A prospective trial of primary inguinal hernia repair by surgical trainees.

The main hypotheses were that the Lichtenstein inguinal hernia repair has a lower recurrence rate and similar incidence of chronic groin pain compared to sutured repairs when performed by surgical trainees. In a U.S. Veterans Administration Hospital, 150 primary hernia repairs were randomized to a Lichtenstein, McVay, or Shouldice repair. The Shouldice repair included a routine relaxing incision. First- and second-year residents, under the supervision of an experienced general surgeon, performed the procedure. Long-term follow-up was obtained in 81% of patients. Hernia recurrence rate was Lichtenstein 8%, McVay 10%, Shouldice 5% ( P>0.1) at 6-9 years follow-up. More patients had chronic groin pain following Lichtenstein repair (38%) than after Shouldice repair (7%) ( P<0.05). More information is needed on long-term groin pain following anterior mesh repair. The Shouldice inguinal hernia repair may have a role in open primary herniorrhaphy to decrease the risk of chronic groin pain.

Interval breast cancers are not biologically distinct--just more difficult to diagnose.

BACKGROUND: Breast cancer diagnosed within 1 year of a negative annual screening examination is called interval breast cancer (IBC) and is considered to be a more virulent subtype of disease. METHODS: We reviewed clinical data on 24 women who were diagnosed as having IBC while participating in the Breast Cancer Detection Demonstration Project at Ellis Fischel Cancer Hospital and the Women's Cancer Control Program screening project in Columbia, Missouri, between 1974 and 1992. We reinterpreted mammograms from the visit prior to the diagnosis of IBC for possible misdiagnosis, changes suggestive of malignancy, and Wolfe's patterns. Archival paraffin blocks from 19 patients were used to determine qualitative expression of tumor markers. RESULTS: Observed 5-, 8-, and 10-year survival rates were identical to published data for patients with non-IBC. Seventy-four percent of the mammograms evidenced dysplastic Wolfe's patterns (P2 and DY), and one patient was found retrospectively to have shown evidence of cancer which was missed. Compared to breast cancers in general, fewer IBC tumors expressed tumor markers associated with poor prognosis. CONCLUSIONS: Survival rates and tumor marker expressions in this retrospective cohort suggest that IBC tumors are not more biologically aggressive than noninterval tumors. They are more difficult to diagnose both by physical examination and mammography.

Pressor responsiveness in rats with hypertension induced by mestranol.

The aim of this study was to determine if pressor hyper-responsiveness is associated with the hypertension that results from the ingestion of the synthetic estrogen, mestranol. Rats were fed a diet containing mestranol for 6 months, while control rats were fed the same diet without mestranol. Catheters were then placed in the carotid artery and jugular vein of all rats, under halothane anesthesia. When the rats had recovered from the anesthesia, blood pressure was measured through the carotid catheter in conscious rats. Each rat received IV injections of norepinephrine (NE) at 2, 4, 8, and 16 ng per 100 gm body weight, and the pressor responses were recorded. The rats fed mestranol had significantly higher arterial pressures than did the control rats. However, the pressor responses to NE were significantly less in the mestranol-treated rats than in the controls, indicating that pressor hyper-responsiveness does not contribute to this form of hypertension.

Effect on pressor and vascular responsiveness in rabbits of drugs that decrease norepinephrine uptake.

The purpose of this study was to determine if decreases in norepinephrine (NE) uptake would result in pressor and vascular hyperresponsiveness to vasoconstrictor substances. These experiments examined the effects of cocaine and imipramine, drugs known to decrease NE uptake, on the changes in arterial pressure and total peripheral resistance (TPR) in response to NE and arginine vasopressin (AVP) in conscious rabbits. The infusion of graded doses of NE resulted in significantly greater increases in mean arterial pressure at all dose levels following the administration of cocaine (0.6 mg/kg iv) or imipramine (0.5 mg/kg) than following the administration of the vehicle alone. The infusion of NE also resulted in greater increases in TPR as well as blood pressure following cocaine or imipramine administration than occurred prior to the administration of these drugs. The infusion of AVP caused significantly larger increases in arterial pressure and in TPR following cocaine or imipramine administration than was seen after the administration of AVP to control rabbits not treated with these drugs. These studies demonstrated that cocaine and imipramine, substances known to decrease NE uptake by the sympathetic nerve terminals, will induce pressor and vascular hyperresponsiveness to NE and AVP in rabbits. These results are in keeping with the concept that pressor and vascular hyperresponsiveness in renal prehypertensive rabbits may be the result of decreases in NE uptake by sympathetic fibers supplying vascular smooth muscle cells.

Arterial sodium concentration in rats with hypertension induced by mestranol.

Rats were made hypertensive by the oral ingestion of mestranol for 6 months. Carotid arteries from these hypertensive rats and from control rats were incubated in an extract of plasma from these rats, which contained 24Na and 14C-sucrose (an extracellular fluid marker). After sufficient time for equilibration, the vessels were removed and counted for 24Na; an aliquot of the incubation fluid was also counted for 24Na. At least 7 days later, after the 24Na had decayed away, the samples were counted for 14C-sucrose. By knowing the specific activity of the 24Na and the ratio of 24Na/14C in the bathing fluid, the amount of intracellular Na could be calculated for each carotid artery. The total protein content of each vessel was determined, and the results were expressed as nEq of Na per mg of vessel. The Na content of carotids from mestranol treated rats averaged 135 +/- 11 (SEM) while the carotids from the control rats averaged 125 +/- 8 nEq/mg protein. Because these values were not significantly different, this study provided no evidence that increases in arterial Na content contributed to the hypertension associated with the ingestion of mestranol in this rat model.

Not all "occult" papillary carcinomas are "minimal".

"Occult" papillary carcinomas are characterized as small papillary tumors of less than 1.5 cm in maximum diameter, with or without bulky metastatic deposits in cervical nodes. The primary lesion is usually not palpable, and although the clinical behavior usually follows a benign course, tumors with unfavorable histologic features (invasiveness, multifocality) or extrathyroidal disease or a combination of both may not do so. In this report six cases are presented to illustrate this entity. No patient had a history of irradiation to the head or neck. All had primary lesions smaller than 1.5 cm. None had a palpable nodule or abnormal thyroid scan results, and the diagnosis of thyroid cancer was based on cervical lymph node or lung biopsy specimens, which revealed papillary thyroid cancer. All of the patients underwent total or near-total thyroidectomies and were found to have small, invasive papillary lesions with additional metastases to cervical nodes noted at the time of thyroidectomy. Adjunctive treatment consisted of a 5 mCi iodine-131 scan, ablative iodine-131 therapy, and suppression with L-thyroxine. Although distant metastasis to lung or other organs is uncommon and the mortality rate is low (as in larger papillary cancers), these invasive lesions--despite their small size--have a high propensity for recurrence and should be considered to behave more like encapsulated papillary tumors with extrathyroidal extension than like their small, unencapsulated intrathyroidal counterparts.

Early postoperative function of suppressed parathyroid glands with microscopic hyperplasia.

Calcium-parathyroid hormone (Ca-PTH) relationships were studied perioperatively in 35 patients with primary hyperparathyroidism. Twenty-nine patients had solitary adenomas that caused preoperative hypercalcemia; those patients whose remaining glands were subjected to biopsy were classified as having either microscopic evidence of suppression in those glands (15 patients) or no evidence of suppression (less than or equal to 30% stromal fat on biopsy cross sections, 11 patients). Before surgery, all patients showed the expected positive slopes for Ca-PTH linear regression curves. After surgery, all patients with adenomas showed an immediate and sustained shift of the Ca-PTH regression to the right; this shift achieved statistical significance only in those patients whose remaining glands showed microscopic evidence of suppression (greater than 30% fat, p less than 0.05). Moreover, the slope of the Ca-PTH regression curve for these patients assumed a negative value 1 month after surgery. All patients with adenomas were eucalcemic after surgery, regardless of the cellularity of the remaining in situ glands. We conclude that the absence of microscopic suppression in grossly suppressed parathyroid glands at the time of adenoma resection for hyperparathyroidism does not affect postoperative results. However, the presence of microscopic hyperplasia in macroscopically normal or suppressed glands may represent a persistent alteration in biologic function, evidenced by failure of these glands to achieve negative calcium regulation.

Angiotensin receptors and pressor hyperresponsiveness in renal prehypertensive rabbits.

This study consisted of five different experiments with conscious rabbits. In experiment 1, the angiotensin II (ANG II) antagonist [Sar1-Ala8]ANG II infused iv into one-kidney rabbits with renal artery stenosis (RAS) of 3 days' duration, at a dose that blocked pressor responses to ANG II, did not decrease the exaggerated pressor responses to norepinephrine (NE). In experiment 2, captopril infused iv into one-kidney, 3-day, RAS rabbits blocked pressor hyperresponsiveness to NE, and the concurrent infusion of [Sar1-Ala8]ANG II did not reestablish pressor hyperresponsiveness, indicating that this ANG II analogue had no agonistic action to promote hyperresponsiveness to NE. In experiment 3, infusion of ANG II at a subpressor dose (6.7 pmol . min-1 . kg body wt-1) into normal rabbits resulted in pressor hyperresponsiveness to NE, which was blocked by [Sar1-Ala8]ANG II. Experiment 4 involved infusing [Sar1-Ala8]ANG II or [Sar1-Ile8]ANG II at various doses into 3-day RAS rabbits, to determine their abilities to attenuate the pressor responses to ANG II (100 ng/kg) and the pressor hyper-responses to NE (800 ng . min-1 . kg-1). [Sar1-Ile8]ANG II decreased the ANG II pressor responses at an ID50 dose of 64 +/- 5 (SEM) pmol . min-1 . kg-1 and attenuated the NE pressor hyper-response at an ID50 dose of 65 +/- 5 pmol . min-1 . kg-1; [Sar1-Ala8]ANG II diminished the ANG II pressor response at an ID50 dose of 757 +/- 247 and the NE pressor hyper-response at an ID50 dose of 10,061 +/- 944 pmol . min-1 . kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Thallium-technetium parathyroid scan. A useful noninvasive technique for localization of abnormal parathyroid tissue.

We studied the usefulness of the thallium-technetium scan in 60 patients with suspected parathyroid disorders. The scan correctly localized abnormal parathyroid tissue in 82% of patients with surgically proved primary hyperparathyroidism due to a single adenoma and in 60% of patients operated on for primary hyperplasia. The scan was particularly useful in patients who had undergone previous neck explorations, since it successfully identified residual adenomatous or hyperplastic tissue in six of seven patients. False-positive images were consistently produced in all patients with coexisting thyroid disease. We conclude that the thallium-technetium scan is useful for localizing abnormal parathyroid tissue. We recommend its routine use in patients with persistent or recurrent hypercalcemia following neck exploration for primary hyperparathyroidism who have no evidence of thyroid disorders.

Pressor responsiveness in renal prehypertensive rabbits with a denervated kidney.

Norepinephrine was infused iv at several doses into four groups of conscious rabbits (six per group), and the pressor responses were recorded. The groups were 3-day sham-operated rabbits; 3-day, two-kidney rabbits with unilateral renal artery stenosis (RAS); 3-day, two-kidney rabbits with unilateral renal denervation; and 3-day, two-kidney rabbits with unilateral renal denervation plus RAS of the denervated kidney. The rabbits with RAS of an innervated kidney and those with RAS of a denervated kidney had the same pressor responses to norepinephrine, which were greater than the pressor responses in the sham-operated rabbits or in the rabbits with a denervated kidney but without RAS. Four additional groups of similarly prepared rabbits were infused with norepinephrine at 800 ng/min/kg body wt, and mean arterial pressure and cardiac output were determined before and during norepinephrine infusion. The rabbits with RAS of an innervated or of a denervated kidney had greater increases in total peripheral resistance as well as in mean arterial pressure during norepinephrine infusion than did the two groups of rabbits without RAS. This indicated that the rabbits with RAS also had increased vascular responses to norepinephrine. The concentration of norepinephrine in six denervated kidneys was extremely low as compared to that of six innervated kidneys. Because renal denervation did not diminish pressor and vascular hyperresponsiveness in 3-day RAS rabbits, the signal that originates in the kidney following RAS and that results ultimately in pressor and vascular hyperresponsiveness is not mediated by renal nerves.

A fast-acting humoral factor mediates pressor hyperresponsiveness in deoxycorticosterone-salt rabbits.

Six rabbits were sham operated and were given water to drink (sham-water group); six additional rabbits were sham operated and were given saline to drink (sham-salt group); another six rabbits received an implant of deoxycorticosterone (DOCA) and were given water to drink (DOCA-water group); a final group of six rabbits received implants of DOCA and were given saline to drink (DOCA-salt group). Two weeks later, all four groups of rabbits had approximately the same mean arterial pressures, and the sham-salt, DOCA-water, and DOCA-salt groups all had plasma renin activity values less than the sham-water group. The DOCA-salt group had greater pressor responses to norepinephrine (NE) at several doses than did the other three groups of rabbits. In another group of six sham-water and six DOCA-salt rabbits, measurements of cardiac output before and during infusions of NE at 800 ng/min/kg body wt revealed no changes in cardiac output before or during NE infusion, but the DOCA-salt group had significantly greater increases in mean arterial pressure and total peripheral resistance during NE than did the sham-water group. In another group of six DOCA-salt rabbits, the pressor response to several doses of NE were determined during infusion of the angiotensin II (AII) antagonist, [Sar1, Ile8] AII; this AII antagonist failed to alter the enhanced pressor responses to NE. A final experiment examined pressor responses to NE in six normal rabbits before and after cross circulation of blood with six DOCA-salt rabbits. After blood cross circulation the normal rabbits had exaggerated pressor responses to NE at 5, 15, and 30 min, but not at 60 min. Similar cross-circulation experiments between six pairs of normal rabbits did not show any transfer of pressor hyperresponsiveness. These studies indicated that pressor and vascular hyperresponsiveness in DOCA-salt rabbits is conveyed by a fast-acting hormonal factor and that AII probably is not involved in mediating this hyperresponsiveness.

Pressor hyperresponsiveness in saline-infused rabbits.

Conscious rabbits infused intravenously (i.v.) with isotonic saline at 1.5 to 1.8 ml/min for 24 hours had greater pressor responses to norepinephrine (NE) than did normal control rabbits. Infusion of the angiotension II (ANG II) antagonist [Sar1, Ile8] ANG II did not decrease the exaggerated pressor responses to NE in saline-infused rabbits. Measurements of cardiac output (CO) as well as the pressor responses to NE before and after saline infusion revealed that, although saline infusion increased the CO and decreased total peripheral resistance (TPR), CO did not change during NE infusion either before or after saline infusion, but NE produced significantly greater increases in mean arterial pressure (MAP) and TPR after saline infusion than before the saline infusion. The cross-circulation of blood at 10 ml/min for 5 minutes between saline-infused donor rabbits and normal recipient rabbits resulted in pressor hyperresponsiveness to NE in the normal recipients. Similar cross-circulation experiments between pairs of normal rabbits did not alter the pressor responses to NE. These studies provided direct evidence that expansion of body fluid volumes by saline infusion results in pressor and vascular hyperresponsiveness. There was no evidence to indicate that ANG II was involved in the mechanisms producing this pressor hyperresponsiveness. Some circulating hormonal factor, however, was involved in mediating the pressor hyperresponsiveness following saline infusion. The results of this study are compatible with the concept that natriuretic hormone may play a role in promoting pressor hyperresponsiveness in saline-expanded animals.

Humoral factor in pressor hyperresponsiveness in renal prehypertensive rabbits.

Prehypertensive rabbits with renal artery stenosis of 3 days' duration (one-kidney, one clip) are known to have increased pressor responses to norepinephrine and vasopressin; this pressor hyperresponsiveness is restored to normal by the angiotensin II (AII) antagonist, [ Sar1, Ile8 ] AII, even though plasma renin activity (PRA) and plasma AII concentrations are not elevated. In the present study, the cross-circulation of blood between conscious one-kidney, 3-day renal artery stenosis rabbits and conscious normal rabbits resulted in the transfer of pressor hyperresponsiveness to the normal rabbits, although both groups of rabbits had normal values for PRA. A similar cross-circulation of blood between one-kidney rabbits without renal artery stenosis and normal rabbits did not alter the pressor responsiveness of the normal rabbits to norepinephrine. It was concluded that a circulating humoral factor is involved in mediating pressor hyperresponsiveness in 3-day renal artery stenosis rabbits. To evaluate the interrelationship between AII and the hormonal hyperresponsiveness factor, an additional experiment was performed in which blood was cross-circulated between one-kidney, 3-day renal artery stenosis rabbits and normal rabbits, with the normal rabbits receiving [ Sar1, Ile8 ] AII immediately following cross-circulation. Administration of this AII antagonist to the normal rabbits prevented them from showing pressor hyperresponsiveness following the cross-circulation of blood. It is concluded that in this prehypertensive renal artery stenosis model the humoral hyperresponsiveness factor exerts its effect through AII mechanisms, rather than AII acting to increase the release or secretion of the hyperresponsiveness factor.

Vascular trauma in a rural population.

Most reports on vascular trauma from metropolitan centers indicate that prompt repair of injuries contributes to significant limb salvage. A review of 89 cases of vascular trauma seen during the past 10 years revealed higher amputation and complication rates than are usually experienced at urban centers. The University of Missouri Health Sciences Center serves a predominately rural area of 10,000 square miles. The average delay between injury and arrival at the center was 3.4 hours. Farm and industrial accidents accounted for 16% of the cases, motor vehicle accidents 33%, and penetrating wounds from guns, knives, and glass the remainder. Eighty-two percent of the injuries involved extremities, and 12 of 116 injured vessels were veins. Arteriography was performed in 34% of the patients. Surgery consisted of primary repair or autogenous vein graft in 60% of the vessels and ligation in approximately 35%. Thirteen primary amputations were performed for extensive tissue damage. There were six additional delayed amputations, yielding an overall amputation rate of 16.4%. The mortality rate was 5.6%, with deaths occurring only in patients with multiple severe injuries. The complication rate associated with vascular repair was 12.4%. Most complications and all deaths and amputations occurred in patients suffering trauma from farm, industrial, and motor vehicle accidents. These patients also had longer times in transit. The increased amputation and complication rates appear to be related to the severity of injuries and the time lapse before initiation of definitive therapy.