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A study comprising 221 women sterilized laparoscopically with Filshie Clips is presented. The pregnancy rate was 1.36%, which is considered acceptable as the method was new in the Department and performed by 10 surgeons with different degrees of skill in laparoscopy.
A 69-year-old male underwent a radical retropubic prostatectomy for prostate cancer. He presented severe perineal pain that prevented him from sitting normally after removal of the urethral catheter. Cystography and echography disclosed a possible aetiology that was later confirmed by cystoscopy: a metal clip protruding into the urethra through the urethrovesical anastomosis.
We report a case of a 58-year-old woman who presented with an aneurysmal subarachnoid haemorrhage. Immediately following clipping of this aneurysm, she had a spontaneous hypertensive bleed in the contralateral hemisphere. Although very unusual, hypertensive episodes following aneurysmal subarachnoid haemorrhage must carry a risk of such an intracranial event.
An endoscopic probe has been used intraoperatively to facilitate the obliteration of cerebral aneurysms. This method has been used in 24 patients with 30 arterial aneurysms. There were 13 males and 11 females. They ranged in age from 22 to 73 years (mean age 48 years). The mean time of surgery was 7.3 days after subarachnoid haemorrhage (ranging from 2 to 24 days). In three cases there was intraoperative rupture of the aneurysm and with one patient the operation had to be abandoned because of severe brain oedema. The follow-up ranged from 12 to 48 weeks (average 31.8 weeks). The overall outcome was good in 14 cases (58.3%), eight patients (33.3%) showed moderate disability, severe disability occurred in one patient (4%) and one patient (4%) died. In all cases when the endoscope was used, there was a striking improvement in the visualisation of the anatomy of the aneurysm and surrounding structures. Furthermore, the position of the clip and the state of the vessels leading to and from the aneurysm could be easily examined.
For those patients with reduced dynamic range of hearing, accomodation of normal dynamic range of speech has always presented a problem. This paper describes a method of overcoming the problem, a method which has the added benefit of offering improved speech discrimination as well as limiting the output from a hearing aid system. The principle employed is the presentation of taped speech material processed through clipping of a radio frequency single side side band suppressed carrier signal, which is filtered to remove the Fourier components and demodulated to obtain the modified speech material. Groups of normally hearing and hearing impaired subjects undergo speech audiometry testing to assess what improvement can be effected by this system. The majority of subjects tested both normal and hearing impaired achieve improved speech discrimination when using the system described. Further once the output was set no increase in the input signal could produce a level in excess of that set by the output control.
The effect of the increased cardiac output of two-kidney, one-clip Goldblatt hypertension (2-KGH) on the altered vascular responses to vasoactive agents was examined in the conscious, chronically instrumented dog. The early stage of 2-KGH is characterized by an increased arterial pressure, an increased aortic flow, a decreased total peripheral resistance, and enhanced responses to angiotensin II and serotonin. As the aortic flow increases the responses to norepinephrine are enhanced, and the dilator responses to acetyl-choline and nitroglycerin are depressed. Aortic flow then returns to control values and the increased arterial pressure is maintained by an increase in peripheral resistance. When the increased aortic flow is prevented by occluding the vena cava to maintain flow at control values, the vascular responses to each of the agonists do not differ from that obtained when the aortic flow is elevated. Moreover, the temporal development and magnitude of the elevation in arterial pressure resulting from the increased vascular resistance is similar in dogs with an increased and normal aortic flows. The results suggest that increased aortic flow is not essential for the increased vascular resistance or the vascular changes in the canine model of 2-KGH.
Cumulative contractile responses to norepinephrine (NE), their potentiation with cocaine and their inhibition by diltiazem, cumulative relaxation responses to adenosine and acetylcholine, and contractile responses to 140 mM K+ were studied in isolated mesenteric resistance vessels (ca 175 mu internal diameter) from 2-kidney, 1 clip (2K-1C) Goldblatt hypertensive Wistar rats (2 week duration) and sham-operated controls. No difference in calculated internal diameter, NE sensitivity (before or after inclusion of cocaine in the bath), maximum NE-induced tension, or rate of relaxation after NE washout was found between the two groups. However, the contractile responses to NE in the presence of diltiazem were greater, and acetylcholine and adenosine were less effective in relaxing NE-induced contractions in vessels from 2K-1C Goldblatt hypertensive rats. Depolarization with 140 mM K+ induced equivalent contractions in the two groups and were inhibited to the same extent by 10(-6) M phentolamine, indicating that the contribution of catecholamines released from sympathetic nerve endings by the 140 mM K+ to the K+ induced contraction was equivalent in the two groups. Decreased relaxation of NE-induced contractions reflects a functional alteration in vascular smooth muscle of resistance vessels from 2K-1C rats that may contribute to the development of elevated total peripheral resistance in this model of hypertension.
Hemodynamic effects of captopril were examined in chronic one-kidney, one clip renal hypertensive rabbits and normotensive controls either in normal sodium or in sodium depletion. The mean arterial pressure (MAP) of hypertensive and normotensive rabbits in sodium depletion did not differ from that in normal sodium, while plasma renin activity (PRA) was elevated by sodium depletion. The cardiac output of sodium depleted groups decreased slightly. The increase in total peripheral resistance was greater in hypertensive than in normotensive groups. The MAP in all groups was decreased by acute administration of captopril irrespective of sodium intake. The decrease in MAP in the sodium-depleted hypertensive group was correlated with the control values of PRA, but no correlation was observed in other groups. Captopril significantly reduced the cardiac output of the sodium-depleted hypertensive group, but not of the other groups. These results show that: (1) the lowering effect of captopril on arterial pressure is not mediated only by blocking of the renin-angiotensin system, and (2) the decrease in cardiac output with captopril in sodium depleted hypertensive rabbits is an important factor in the reduction in the arterial pressure.
Exchangeable 22Na (ExNa), total body water (TBW) and the inulin space (InSp) were determined in two-kidney, two-clip (2K-2C) hypertensive and sham operated (normotensive) control rats 6-8 weeks after surgery. TBW (ml/kg lean body weight) was the same in hypertensive and sham rats. In contrast, ExNa (mEq/kglbw) and InSp (ml/kglbw) significantly increased (p less than 0.01) in rats whose hypertension did not exceed 170 mmHg. Consequently, sham, moderate hypertensive (less than 170 mmHg) and severe hypertensive (less than 170 mmHg) animals showed equal TBW but differed in body water distribution in that moderately hypertensive animals displayed a redistribution of water in favor of the extracellular space.
Television microscopy was used to quantify in vivo resting venular diameters and the responses to topically applied norepinephrine in the cremaster muscle of two groups of urethanchloralose anesthetized rats: normotensive rats (NT) and one-kidney, one-clip Goldblatt hypertensive rats (1K1C). Observations were made two weeks after the surgery which was used to induce renovascular hypertension. At this stage, we have previously observed an increase in arteriolar reactivity (1). In the current study, mean arterial blood pressures for 1K1C (149 +/- 5 mmHg) were significantly higher than pressures for NT (102 +/- 3 mmHg). Venules were categorized by branching order and venular diameters were measured at three different levels of the microcirculation: first (1V), second (2V), and third order (3V) venules. Reactivity to norepinephrine at all venular levels in the 1K1C group was similar to that recorded for the NT group. Resting venular luminal diameters, however, were significantly smaller (20%) for large (1V) venules of the HT group (137 +/- 9 micron) compared to those for the NT group (171 +/- 10 micron). Thus, in contrast to previously reported data for arterioles, a structural venoconstriction and not an increase in venular reactivity appears to characterize the early vascular changes associated with this form of renovascular hypertension.
The in vivo reactivity of small arterioles to norepinephrine and to changes in external calcium was investigated in normotensive (NT) and one-kidney, one-clip Goldblatt hypertensive rats (1K1C). Rats were anesthetized with sodium pentobarbital (50 mg/kg) and arterioles in the cremaster muscle were exposed to increasing concentrations of either norepinephrine (10(-10) to 10(-5) M) or of bath calcium (0 to 5.1 mM). Third-order arterioles of 1K1C showed almost a ten-fold increased reactivity to NE compared to arterioles of NT rats (pD2 values of 7.88 +/- .43 vs 6.92 +/- .30). Arterioles of 1K1C rats showed an increased reactivity to re-exposure to calcium (0.65 to 5.10 mM). Following exposure to phentolamine this hyper-reactivity was abolished and arterioles of 1K1C and NT exhibited similar responses to changes in bath calcium concentrations, suggesting that the increased reactivity in the 1K1C was due to stimulation of endogenous norepinephrine release. When arterioles were exposed to increasing bath concentrations of the calcium entry blockers, verapamil and diltiazem, dilator responses were similar for 1K1C and NT groups. Collectively, these data suggest that during the development of renovascular hypertension, observed increases in arteriolar reactivity involve an increase in the receptor mediated entry of extracellular calcium into vascular smooth muscle and no change in non-receptor-mediated entry of calcium.
We reported that the pups of one kidney:one-clip Goldblatt hypertensive (HT) rats have a predisposition to the induction of experimental hypertension. To investigate the nature of the predisposition, pups of HT dams were challenged with vasopressor agents at 28-days-of-age or treated with DOCA and 6.5% salt diet between 35 and 81 days-of-age. Pups of HT dams had a significantly greater blood pressure between 28 and 81 days-of-age and also showed a greater change in blood pressure when provided a 6.5% salt diet than did pups of normotensive dams. Pups of HT dams demonstrated a decreased bradycardic response after injection of angiotensin II (p less than .05) and a lesser change in mean arterial blood pressure after injection of angiotensin II or norepinephrine than did the pups from normotensive dams. These results suggest an effect of maternal hypertension on the development of cardiovascular control mechanisms in her offspring. The decreased pressor response suggests the predisposition is not due to an increased vascular sensitivity to vasopressors.
The role of vasopressin (AVP) in the maintenance of hypertension in the rat model of two-kidney, one-clip (2K1C) Goldblatt hypertension was assessed using the nonpeptide orally effective V1a receptor antagonist, OPC-21268. Rats were studied eight weeks after surgery when mean arterial pressure (MAP) was significantly increased in 2K1C rats compared to SHAM operated controls (2K1C 139 +/- 6, SHAM 106 +/- 3, P < 0.01). Neither acute (OPC-21268, 30 mg/kg) nor chronic (OPC-21268, 30 mg/kg twice daily) V1a receptor blockade reduced blood pressure in either 2K1C or SHAM rats. The results of binding kinetic studies confirmed that OPC-21268 was effective at its putative site of action, the V1a receptor in both 2K1C and SHAM rats. These results indicate AVP is not involved in the maintenance of blood pressure in the 2K1C model of renovascular hypertension.
An 82-year-old woman was admitted to our hospital because of hematemesis. She had had a feeling of a foreign substance in her throat for one week after having eaten fish. On admission she had a fever of 38 degrees C, Hb of 5.8 g/dl, CRP level of 8.8 mg/dl, and bilateral pleural effusions. Endoscopy revealed a deep longitudinal laceration with active bleeding in the esophagus that also caused mediastinitis. Endoscopic hemostasis and closure of the laceration was done with hemostatic clips. The esophageal injury seemed to have been caused by a fish bone. After the treatments described here were carried out, the patient's condition rapidly improved.
The opening force of aneurysm clips can be determined easily with a dynamometer tension guage. The method is described.
A case is reported in which a Heifetz aneurysm clip, applied for the treatment of an aneurysm of the posterior inferior cerebellar artery, slipped and migrated into the cauda equina resulting in lumbar radiculopathy. Related reports are discussed briefly.
If the main feeder of an arteriovenous malformation (AVM) is a branch of the middle cerebral artery, one segment of which lies on the brain surface, it is advisable to clip it through a burr hole placed at an angiographically preselected point. The technical details of the procedure are described. This simple maneuver performed directly prior to radical surgery decreases the risk of possible rupture of an AVM during craniotomy and facilitates radical AVM excision.
The author reports a case in which a subchiasmal carotid-ophthalmic artery aneurysm was clipped through a bifrontal interhemispheric approach. This approach is feasible for carotid-ophthalmic artery aneurysms with a variety of anatomical correlations between the optic nerve and the aneurysmal neck.