperfusion. CONCLUSION: Mucosal injury following warm or cold intestinal ischemia and reperfusion is caused by factors other than or in addition to lipid peroxidation, which is preventable by use of a 21-aminosteroid.

Animals↗
PubMed1992

Regeneration of small bowel mucosa after intestinal ischemia.

BACKGROUND AND METHODS: The objective of this study was to evaluate the histologic reconstitution of the small intestinal mucosa after a standardized ischemic injury and to determine if the early repair process takes place by cell renewal or migration of existing mucosal cells. Therefore, male Wistar rats, weighing 190 to 320 g, were subjected to total warm intestinal ischemia by means of a hydrostatic pressure clamp for 45 or 90 mins. These rats were compared to sham-operated controls. Intestinal biopsies were obtained just before reperfusion and at various times up to 48 hrs thereafter. Mucosal injury was evaluated microscopically by a blinded examiner. RESULTS: Variable mucosal reconstitution occurred within 3 hrs, after 45 mins of ischemia, whereas mucosal repair required up to 18 hrs after 90 mins of ischemia. In a second series of experiments, 45 or 90 mins of ischemia and 5 hrs of reperfusion were followed by the iv administration of radioactively labeled thymidine. Intestinal biopsies were taken 1 hr later and prepared for autoradiography. No increase in mucosal mitoses was observed. CONCLUSIONS: The mucosal reconstitution occurred rapidly after 45 mins and 90 mins of total warm intestinal ischemia and primarily through mucosal cell migration.

Animals↗
PubMed1991

Cold ischemic and reperfusion injury in a model of small bowel transplantation in the rat.

Following 0, 5, or 18 h of cold ischemia in the University of Wisconsin or Sacks' solution syngenic small bowel transplantation was performed to the renal vessels. Mucosal injury during ischemia or at reperfusion was evaluated microscopically using a grading scale from 0 to 8. The series subjected to small bowel transplantation without cold ischemia showed superficial damage to the tips of the villi (median grade 2) with no further exacerbation at reperfusion and complete healing 24 h thereafter. Moderate villous injury (median grade 3) was demonstrated following 5 h of cold ischemia. This injury was exacerbated to grade 4 (p less than 0.05) following reperfusion but was almost completely healed 24 h later. Grade 4 tissue injury was seen following 18 h of cold ischemia without further exacerbation at reperfusion and no clear tendency to healing 24 h later.

Animals↗
PubMed1990

The influence of a histamine2-receptor antagonist on the healing of an experimentally induced gastric mucosal lesion.

The effect of an H2-receptor antagonist (ranitidine) on the healing of gastric mucosal lesions was studied. Mucosal lesions were induced by a standardized thermo-mechanical technique. The healing process was assessed by macro- and light microscopical examination. It was further evaluated by measurements of the tissue contents of hydroxyproline, a chemical compound reflecting collagen, and of DNA and RNA, reflecting cell frequency and protein synthesis respectively, in the gastric wall from both injured and wound-free areas. The healing process was more rapid in ranitidine-treated animals than in controls. After four weeks, however, the lesion in nine out of ten animals had healed in the ranitidine-treated group and seven of nine rats in the control group. At that time the amounts of hydroxyproline, DNA and RNA did not differ between the two groups. These findings may be taken as an indication that the tissue components of the healed lesions were similar in ranitidine-treated rats and in the saline controls, i.e. the different speeds of the healing process did not seem to influence the components of the scar tissue.

Animals↗
PubMed1990

The sequence of development of intestinal tissue injury after strangulation ischemia and reperfusion.

Tissue injury at reperfusion has been reported after partial ischemia. However, previous attempts to demonstrate a component of injury caused by reperfusion after total ischemia have failed. This study was performed to evaluate the hypothesis that in such situations the extent of the tissue injury caused by ischemia itself prevented detection of a reperfusion component. Rats were subjected to near-total intestinal ischemia by means of a hydrostatic pressure clamp that produced preferential venous occlusion (strangulation) for periods from 1 to 90 minutes. Tissue injury was evaluated microscopically by a blinded examiner. Ischemic periods of 20 minutes or less did not induce detectable tissue injury. Longer durations of ischemia caused villous injury: the longer the period of ischemia, the more extensive the tissue injury. However, there was no exacerbation of injury seen after reperfusion, regardless of the duration of ischemia. In a separate series of rats, total arterial occlusion was employed without concomitant venous congestion. Such isolation arterial occlusion of 40 to 60 minutes' duration was followed by a statistically significant exacerbation of tissue injury at reperfusion. Thus total intestinal ischemia may be followed by reperfusion injury if there is no concomitant congestion and if ischemic injury is not too extensive.

Animals↗